Статті в журналах: "CAPNS1"

1

Kumar, Vijay, Chris Hall, Peter Greer, and Andrew Craig. "Calpain proteases are required for effective clearance of enterobacteria within the peritoneum of mice to prevent systemic infection (112.5)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 112.5. http://dx.doi.org/10.4049/jimmunol.188.supp.112.5.

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Abstract The ubiquitously expressed calpain 1 and 2 isoforms are heterodimers consisting of a catalytic subunit (capn1 or capn2), and a common regulatory capns1-encoded subunit, which is required for protease stability and activity. Although calpains regulate neutrophil and macrophage activation, their roles in immunity remain poorly defined. Here, we use fes-driven Cre recombinase (fes-Cre) to delete capns1 in mice, thus eliminating calpain 1/2 activity in Cre-expressing cells. We detect near complete capns1 deletion in hematopoietic cells, consistent with the tissue-specific expression pattern of fes. Next, we compared the response of control and capns1 targeted mice in the feces-in-peritoneum (FIP) model of sepsis (i.p. injection of enterobacteria). At 2-6 hours post infection, mice were sacrificed and bacterial load, neutrophil recruitment, and cytokine levels in peritoneal lavage fluid (PLF) and peripheral blood were compared between genotypes. We observed comparable levels of neutrophil infiltration and cytokine production in PLF from control and capns1 targeted FIP-treated mice. However, bacterial killing was highly reduced (>10-fold) in capns1 targeted compared to control mice; and this correlated with increased enterobacterial escape to the peripheral blood. These observations suggest that calpains are not required for inflammatory cytokine production or neutrophil recruitment, but they are required for bacterial clearance, and may protection against development of sepsis.

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2

Piper, Ann-Katrin, Reece A. Sophocleous, Samuel E. Ross, Frances J. Evesson, Omar Saleh, Adam Bournazos, Joe Yasa, et al. "Loss of calpains-1 and -2 prevents repair of plasma membrane scrape injuries, but not small pores, and induces a severe muscular dystrophy." American Journal of Physiology-Cell Physiology 318, no. 6 (June 1, 2020): C1226—C1237. http://dx.doi.org/10.1152/ajpcell.00408.2019.

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The ubiquitous calpains, calpain-1 and -2, play important roles in Ca2+-dependent membrane repair. Mechanically active tissues like skeletal muscle are particularly reliant on mechanisms to repair and remodel membrane injury, such as those caused by eccentric damage. We demonstrate that calpain-1 and -2 are master effectors of Ca2+-dependent repair of mechanical plasma membrane scrape injuries, although they are dispensable for repair/removal of small wounds caused by pore-forming agents. Using CRISPR gene-edited human embryonic kidney 293 (HEK293) cell lines, we established that loss of both calpains-1 and -2 ( CAPNS1−/−) virtually ablates Ca2+-dependent repair of mechanical scrape injuries but does not affect injury or recovery from perforation by streptolysin-O or saponin. In contrast, cells with targeted knockout of either calpain-1 ( CAPN1−/−) or -2 ( CAPN2−/−) show near-normal repair of mechanical injuries, inferring that both calpain-1 and calpain-2 are equally capable of conducting the cascade of proteolytic cleavage events to reseal a membrane injury, including that of the known membrane repair agent dysferlin. A severe muscular dystrophy in a murine model with skeletal muscle knockout of Capns1 highlights vital roles for calpain-1 and/or -2 for health and viability of skeletal muscles not compensated for by calpain-3 ( CAPN3). We propose that the dystrophic phenotype relates to loss of maintenance of plasma membrane/cytoskeletal networks by calpains-1 and -2 in response to directed and dysfunctional Ca2+-signaling, pathways hyperstimulated in the context of membrane injury. With CAPN1 variants associated with spastic paraplegia, a severe dystrophy observed with muscle-specific loss of calpain-1 and -2 activity identifies CAPN2 and CAPNS1 as plausible candidate neuromuscular disease genes.

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3

Mellgren, Ronald L., and Xinhua Huang. "Fetuin A Stabilizes m-Calpain and Facilitates Plasma Membrane Repair." Journal of Biological Chemistry 282, no. 49 (October 17, 2007): 35868–77. http://dx.doi.org/10.1074/jbc.m706929200.

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Yeast two-hybrid experiments identified α2-Heremans-Schmid glycoprotein (human fetuin A) as a binding partner for calpain domain III (DIII). The tandem DIIIs of calpain-10 interacted under the most selective culture conditions, but DIIIs of m-calpain, calpain-3, and calpain-5 also interacted under less stringent selection. DIIIs of μ-calpain, calpain-6, and the tandem DIII-like domains of the Dictyostelium Cpl protein did not interact with α2-Heremans-Schmid glycoprotein in the yeast two-hybrid system. Bovine fetuin A stabilized proteolytic activity of purified m-calpain incubated in the presence of mm calcium chloride and prevented calcium-dependent m-calpain aggregation. Consistent with the yeast two-hybrid studies, fetuin A neither stabilized μ-calpain nor prevented its aggregation. Confocal immunofluorescence microscopy of scratch-damaged L6 myotubes demonstrated accumulation of m-calpain at the wound site in association with the membrane repair protein, dysferlin. m-Calpain also co-localized with fluorescein-labeled fetuin A at the wound site. The effect of fetuin A on calpain-mediated plasma membrane resealing was investigated using fibroblasts from Capns1-/- and Capns1+/+ mouse embryos. Capns1 encodes the small noncatalytic subunit that is required for the proteolytic function of m- and μ-calpains. Thus, Capns1-/- fibroblasts do not express these calpains in active form. Fetuin A increased resealing of scrape-damaged wild-type fibroblasts but not Capns1-/- fibroblasts. These studies identify fetuin A as a potential extracellular regulator of m-calpain at nascent sites of plasma membrane wounding.

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4

Tyagi, Tarun, Shadab Ahmad, Neha Gupta, Anita Sahu, Yasmin Ahmad, Velu Nair, Tathagat Chatterjee, et al. "Altered expression of platelet proteins and calpain activity mediate hypoxia-induced prothrombotic phenotype." Blood 123, no. 8 (February 20, 2014): 1250–60. http://dx.doi.org/10.1182/blood-2013-05-501924.

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Key Points Hypoxia induces altered platelet proteome/reactivity, which correlates with a prothrombotic phenotype. CAPNS1-dependent calpain activity in platelet activation cascade is associated with hypoxia-induced thrombogenesis.

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5

Demarchi, Francesca, Cosetta Bertoli, Tamara Copetti, Isei Tanida, Claudio Brancolini, Eeva-Liisa Eskelinen, and Claudio Schneider. "Calpain is required for macroautophagy in mammalian cells." Journal of Cell Biology 175, no. 4 (November 13, 2006): 595–605. http://dx.doi.org/10.1083/jcb.200601024.

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Ubiquitously expressed micro- and millicalpain, which both require the calpain small 1 (CAPNS1) regulatory subunit for function, play important roles in numerous biological and pathological phenomena. We have previously shown that the product of GAS2, a gene specifically induced at growth arrest, is an inhibitor of millicalpain and that its overexpression sensitizes cells to apoptosis in a p53-dependent manner (Benetti, R., G. Del Sal, M. Monte, G. Paroni, C. Brancolini, and C. Schneider. 2001. EMBO J. 20:2702–2714). More recently, we have shown that calpain is also involved in nuclear factor κB activation and its relative prosurvival function in response to ceramide, in which calpain deficiency strengthens the proapoptotic effect of ceramide (Demarchi, F., C. Bertoli, P.A. Greer, and C. Schneider. 2005. Cell Death Differ. 12:512–522). Here, we further explore the involvement of calpain in the apoptotic switch and find that in calpain-deficient cells, autophagy is impaired with a resulting dramatic increase in apoptotic cell death. Immunostaining of the endogenous autophagosome marker LC3 and electron microscopy experiments demonstrate that autophagy is impaired in CAPNS1-deficient cells. Accordingly, the enhancement of lysosomal activity and long-lived protein degradation, which normally occur upon starvation, is also reduced. In CAPNS1-depleted cells, ectopic LC3 accumulates in early endosome-like vesicles that may represent a salvage pathway for protein degradation when autophagy is defective.

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6

Liang, Liwen, Huili Li, Ting Cao, Lina Qu, Lulu Zhang, Guo-Chang Fan, Peter A. Greer, Jianmin Li, Douglas L. Jones, and Tianqing Peng. "Calpain activation mediates microgravity-induced myocardial abnormalities in mice via p38 and ERK1/2 MAPK pathways." Journal of Biological Chemistry 295, no. 49 (September 28, 2020): 16840–51. http://dx.doi.org/10.1074/jbc.ra119.011890.

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The human cardiovascular system has adapted to function optimally in Earth's 1G gravity, and microgravity conditions cause myocardial abnormalities, including atrophy and dysfunction. However, the underlying mechanisms linking microgravity and cardiac anomalies are incompletely understood. In this study, we investigated whether and how calpain activation promotes myocardial abnormalities under simulated microgravity conditions. Simulated microgravity was induced by tail suspension in mice with cardiomyocyte-specific deletion of Capns1, which disrupts activity and stability of calpain-1 and calpain-2, and their WT littermates. Tail suspension time-dependently reduced cardiomyocyte size, heart weight, and myocardial function in WT mice, and these changes were accompanied by calpain activation, NADPH oxidase activation, and oxidative stress in heart tissues. The effects of tail suspension were attenuated by deletion of Capns1. Notably, the protective effects of Capns1 deletion were associated with the prevention of phosphorylation of Ser-345 on p47phox and attenuation of ERK1/2 and p38 activation in hearts of tail-suspended mice. Using a rotary cell culture system, we simulated microgravity in cultured neonatal mouse cardiomyocytes and observed decreased total protein/DNA ratio and induced calpain activation, phosphorylation of Ser-345 on p47phox, and activation of ERK1/2 and p38, all of which were prevented by calpain inhibitor-III. Furthermore, inhibition of ERK1/2 or p38 attenuated phosphorylation of Ser-345 on p47phox in cardiomyocytes under simulated microgravity. This study demonstrates for the first time that calpain promotes NADPH oxidase activation and myocardial abnormalities under microgravity by facilitating p47phox phosphorylation via ERK1/2 and p38 pathways. Thus, calpain inhibition may be an effective therapeutic approach to reduce microgravity-induced myocardial abnormalities.

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7

Cataldo, F., L. Y. Peche, E. Klaric, C. Brancolini, M. P. Myers, F. Demarchi, and C. Schneider. "CAPNS1 Regulates USP1 Stability and Maintenance of Genome Integrity." Molecular and Cellular Biology 33, no. 12 (April 15, 2013): 2485–96. http://dx.doi.org/10.1128/mcb.01406-12.

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8

Pisanu, Merkouri Papadima, Melis, Congiu, Loizedda, Orrù, Calza, et al. "Whole Genome Expression Analyses of miRNAs and mRNAs Suggest the Involvement of miR-320a and miR-155-3p and their Targeted Genes in Lithium Response in Bipolar Disorder." International Journal of Molecular Sciences 20, no. 23 (November 30, 2019): 6040. http://dx.doi.org/10.3390/ijms20236040.

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Lithium is the mainstay in the maintenance of bipolar disorder (BD) and the most efficacious pharmacological treatment in suicide prevention. Nevertheless, its use is hampered by a high interindividual variability and important side effects. Genetic and epigenetic factors have been suggested to modulate lithium response, but findings so far have not allowed identifying molecular targets with predictive value. In this study we used next generation sequencing to measure genome-wide miRNA expression in lymphoblastoid cell lines from BD patients excellent responders (ER, n = 12) and non-responders (NR, n = 12) to lithium. These data were integrated with microarray genome-wide expression data to identify pairs of miRNA/mRNA inversely and significantly correlated. Significant pairs were prioritized based on strength of association and in-silico miRNA target prediction analyses to select candidates for validation with qRT-PCR. Thirty-one miRNAs were differentially expressed in ER vs. NR and inversely correlated with 418 genes differentially expressed between the two groups. A total of 331 of these correlations were also predicted by in-silico algorithms. miR-320a and miR-155-3p, as well as three of their targeted genes (CAPNS1 (Calpain Small Subunit 1) and RGS16 (Regulator of G Protein Signaling 16) for miR-320, SP4 (Sp4 Transcription Factor) for miR-155-3p) were validated. These miRNAs and mRNAs were previously implicated in psychiatric disorders (miR-320a and SP4), key processes of the central nervous system (CAPNS1, RGS16, SP4) or pathways involved in mental illnesses (miR-155-3p). Using an integrated approach, we identified miRNAs and their targeted genes potentially involved in lithium response in BD.

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9

Rodríguez-Fernández, Lucía, Iván Ferrer-Vicens, Concha García, Sara S. Oltra, Rosa Zaragozá, Juan R. Viña, and Elena R. García-Trevijano. "Isoform-specific function of calpains in cell adhesion disruption: studies in postlactational mammary gland and breast cancer." Biochemical Journal 473, no. 18 (September 12, 2016): 2893–909. http://dx.doi.org/10.1042/bcj20160198.

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Cleavage of adhesion proteins is the first step for physiological clearance of undesired cells during postlactational regression of the mammary gland, but also for cell migration in pathological states such as breast cancer. The intracellular Ca2+-dependent proteases, calpains (CAPNs), are known to cleave adhesion proteins. The isoform-specific function of CAPN1 and CAPN2 was explored and compared in two models of cell adhesion disruption: mice mammary gland during weaning-induced involution and breast cancer cell lines according to tumor subtype classification. In both models, E-cadherin, β-catenin, p-120, and talin-1 were cleaved as assessed by western blot analysis. Both CAPNs were able to cleave adhesion proteins from lactating mammary gland in vitro. Nevertheless, CAPN2 was the only isoform found to co-localize with E-cadherin in cell junctions at the peak of lactation. CAPN2/E-cadherin in vivo interaction, analyzed by proximity ligation assay, was dramatically increased during involution. Calpain inhibitor administration prevented the cytosolic accumulation of truncated E-cadherin cleaved by CAPN2. Conversely, in breast cancer cells, CAPN2 was restricted to the nuclear compartment. The isoform-specific expression of CAPNs and CAPN activity was dependent on the breast cancer subtype. However, CAPN1 and CAPN2 knockdown cells showed that cleavage of adhesion proteins and cell migration was mediated by CAPN1, independently of the breast cancer cell line used. Data presented here suggest that the subcellular distribution of CAPN1 and CAPN2 is a major issue in target-substrate recognition; therefore, it determines the isoform-specific role of CAPNs during disruption of cell adhesion in either a physiological or a pathological context.

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10

Santos, Sara Costa, Lucas De Sousa Pontes, Maria Elisabete Amaral De Moraes, and Caroline De Fátima Aquino Moreira-Nunes. "Identificação de alterações genéticas relacionadas à síndrome do X frágil e ao transtorno de espectro do autismo por meio de ferramentas de bioinformática." Revista de Ciências Médicas e Biológicas 19, no. 2 (September 24, 2020): 292. http://dx.doi.org/10.9771/cmbio.v19i2.34910.

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Introdução: a Síndrome do X Frágil (FXS) é a forma mais prevalente de deficiência intelectual herdável, e é a principal causa monogênica para o desenvolvimento de Transtorno de Espectro do Autismo (TEA). Objetivo: o objetivo do presente estudo é identificar RNAm associados à possíveis vias neurocomportamentais na SFX como no TEA, através de ferramentas de bioinformática. Metodologia: para identificação de possíveis vias alteradas entre a SFX e pacientes com TEA, utilizamos os bancos de dados GSE65106 e GSE21348 para anotação, visualização e descoberta integrada (DAVID 6.8). O valor de p <0,05 e fold change maior que 2 vezes (FC > 2) definidos como os limiares para a identificação de genes diferencialmente expressos (DE-RNAm). Resultados: foi possível identificar cerca de 32 DE-RNAm com funções em vias de spliceossomo, apoptose, transcrição, e em vias neurológicas comportamentais expressos exclusivamente na SFX. Os genes CAPNS1, HNRNPK, HNRPM, foram identificados como hipoexpressos em indivíduos com síndrome do X Frágil. Estes genes tem importante função moduladora nas respostas do potencial de longo prazo (LTP), plasticidade neural, e em transportadores de serotonina (SERT) alterando respostas que englobam humor, cognição e comportamentos, além de interferirem no receptor de dopamina (D2R) alterando as funções motoras e circuitos de recompensa. Conclusão: os genes CAPNS1, HNRNPK, HNRNPM foram identificados como marcadores genéticos neurocomportamentais importantes para a síndrome do X-frágil com expressão diminuída na doença, indicando uma possível modulação desses genes em aspectos fenotípicos marcantes da doença.

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11

Gandolfi, G., M. U. Cinar, S. Ponsuksili, K. Wimmers, D. Tesfaye, C. Looft, H. Jüngst, et al. "Association of PPARGC1A and CAPNS1 gene polymorphisms and expression with meat quality traits in pigs." Meat Science 89, no. 4 (December 2011): 478–85. http://dx.doi.org/10.1016/j.meatsci.2011.05.015.

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12

Zhang, Yajie, Wenxia Xu, Pan Ni, Aiping Li, Jianwei Zhou, and Shan Xu. "MiR-99a and MiR-491 Regulate Cisplatin Resistance in Human Gastric Cancer Cells by Targeting CAPNS1." International Journal of Biological Sciences 12, no. 12 (2016): 1437–47. http://dx.doi.org/10.7150/ijbs.16529.

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13

Grochowska, E., B. Borys, E. Grześkowiak, and S. Mroczkowski. "Effect of the calpain small subunit 1 gene ( CAPNS1 ) polymorphism on meat quality traits in sheep." Small Ruminant Research 150 (May 2017): 15–21. http://dx.doi.org/10.1016/j.smallrumres.2017.02.022.

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14

Juszczuk-Kubiak, E., K. Flisikowski, and K. Wicińska. "A new SNP in the 3′UTR region of the bovine calpain small subunit (CAPNS1) gene." Molecular Biology Reports 37, no. 1 (August 2, 2009): 473–76. http://dx.doi.org/10.1007/s11033-009-9654-8.

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15

Drögemüller, C., and T. Leeb. "Molecular characterization of the porcine gene CAPNS1 encoding the small subunit 1 of calpain on SSC6q1.1→q1.2." Cytogenetic and Genome Research 98, no. 2-3 (2002): 206–9. http://dx.doi.org/10.1159/000069809.

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16

Asangani, Irfan A., Suhail A. K. Rasheed, Jörg H. Leupold, Stefan Post, and Heike Allgayer. "NRF-1, and AP-1 regulate the promoter of the human calpain small subunit 1 (CAPNS1) gene." Gene 410, no. 1 (February 2008): 197–206. http://dx.doi.org/10.1016/j.gene.2007.12.009.

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17

Xiao, Zilong, Xiang Wei, Minghui Li, Kun Yang, Ruizhen Chen, Yangang Su, Ziqing Yu, Yixiu Liang, and Junbo Ge. "Myeloid-specific deletion of Capns1 attenuates myocardial infarction injury via restoring mitochondrial function and inhibiting inflammasome activation." Journal of Molecular and Cellular Cardiology 183 (October 2023): 54–66. http://dx.doi.org/10.1016/j.yjmcc.2023.08.006.

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18

Fairfax, Benjamin P., Fredrik O. Vannberg, Jayachandran Radhakrishnan, Hakon Hakonarson, Brendan J. Keating, Adrian V. S. Hill, and Julian C. Knight. "An integrated expression phenotype mapping approach defines common variants in LEP, ALOX15 and CAPNS1 associated with induction of IL-6." Human Molecular Genetics 19, no. 4 (November 26, 2009): 720–30. http://dx.doi.org/10.1093/hmg/ddp530.

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19

Pamonsinlapatham, Perayot, Brunilde Gril, Sylvie Dufour, Réda Hadj-Slimane, Véronique Gigoux, Stéphanie Pethe, Sébastien L'Hoste, et al. "Capns1, a new binding partner of RasGAP-SH3 domain in K-RasV12 oncogenic cells: Modulation of cell survival and migration." Cellular Signalling 20, no. 11 (November 2008): 2119–26. http://dx.doi.org/10.1016/j.cellsig.2008.08.005.

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20

Gross, Johann, Heidi Olze, and Birgit Mazurek. "Gene Expression Patterns in Functionally Different Cochlear Compartments of the Newborn Rat." Journal of Molecular Biology Research 5, no. 1 (January 12, 2015): 20. http://dx.doi.org/10.5539/jmbr.v5n1p20.

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In an experimental model of organotypic cultures of the stria vascularis (SV), the organ of Corti (OC) and the modiolus (MOD), we compared the expression levels and injury/hypoxia induced response of 36 genes associated with the cells´ energy-producing and energy-consuming processes, using the microarray technique. A decrease of expression was observed for most of the voltage-dependent K+- and Ca++- channels as an effective mechanism to lower energetic demands. We identified two gene networks of transcripts that are differentially expressed across the three regions. One cluster is associated with the transcription factor hypoxia-inducing factor (Hif-1a) and the second one with the caspase and calpain cell death genes Casp3, Capn1, Capn2 and Capns1. The Hif-1a gene subset consists of genes belonging to the glucose metabolism (glucose transporter Slc2a1, glycolytic enzymes Gapdh, Hk1 and Eno2), the Na+/K+ homeostasis (ATPase Atp1a1) and the glutamate pathway (NMDA receptor associated protein 1 Grina, glutamate transporter Slc1a1, Slc1a3). The Slc2a1, Gapdh, Hk1, Slc1a3, Grina and Atp1a1 transcripts are also members of the cell death subset indicating a role they have to play in the differential regional cell death rates. The newly identified genes Grina and calnexin (Canx) may play specific and yet unknown roles in regulating cell death induced by injury and hypoxia in the inner ear. We assume that the differential regional response occurs on the basis of endogenous gene regulatory mechanisms and may be important to maintaining the cochlea’s function following damage from trauma and hypoxia.

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21

Lin, Yi-Wei, Bomi Lee, Pu-Ste Liu, and Li-Na Wei. "Receptor-Interacting Protein 140 Orchestrates the Dynamics of Macrophage M1/M2 Polarization." Journal of Innate Immunity 8, no. 1 (July 23, 2015): 97–107. http://dx.doi.org/10.1159/000433539.

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Macrophage classical (M1) versus alternative (M2) polarization is critical for the homeostatic control of innate immunity. Uncontrolled macrophage polarization is frequently implicated in diseases. This study reports a new functional role for receptor-interacting protein 140 (RIP140) in regulating this phenotypic switch. RIP140 is required for M1 activation, and its degradation is critical to LPS-induced endotoxin tolerance (ET). Here, we found that failure to establish RIP140 degradation-mediated ET prevents M2 polarization, and reducing RIP140 level facilitates an M1/M2 switch, resulting in more efficient wound healing in animal models generated with either transgenic or bone marrow transplant procedures. The M2-suppressive effect is elicited by a new function of RIP140 that, in macrophages exposed to M2 cues, is exported to cytosol, forming complexes with CAPNS1 (calpain regulatory subunit) to activate calpain 1/2, that activates PTP1B phosphatase. The activated PTP1B then reduces STAT6 phosphorylation, thereby suppressing the efficiency of M2 polarization. It is concluded that RIP140 plays dual roles in regulating the M1-M2 phenotype switch: the first, in the nucleus, is an M1 enhancer and the second, in the cytosol, is an M2 suppressor. Modulating the level and/or subcellular distribution of RIP140 can be a new therapeutic strategy for diseases where inflammatory/anti-inflammatory responses are critical.

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Salgado, Iván, Ernesto Prado Montes de Oca, Isaac Chairez, Luis Figueroa-Yáñez, Alejandro Pereira-Santana, Andrés Rivera Chávez, Jesús Bernardino Velázquez-Fernandez, Teresa Alvarado Parra, and Adriana Vallejo. "Deep Learning Techniques to Characterize the RPS28P7 Pseudogene and the Metazoa-SRP Gene as Drug Potential Targets in Pancreatic Cancer Patients." Biomedicines 12, no. 2 (February 8, 2024): 395. http://dx.doi.org/10.3390/biomedicines12020395.

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The molecular explanation about why some pancreatic cancer (PaCa) patients die early and others die later is poorly understood. This study aimed to discover potential novel markers and drug targets that could be useful to stratify and extend expected survival in prospective early-death patients. We deployed a deep learning algorithm and analyzed the gene copy number, gene expression, and protein expression data of death versus alive PaCa patients from the GDC cohort. The genes with higher relative amplification (copy number >4 times in the dead compared with the alive group) were EWSR1, FLT3, GPC3, HIF1A, HLF, and MEN1. The most highly up-regulated genes (>8.5-fold change) in the death group were RPL30, RPL37, RPS28P7, RPS11, Metazoa_SRP, CAPNS1, FN1, H3−3B, LCN2, and OAZ1. None of their corresponding proteins were up or down-regulated in the death group. The mRNA of the RPS28P7 pseudogene could act as ceRNA sponging the miRNA that was originally directed to the parental gene RPS28. We propose RPS28P7 mRNA as the most druggable target that can be modulated with small molecules or the RNA technology approach. These markers could be added as criteria to patient stratification in future PaCa drug trials, but further validation in the target populations is encouraged.

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Hafidh, Rand R., Zahraa Q. Ali, and Ahmed S. Abdulamir. "Autophagy or Apoptosis: Anticancer Molecular Mechanism of Epigallocatechin Gallate with Natural Polyphenol Effect on HepG2 Cells Viability." Iraqi Journal of Pharmaceutical Sciences ( P-ISSN 1683 - 3597 E-ISSN 2521 - 3512) 32, no. 1 (June 16, 2023): 167–76. http://dx.doi.org/10.31351/vol32iss1pp167-176.

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Background: The anticancer impact of Epigallocatechin gallate (EGCG) the highly active polyphenol of green tea was abundantly studied. Though, the exact mechanism of its cytotoxicity is still under investigation. Objectives: Hence, the current study designed to investigate the molecular target of EGCG in HepG2 cells on thirteen autophagy- and/or apoptosis- related genes. Methods: The apoptosis detection analyses such as flow cytometry and dual apoptosis assay were used. The genes expression profile was explored by the real-time quantitative-PCR. Results: EGCG increases G0/G1 cell cycle arrest and the real-time apoptosis markers proteins leading to stimulate apoptosis in 70% of the treated HepG2 cells. The up-regulation was recorded in two of autophagy inhibitory genes (FOS-1, FOS-2) and apoptosis inducer gene (DDIT3). While the other ten genes expressed down-regulation after treatment. The down regulation was manifested in the genes of mitochondrial autophagy marker proteins (BNIP3, BNIP3L, and NBR1), the autophagy regulator genes (BIRC5, MAPK9), and the gene that implicated in protein biosynthesis and protein modification (ITGB1). The genes that have pro-apoptotic function in cells (CAPNS1, CFLAR, EIF4G, and RB1) were also showed down-regulation after treatment. Conclusion: Thus, the results demonstrated a potential effect of EGCG to induce apoptosis rather than autophagy in the treated HepG2 cells that could play a good target for therapy.

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Ghoreishifar, Seyed Mohammad, Christina Marie Rochus, Sima Moghaddaszadeh-Ahrabi, Pourya Davoudi, Siavash Salek Ardestani, Natalia A. Zinovieva, Tatiana E. Deniskova, and Anna M. Johansson. "Shared Ancestry and Signatures of Recent Selection in Gotland Sheep." Genes 12, no. 3 (March 17, 2021): 433. http://dx.doi.org/10.3390/genes12030433.

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Gotland sheep, a breed native to Gotland, Sweden (an island in the Baltic Sea), split from the Gute sheep breed approximately 100 years ago, and since, has probably been crossed with other breeds. This breed has recently gained popularity, due to its pelt quality. This study estimates the shared ancestors and identifies recent selection signatures in Gotland sheep using 600 K single nucleotide polymorphism (SNP) genotype data. Admixture analysis shows that the Gotland sheep is a distinct breed, but also has shared ancestral genomic components with Gute (~50%), Karakul (~30%), Romanov (~20%), and Fjällnäs (~10%) sheep breeds. Two complementary methods were applied to detect selection signatures: A Bayesian population differentiation FST and an integrated haplotype homozygosity score (iHS). Our results find that seven significant SNPs (q-value < 0.05) using the FST analysis and 55 significant SNPs (p-value < 0.0001) using the iHS analysis. Of the candidate genes that contain significant markers, or are in proximity to them, we identify several belongings to the keratin genes, RXFP2, ADCY1, ENOX1, USF2, COX7A1, ARHGAP28, CRYBB2, CAPNS1, FMO3, and GREB1. These genes are involved in wool quality, polled and horned phenotypes, fertility, twining rate, meat quality, and growth traits. In summary, our results provide shared founders of Gotland sheep and insight into genomic regions maintained under selection after the breed was formed. These results contribute to the detection of candidate genes and QTLs underlying economic traits in sheep.

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Arce-Recinos, Carlos, Alfonso Juventino Chay-Canul, Baldomero Alarcón-Zúñiga, Jesús Alberto Ramos-Juárez, Luis Manuel Vargas-Villamil, Emilio Manuel Aranda-Ibáñez, Nathaly Del Carmen Sánchez-Villegas, and Ricardo Lopez Dias da Costa. "Índices de eficiencia alimenticia en ovinos de pelo: calidad de la carne y genes asociados. Revisión." Revista Mexicana de Ciencias Pecuarias 12, no. 2 (September 15, 2021): 523–52. http://dx.doi.org/10.22319/rmcp.v12i2.5642.

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Los ovinos de pelo desempeñan un papel importante en la producción de carne en zonas tropicales, donde los estudios de eficiencia alimenticia han sido poco evaluados. El consumo de alimento representa más del 70 % de los costos; por lo tanto, la selección de animales con alta eficiencia alimenticia puede mejorar la rentabilidad del sistema de producción. Se han desarrollado herramientas que permiten seleccionar individuos con mayor eficiencia alimenticia sin comprometer la calidad del producto. Por lo que esta revisión tiene la finalidad de identificar estas herramientas genético-moleculares y estadísticas, como son, el consumo de alimento residual (CAR) y ganancia e ingesta residual (GIR). En la literatura consultada, se reportan diferencias en el consumo de materia seca (CMS) en un rango del 9 al 30 % entre animales eficientes e ineficientes, manteniendo una ganancia diaria de peso (GDP) similar empleando el índice CAR. Por otro lado, utilizando el índice GIR los CMS son similares, aunque la GDP en animales eficientes es mayor hasta en 50 g día-1, reduciendo la conversión alimenticia en un kilo. Esta diferencia se asume a un conjunto de genes asociados a la eficiencia alimenticia (Adra2a, Gfra1, Gh, Glis1, Il1rapl1, Lep, Lepr, Mc4r, Oxsm, Pde8b, Rarb, Ryr2, Sox5 y Sox6, Trdn), que pudieran ser utilizados para la selección de ovinos de razas de pelo con alta eficiencia alimenticia, teniendo en cuenta los genes relacionados con la calidad de carne (Capns1, Cast, Dgat1, Fabp4, Igf-i, Lep, Mstn y Scd).

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Luo, Dan, Shaohua Zhan, Wenchao Xia, Liang Huang, Wei Ge, and Tianxiao Wang. "Proteomics study of serum exosomes from papillary thyroid cancer patients." Endocrine-Related Cancer 25, no. 10 (October 2018): 879–91. http://dx.doi.org/10.1530/erc-17-0547.

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Lymph node metastasis (LNM) in papillary thyroid cancer (PTC) is related to increased risk of recurrence and poor prognosis. Tumour exosomes have been shown to be associated with metastasis of cancer cells. Therefore, we aim to identify the characteristics and biological functions of serum exosomes in lymph node metastases of PTC. We compared proteome profiles of serum-purified exosomes (SPEs) from PTC patients with LNM, PTC patients without LNM, and healthy donors, using a combination of liquid chromatography-tandem mass spectroscopy analyses and tandem mass tag label quantitation analysis. We identified 1569 proteins by two or more unique peptides. Compared with the SPEs of PTC patients without LNM, we found 697 differentially expressed proteins in the SPEs of PTC patients with LNM. Our results revealed overexpression of specific proteins with well-established links to cancer cell metastasis, such as SRC, TLN1, ITGB2 and CAPNS1. Consistent with mass spectrum results, we performed Western blot to detect the expression of these proteins in individual sample. Biological pathway analyses showed that integrin signalling was aberrantly activated in the SPEs of PTC patients with LNM compared to those without LNM. Our study reveals that SPEs of PTC patients with lymph node metastases promote BHT101 thyroid cancer cell invasiveness, but have no apparent influence on cell migration. In the serum exosomes of PTC patients with LNM, integrin-associated proteins are obviously upregulated. These proteomic findings will contribute to elucidation of the pathophysiological functions of tumour-derived exosomes.

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Abrouk-Vérot, Lucie, Claire Brun, and Jean-Marie Exbrayat. "Expression Patterns of CAPN1 and CAPN8b Genes during Embryogenesis in Xenopus laevis." CellBio 02, no. 04 (2013): 211–16. http://dx.doi.org/10.4236/cellbio.2013.24024.

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Kulkarni, Yogesh M., Changxing Liu, Qi Qi, Yanmei Zhu, David J. Klinke II, and Jun Liu. "Differential proteomic analysis of caveolin-1 KO cells reveals Sh2b3 and Clec12b as novel interaction partners of caveolin-1 and Capns1 as a potential mediator of caveolin-1-induced apoptosis." Analyst 138, no. 22 (2013): 6986. http://dx.doi.org/10.1039/c3an36819j.

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Perelló-Amorós, Miquel, Isabel García-Pérez, Albert Sánchez-Moya, Arnau Innamorati, Emilio J. Vélez, Isabel Achaerandio, Montserrat Pujolà, et al. "Diet and Exercise Modulate GH-IGFs Axis, Proteolytic Markers and Myogenic Regulatory Factors in Juveniles of Gilthead Sea Bream (Sparus aurata)." Animals 11, no. 8 (July 23, 2021): 2182. http://dx.doi.org/10.3390/ani11082182.

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The physiological and endocrine benefits of sustained exercise in fish were largely demonstrated, and this work examines how the swimming activity can modify the effects of two diets (high-protein, HP: 54% proteins, 15% lipids; high-energy, HE: 50% proteins, 20% lipids) on different growth performance markers in gilthead sea bream juveniles. After 6 weeks of experimentation, fish under voluntary swimming and fed with HP showed significantly higher circulating growth hormone (GH) levels and plasma GH/insulin-like growth-1 (IGF-1) ratio than fish fed with HE, but under exercise, differences disappeared. The transcriptional profile of the GH-IGFs axis molecules and myogenic regulatory factors in liver and muscle was barely affected by diet and swimming conditions. Under voluntary swimming, fish fed with HE showed significantly increased mRNA levels of capn1, capn2, capn3, capns1a, n3, and ub, decreased gene and protein expression of Ctsl and Mafbx and lower muscle texture than fish fed with HP. When fish were exposed to sustained exercise, diet-induced differences in proteases’ expression and muscle texture almost disappeared. Overall, these results suggest that exercise might be a useful tool to minimize nutrient imbalances and that proteolytic genes could be good markers of the culture conditions and dietary treatments in fish.

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Zhou, Jingran, Min Li, Zheng Luo, Ke Zou, Zhenzhen Chen, Baoping Yang та Zhenyu Tang. "Downregulation of Calpain 1 Causes Neurotoxicity and Apoptosis in Primary Neurons Induced by Aβ25-35". Nanoscience and Nanotechnology Letters 11, № 5 (1 травня 2019): 696–703. http://dx.doi.org/10.1166/nnl.2019.2928.

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Amyloid-peptides (Aβ), which can aggregate oligomers or fibrils into neurons, play a critical role in Alzheimer's disease (AD). Calpain 1 (CAPN1) is one of the Ca2+ regulated proteases, involved in cell death, apoptosis, and motility. As an important signal transduction pathway, it has been reported to be closely related to muscle atrophy, myoblast fusion, diabetes mellitus, and neurode-generative diseases, including Alzheimer's disease. Our previous study investigated the effect of CAPN1 RNAi on neurotoxicity and apoptosis in primary neurons induced by Aβ25-35. The primary neurons were cultured and separated into different groups pretreated with Aβ25-35 (10 μM). Three groups were treated with CAPN1 shRNA, while one group was not. Along with CAPN1 shRNA, P25 (2 μg/mL) and rapamycin (20 ng/mL) were added to the culture. The results showed that CAPN1 RNAi enhanced the formation of autophagosomes in cells, as observed by confocal microscopy. Parallelly, CAPN1 RNAi enhanced the cell viability, as observed by Cell Counting Kit-8 (CCK8) assay, and decreased the apoptotic rate, as observed by flow cytometry. In addition, CAPN1 RNAi decreased the mRNA level of CAPN1 and downregulated the expression levels of CDK5, GSK3β, and p-tau in primary neurons induced by Aβ25-35. All these results indicated the effect of CAPN1 RNAi against Aβ-induced neurotoxicity. Our results suggested that CAPN1 RNAi exhibits a neuroprotective effect on the treatment of AD and provided a pharmacological basis for its clinical treatment.

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Liu, Yueyang, Xiaohang Che, Haotian Zhang, Xiaoxiao Fu, Yang Yao, Jun Luo, Yu Yang, et al. "CAPN1 (Calpain1)-Mediated Impairment of Autophagic Flux Contributes to Cerebral Ischemia-Induced Neuronal Damage." Stroke 52, no. 5 (May 2021): 1809–21. http://dx.doi.org/10.1161/strokeaha.120.032749.

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Background and Purpose: CAPN1 (calpain1)—an intracellular Ca 2+ -regulated cysteine protease—can be activated under cerebral ischemia. However, the mechanisms by which CAPN1 activation promotes cerebral ischemic injury are not defined. Methods: In the present study, we used adeno-associated virus-mediated genetic knockdown and pharmacological blockade (MDL-28170) of CAPN1 to investigate the role of CAPN1 in the regulation of the autophagy-lysosomal pathway and neuronal damage in 2 models, rat permanent middle cerebral occlusion in vivo model and oxygen-glucose–deprived primary neuron in vitro model. Results: CAPN1 was activated in the cortex of permanent middle cerebral occlusion–operated rats and oxygen-glucose deprivation–exposed neurons. Genetic and pharmacological inhibition of CAPN1 significantly attenuated ischemia-induced lysosomal membrane permeabilization and subsequent accumulation of autophagic substrates in vivo and in vitro. Moreover, inhibition of CAPN1 increased autophagosome formation by decreasing the cleavage of the autophagy regulators BECN1 (Beclin1) and ATG (autophagy-related gene) 5. Importantly, the neuron-protective effect of MDL-28170 on ischemic insult was reversed by cotreatment with either class III-PI3K (phosphatidylinositol 3-kinase) inhibitor 3-methyladenine or lysosomal inhibitor chloroquine (chloroquine), suggesting that CAPN1 activation-mediated impairment of autophagic flux is crucial for cerebral ischemia-induced neuronal damage. Conclusions: The present study demonstrates for the first time that ischemia-induced CAPN1 activation impairs lysosomal function and suppresses autophagosome formation, which contribute to the accumulation of substrates and aggravate the ischemia-induced neuronal cell damage. Our work highlights the vital role of CAPN1 in the regulation of cerebral ischemia–mediated autophagy-lysosomal pathway defects and neuronal damage.

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Ropka-Molik, Katarzyna, Robert Eckert та Katarzyna Piórkowska. "New Polymorphisms in Regulatory Regions of Porcine μ-Calpain Gene and Their Association with CAPN1 Transcript Abundance". Annals of Animal Science 14, № 3 (29 липня 2014): 525–35. http://dx.doi.org/10.2478/aoas-2014-0027.

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AbstractThe activity of calpains, in particular μ-calpain, is associated with several processes occurring in muscle tissue postmortem and influences meat quality parameters. Therefore, the CAPN1 gene coding for large subunit of μ-calpain is considered as a candidate gene associated with meat quality traits. The aim of our study was to identify new polymorphisms in regulatory regions of the porcine CAPN1 gene and to estimate their impact on CAPN1 transcript abundance. In the present study, 7 polymorphisms in the porcine CAPN1 gene were identified, of which 5 were localized in introns (g.1195_1197insCCT; g.1429G>A; g. [4479A>G; 4526A>T; 4529_4530delAG]), one in 3’ untranslated region (g.25676C>T) and one microsatellite sequence in promoter region (c.-155- AGGG [3_5]). The analysed populations (a total of 451 gilts representing three pure breeds: Pietrain, P lish Landrace, Polish Large White and one conservation breed Pu.awska) were not in Hardy-Weinberg equilibrium according to mutation g.25676C>T in 3’ untranslated region (all breeds), g.1429G>A (Pu.awska pigs) and g. [4479A>G; 4526A>T; 4529_4530delAG] (PLW pigs). Furthermore, the analysed SNPs in the porcine CAPN1 gene were in linkage disequilibrium (P≤0.05). The CAPN1 transcript abundance was also estimated in two important muscles (m. longissimus dorsi, m. semimembranosus). In longissimus dorsi muscle, a significant effect of c.-155- AGGG [3_5] polymorphism in promoter region on CAPN1 expression levels was determined. The c.-155AGGG [3/3] pigs showed a statistically higher (P≤0.05) expression level of the CAPN1 gene when compared to c.-155AGGG [4/4] homozygotes. The results obtained suggested that detected SNPs within regulatory regions of the CAPN1 gene could be related to transcript level and activity of μ-calpain. The selected polymorphisms areproposed to be associated with meat production traits.

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Sun, Xiaomei, Xiuxiang Wu, Yongliang Fan, Yongjiang Mao, Dejun Ji, Bizhi Huang, and Zhangping Yang. "Effects of polymorphisms in CAPN1 and CAST genes on meat tenderness of Chinese Simmental cattle." Archives Animal Breeding 61, no. 4 (November 2, 2018): 433–39. http://dx.doi.org/10.5194/aab-61-433-2018.

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Abstract. Considerable evidence has demonstrated that the μ-calpain (CAPN1) gene and its inhibitor calpastatin (CAST) gene are major factors affecting meat quality. Marker-assisted selection (MAS) has been widely used to improve beef quality traits. Therefore, the objective of the present study was to investigate the single nucleotide polymorphisms (SNPs) of bovine CAPN1 and CAST genes using 367 animals representing the four main Chinese cattle breeds and to explore the effects of these SNPs on meat quality traits. Two SNPs within CAPN1 and one SNP in CAST were successfully identified in cattle. Genetic diversity analyses suggested that most SNPs in the four breeds exhibited a moderate genetic diversity. Moreover, associations between individual markers and meat quality traits were analyzed in Chinese Simmental cattle. The CAPN1 4558 A > G locus was found to be significantly associated with shear force value (SFV) and marbling score (BMS), and CAPN1 4684 C > T exerted a significant effect on SFV, while the CAST genotype was not significantly associated with any of the measured traits. SFV, commonly used to measure meat tenderness, represents an important quality trait as it contributes to the flavor of cooked meat. This work confirms the effect of CAPN1 on beef tenderness and lays an important foundation for future cattle breeding.

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Shidiq, Fajrin, Saiful Anwar, Novi Cahya Lestari, and Kusdianawati Kusdianawati. "The Favorable Allele of CAPN1-316 Genetic Marker is Absent in Bali and Sumbawa Cattle." Jurnal Ilmu-Ilmu Peternakan 33, no. 3 (December 1, 2023): 336–46. http://dx.doi.org/10.21776/ub.jiip.2023.033.03.04.

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The micromolar calcium-activated neutral protease 1 (CAPN1) gene encodes the u-calpain enzyme, which plays a crucial role in meat tenderisation. Genetic diversity within the CAPN1 gene, specifically a nucleotide substitution from G to C in exon nine resulting in a change from glycine to alanine at position 316 (CAPN1-316 marker), is known to significantly affect meat tenderness. This study aimed to assess the polymorphism of the CAPN1-316 locus in Bali and Sumbawa cattle. A total of 293 blood samples, 193 from Bali cattle and 100 from Sumbawa cattle were extracted and genotyped using PCR-RFLP with BtgI restriction enzyme (recognition sequence: 5'-C*CRYGG-3') applied to 706 bp PCR products. The results showed the presence of only one genotype (GG genotype) and one allele (G allele) in all DNA samples obtained from the Bali and Sumbawa cattle populations studied. In conclusion, the CAPN1-316 genetic marker showed a lack of diversity or monomorphism in Bali and Sumbawa cattle, making it unsuitable for further association studies in these breeds. Consequently, the CG/AG haplotype identified in Sumbawa cattle warrants further investigation and could serve as an alternative genetic marker, especially due to its monomorphism at the CAPN1-316 locus.

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Cui, Xiaohui, Yan Sun, Xiuge Wang, Chunhong Yang, Zhihua Ju, Qiang Jiang, Yan Zhang, et al. "A g.-1256 A>C in the promoter region of CAPN1 is associated with semen quality traits in Chinese Holstein bulls." Reproduction 152, no. 1 (July 2016): 101–9. http://dx.doi.org/10.1530/rep-15-0535.

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The micromolar calcium-activated neutral protease gene (CAPN1) is a physiological candidate gene for sperm motility. However, the molecular mechanisms involved in regulating the expression of the CAPN1 gene in bulls remain unknown. In this study, we investigated the expression pattern of CAPN1 in testis, epididymis, and sperm at the RNA and protein levels by qRT-PCR, western blot, immunohistochemistry, and immunofluorescence assay. Results revealed that the expression of CAPN1 levels was higher in the sperm head compared with that in other tissues. Moreover, we identified a novel single-nucleotide polymorphism (g.-1256 A>C, ss 1917715340) in the noncanonical core promoter of the CAPN1 gene between base g.-1306 and g.-1012. Additionally, we observed greater sperm motility in bulls with the genotype CC than in those with the genotype AA (P<0.01), indicating that different genotypes were associated with the bovine semen trait. Furthermore, a higher fluorescence intensity of the C allele than that of the A allele at g. -1256 A>C was revealed by transient transfection in MLTC-1 cells and luciferase report assay. Finally, CAPN1 was highly expressed in the spermatozoa with the CC genotype compared with that with the AA genotype by qRT-PCR. This study is the first report on genetic variant g.-1256 A>C in the promoter region of CAPN1 gene association with the semen quality of Chinese Holstein bulls by influencing its expression. g.-1256 A>C can be a functional molecular marker in cattle breeding.

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Mondal, Tanmoy, Zarish Noreen, Christopher A. Loffredo, Jheannelle Johnson, Attya Bhatti, Gail Nunlee-Bland, Ruth Quartey, et al. "Transcriptomic Analysis of Alzheimer’s Disease Pathways in a Pakistani Population1." Journal of Alzheimer's Disease Reports 8, no. 1 (March 19, 2024): 479–93. http://dx.doi.org/10.3233/adr-230146.

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Background: Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder that is most prevalent in elderly individuals, especially in developed countries, and its prevalence is now increasing in developing countries like Pakistan. Objective: Our goal was to characterize key genes and their levels of expression and related molecular transcriptome networks associated with AD pathogenesis in a pilot case-control study in a Pakistani population. Methods: To obtain the spectrum of molecular networks associated with pathogenesis in AD patients in Pakistan (comparing cases and controls), we used high-throughput qRT-PCR (TaqMan Low-Density Array; n = 33 subjects) coupled with Affymetrix Arrays (n = 8) and Ingenuity Pathway Analysis (IPA) to identify signature genes associated with Amyloid processing and disease pathways. Results: We confirmed 16 differentially expressed AD-related genes, including maximum fold changes observed in CAPNS2 and CAPN1. The global gene expression study observed that 61% and 39% of genes were significantly (p-value 0.05) up- and downregulated, respectively, in AD patients compared to healthy controls. The key pathways include, e.g., Amyloid Processing, Neuroinflammation Signaling, and ErbB4 Signaling. The top-scoring networks in Diseases and Disorders Development were Neurological Disease, Organismal Injury and Abnormalities, and Psychological Disorders. Conclusions: Our pilot study offers a non-invasive and efficient way of investigating gene expression patterns by combining TLDA and global gene expression method in AD patients by utilizing whole blood. This provides valuable insights into the expression status of genes related to Amyloid Processing, which could play potential role in future studies to identify sensitive, early biomarkers of AD in general.

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Ardicli, Sena, Hale Samli, Deniz Dincel, Bahadir Soyudal, and Faruk Balci. "Individual and combined effects of CAPN1, CAST, LEP and GHR gene polymorphisms on carcass characteristics and meat quality in Holstein bulls." Archives Animal Breeding 60, no. 3 (September 8, 2017): 303–13. http://dx.doi.org/10.5194/aab-60-303-2017.

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Abstract. The objective of this study was to determine the association of single nucleotide polymorphisms (SNPs) with carcass characteristics and meat quality traits in selected candidate genes in Holstein bulls. Five SNPs in four genes, i.e. calpain 1 (CAPN1), calpastatin (CAST), leptin (LEP) and growth hormone receptor (GHR), were genotyped in 400 purebred bulls using PCR-RFLP. Statistically significant associations were as follows: CAPN1 G316A with live weight, carcass weight, back fat thickness, m. longissimus thoracis et lumborum area and carcass measurements; CAPN1 V530I with pH and L∗; CAST S20T with live weight, inner chest depth and b∗ value; and GHR with ph, a∗ and h∗. In addition, significant genotypic interactions were observed for dressing percentage (LEP A80V × CAST S20T), pH (CAPN1 V530I × GHR S555G and LEP A80V × GHR S555G) and rump width (CAPN1 V530I × CAST S20T). There was no association between the LEP A80V marker and any of the traits evaluated, nor was there any association of the tested SNPs with chest width, C∗ and marbling score. The present results could therefore be indicative for future studies on meat yield and quality.

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Lee, Hyo Jun, Shil Jin, Hyoun-Joo Kim, Mohammad Shamsul Alam Bhuiyan, Doo Ho Lee, Soo Hyun Lee, Sung Bong Jang, Man Hye Han, and Seung Hwan Lee. "Validation Study of SNPs in CAPN1-CAST Genes on the Tenderness of Muscles (Longissimus thoracis and Semimembranosus) in Hanwoo (Korean Cattle)." Animals 9, no. 9 (September 17, 2019): 691. http://dx.doi.org/10.3390/ani9090691.

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Previous studies demonstrated that polymorphisms in the μ-calpain (CAPN1) and calpastatin (CAST) genes had significant effects on meat tenderness in different cattle populations. The aim of this study was to validate the potential association of seven single nucleotide polymorphisms (SNPs) harbored in these two candidate genes with meat tenderness in the Longissimus thoracis (LT) and Semimembranosus (SM) muscles. A total of 1000 animals were genotyped using TaqMan SNP genotyping arrays, and the meat tenderness of two muscle (LT and SM at 7 days post-slaughter) was assessed based on Warner-Bratzler WBSF (WBSF) testing. We observed significant associations of the CAPN1:c.580T>C, CAPN1:c.658T>C and CAST:c.1985G>C polymorphisms (p < 0.05) with the WBSF values in the LT and SM muscles. Additive effects of the C allele in CAPN1:c.580T>C and CAST:c.1985G>C were associated with an increase of 0.16 and 0.15 kg, and 0.08 and 0.26 kg WBSF in the LT and SM, respectively; CAPN1:c.658T>C had negative effects on the WBSFs. Furthermore, six reconstructed haplotypes demonstrated significant associations with WBSF values (p < 0.05). In conclusion, the significant associations identified between the SNPs in CAPN1, CAST and WBSF values could be utilized in marker-assisted selection programs in order to improve the beef tenderness of Hanwoo cattle.

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Landowski, Terry H., Aluvia M. Escalante, Andrew Jefferson, Robert T. Dorr, and Ronald Lynch. "Inhibition of Autophagy Promotes Bortezomib-Mediated Cell Death in Myeloma Cells." Blood 112, no. 11 (November 16, 2008): 3677. http://dx.doi.org/10.1182/blood.v112.11.3677.3677.

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Abstract The 26S proteasome is a key regulator of proteins controlling many important cellular functions, including cell cycle progression, differentiation, gene transcription and apoptosis. Proteasome inhibition is a new therapeutic strategy that has shown promise in the treatment of B cell malignancies, primarily multiple myeloma. We and others have demonstrated that proteasome inhibitors induce endoplasmic reticulum (ER) stress and activate an unfolded protein response (UPR) in transformed cells. Our previous work demonstrated that bortezomib induces an endoplasmic reticulum (ER) stress response ultimately leading to calcium-dependent apoptotic cell death. Co-treatment of myeloma cells with the mitochondrial uniporter inhibitor ruthenium red (RuR) abrogated bortezomib mediated cell death, indicating that the cytotoxic effects of proteasomal inhibition requires dysregulation of intracellular Ca2+. Intracellular Ca2+ has also been implicated in the cellular stress response known as autophagy or “self-eating”. Macroautophagy (hereafter referred to as autophagy) is induced by various cellular stresses including nutrient deprivation, metabolic insufficiency, interruption of growth factor signaling, elevated ROS, accumulation of intracellular Ca2+, and the UPR. The biochemical events linking the cellular stress response with the induction of autophagy, and the relationship between autophagy and apoptosis is not well understood. In this study, we investigate the role of the Ca2+ dependent serine protease, calpain, as a mediator of the conversion from autophagic cell survival to accelerated cell death in the ER stress response. We demonstrate that the proteasome inhibitor, bortezomib, initiates autophagy in myeloma cells, and protection from bortezomib-mediated cell death by mitochondrial Ca2+ inhibitors is associated with a promotion and stabilization of the autophagosome. This response can be reversed, and indeed, accelerated, leading to enhanced cell death, by blockade of calpain activity. Inhibition of calpain activity with the tri-peptide zLLY-FMK (Calpain Inhibitor IV, (CiIV) or the non-peptide inhibitor, PD150606, demonstrated a significant increase in the cytotoxic activity of bortezomib. Similarly, elimination of the small catalytic subunit, CAPNS1, using siRNA, enhanced bortezomib-mediated cell death, and prevented autophagosome-lysosomal progression. Furthermore, inhibition of calpain by clinically approved HIV protease inhibitors including Nelfinavir, Ritonavir, Saquinavir, and Indinavir sulfate, significantly increased the cytotoxic activity of bortezomib in vitro. We suggest that disregulation of Ca2+ by bortezomib-mediated ER stress activates the autophagic survival response. Inhibition of mitochondrial Ca2+ uptake by the uniporter inhibitor RuR promotes autophagy, and confers resistance to bortezomib. Conversely, inhibition of the Ca2+-dependent serine protease, calpain, prevents autophagolysosome maturation, and subverts the survival response to cell death. These data are likely to have important clinical implications for the treatment of refractory myeloma and other B cell malignancies.

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ТЮЛЕБАЕВ, С. Д., and М. Д. КАДЫШЕВА. "INFLUENCE OF POLYMORPHIC GENES ON QUALITATIVE INDICATORS OF MEAT PRODUCTS." VESTNIK RIAZANSKOGO GOSUDARSTVENNOGO AGROTEHNOLOGICHESKOGO UNIVERSITETA IM P A KOSTYCHEVA, no. 2(50) (June 30, 2021): 50–56. http://dx.doi.org/10.36508/rsatu.2021.50.2.007.

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Проблема и цель. Целью данной работы являлось генотипирование животных по генам CAST и CAPN1 c выявлением частот генотипов и аллелей, а также тестирование продукции этих животных, выраженное в оценке выдержанного в течение 8 суток мяса, на показатели, составляющие нежность, сочность, органолептическую оценку вкуса. Методология. Объектом исследований являлись бычки кроссов брединского мясного типа симменталов, полученные от использования выдающихся быков-производителей канадских мясных симменталов на отечественных матках различных линий. Для осуществления полимеразной цепной реакции (ПЦР) по тиражированию участка генома, составляющего ген CAPN1316 и ген CAST2857, использовались праймеры, найденные в открытой печати и синтезированные в фирме «Синтол». Проводилась оценка мяса на нежность (сопротивление усилию на разрез прибором Уорнера-Братцлера + органолептическая оценка варёного и жареного мяса), сочность (p/h, с использованием прокалывающего электрода LoT406-M6-DXK-S7/25 + влагоудерживающая способность). Результаты. В результате показатели мяса бычков, имеющих сочетание генотипов TT* по CAST и СС* по CAPN1, имели превосходство над средними показателями общей выборки (P< 0,001); а также над имеющей наибольшее распространение в выборке группой животных с желательным генотипом СС по гену CAPN1 на 1,22 балла или 15,4 % (P< 0,01) по нежности; на 1,44 балла или 18,2 % (P< 0,05) по сочности; на 1,56 балла или 19,2 % (P< 0,001) по вкусу. Заключение. Таким образом, исследования подтвердили влияние полиморфного состояния гомозиготы СС гена CAPN1 само по себе, а также генов CAST и CAPN1 на нежность говядины в той её части, когда сочетание генотипов ТТ в гене CAST и СС в гене CAPN1 даёт положительный эффект по нежности говядины, вероятно связанный с активизацией деятельности μ-кальпаина в связи с ослаблением влияния кальпастатина как ингибитора на μ-кальпаин. Problem and purpose.The aim of this work was to genotype animals for the CAST and CAPN1 genes with identifying the frequencies of genotypes and alleles, as well as testing the products of these animals, expressed in assessing meat aged for 8 days, for indicators that make up tenderness, juiciness, and organoleptic taste assessment.Methodology. The object of research was the bulls of the breeds of the Bredy meat type of simmentals obtained from the use of outstanding bulls-producers of Canadian meat simmentals on domestic females of various lines. To carry out the polymerase chain reaction (PCR) for replicating a region of the genome constituting the CAPN1316 gene and the CAST2857 gene, primers found in the open press and synthesized by Syntol were used. The meat was evaluated for tenderness (resistance to cutting force with a Warner-Bratzler device + sensory evaluation of cooked and fried meat), juiciness (p/h, using a piercing electrode LoT406-M6-DXK-S7/25 + water-holding capacity). Results. As a result, the meat indicators of bulls with a combination of TT * genotypes for CAST and CC * for CAPN1 were superior over the average indicators of the total sample (P <0.001), as well as over the most common group of animals in the sample with the desired CC genotype for the CAPN1 gene by 1.22 points or 15.4% (P <0.01) for tenderness, 1.44 points or 18.2% (P <0.05) for juiciness, 1.56 points or 19.2% (P <0.001) for taste. Conclusion. Thus, the studies have confirmed the influence of the polymorphic state of the CC homozygote of the CAPN1 gene itself, as well as of the CAST and CAPN1 genes, on the tenderness of beef in that part of it when the combination of TT genotypes in the CAST gene and CC in the CAPN1 gene has a positive effect on the tenderness of beef, probably associated with the activation of the activity of μ-calpain due to the weakening of the effect of calpastatin as an inhibitor on μ-calpain.

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Machado, Alessandro Lima, Ariana Nascimento Meira, Evandro Neves Muniz, Hymerson Costa Azevedo, Luiz Lehmann Coutinho, Gerson Barreto Mourão, Victor Breno Pedrosa, and Luís Fernando Batista Pinto. "Single Loci and Haplotypes in CAPN1 and CAST Genes are Associated with Growth, Biometrics, and in Vivo Carcass Traits in Santa Inês Sheep." Annals of Animal Science 20, no. 2 (April 1, 2020): 465–83. http://dx.doi.org/10.2478/aoas-2020-0007.

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Abstractµ-calpain (CAPN1) and calpastatin (CAST) genes play key roles in protein turnover. The present study aimed to identify the variants in these genes associated with growth and ultrasound carcass traits in Santa Inês sheep. A sample of 192 no full sibling Santa Inês lambs was used. Fragments of the CAST and CAPN1 genes were amplified and next-generation sequencing was performed in the MiSeq platform. Variants in the CAPN1 and CAST sequences were then detected using bioinformatic tools. Withers and croup heights, body length, thoracic and croup widths, thoracic and leg girths, body depth, carcass fat score, rib eye area, fat thickness, body weights were recorded at weaning and at 140 days post-weaning, and average daily gain post-weaning was calculated. Both single-locus and haplotype association analyses were performed with the model as follows: farm (2 levels), year (4 levels), the month of birth (12 levels), and the covariate age of the animal. The fragments amplified included 4,514 bp between the 20th and 23rd exons of CAST as well as 3,927 bp between the 12th and 21st exons of CAPN1. In these regions, 58 (CAST) and 45 (CAPN1) variants were identified. In the CAST gene, the single-locus analysis revealed 22 suggestive additive effects (P<0.05) on several growth and carcass traits. Moreover, haplotype substitutions were associated with rib eye area (–0.689±0.290), average daily gain (–23.6±10.4), thoracic girth (–2.72±1.27), body length (–3.38±1.49), and leg girth (–2.84±1.37). Regarding the CAPN1 gene, the single-locus analysis identified seven suggestive additive effects, while only one haplotype replacement effect on fat thickness (–0.0143±0.0053) was detected. The results of the present study suggest that variants in the CAPN1 and CAST genes are associated with growth and ultrasound carcass traits in Santa Inês sheep, which may be a source of information to improve knowledge regarding the genetic control of these traits.

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42

Ghannoum, Mahmoud A. "Potential Role of Phospholipases in Virulence and Fungal Pathogenesis." Clinical Microbiology Reviews 13, no. 1 (January 1, 2000): 122–43. http://dx.doi.org/10.1128/cmr.13.1.122.

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SUMMARY Microbial pathogens use a number of genetic strategies to invade the host and cause infection. These common themes are found throughout microbial systems. Secretion of enzymes, such as phospholipase, has been proposed as one of these themes that are used by bacteria, parasites, and pathogenic fungi. The role of extracellular phospholipase as a potential virulence factor in pathogenic fungi, including Candida albicans, Cryptococcus neoformans, and Aspergillus, has gained credence recently. In this review, data implicating phospholipase as a virulence factor in C. albicans, Candida glabrata, C. neoformans, and A. fumigatus are presented. A detailed description of the molecular and biochemical approaches used to more definitively delineate the role of phospholipase in the virulence of C. albicans is also covered. These approaches resulted in cloning of three genes encoding candidal phospholipases (caPLP1, caPLB2, and PLD). By using targeted gene disruption, C. albicans null mutants that failed to secrete phospholipase B, encoded by caPLB1, were constructed. When these isogenic strain pairs were tested in two clinically relevant murine models of candidiasis, deletion of caPLB1 was shown to lead to attenuation of candidal virulence. Importantly, immunogold electron microscopy studies showed that C. albicans secretes this enzyme during the infectious process. These data indicate that phospholipase B is essential for candidal virulence. Although the mechanism(s) through which phospholipase modulates fungal virulence is still under investigations, early data suggest that direct host cell damage and lysis are the main mechanisms contributing to fungal virulence. Since the importance of phospholipases in fungal virulence is already known, the next challenge will be to utilize these lytic enzymes as therapeutic and diagnostic targets.

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43

Billhaq, Dody Houston, Galy Hardyta, and Labib Abdillah. "Analisis Perbandingan Sekuens Gen Calpain 1 (CAPN1) pada Sapi, Kerbau, dan Kambing Berdasarkan Database Genbank." AGROVITAL : Jurnal Ilmu Pertanian 8, no. 1 (May 28, 2023): 35. http://dx.doi.org/10.35329/agrovital.v8i1.4009.

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Livestock genetic improvement is the main purpose of animal breeding program. Biotechnology brings novel method to improve the animal breeding program qualitatively and quantitatively. Identification of gene sequence of polymorphism are used widely to analyze gene sequence to understand genetic variation. Calpain 1 (CAPN1) gene is the gene that involve in the process of improving meat quality such as marbling and tenderness of the livestock including the cattle, buffalo, and goat species. CAPN1 is responsible in encoding the µ-calpain that regulate postmortem proteolysis. This study collect the gene database including calpain 1 [Bos taurus (cattle)] NC_037356.1, calpain 1 [Bos indicus (zebu cattle)] NC_032678.1, calpain 1 [Bos indicus x Bos taurus (hybrid cattle)] NC_040104.1, calpain 1 [Bubalus bubalis (water buffalo)] NC_059161.1 calpain 1 [Capra hircus (goat)] NC_030836.1 through NCBI. Those collected gene were analyze using the Clustal W alignment, MEGA 11, and BLAST program. The results indicate that the cattle, buffalo, and goat species CAPN1 gene of the 5’ UTR, Intron, Exon, dan 3’ UTR region show 9 SNPs, 1691 SNPs, 153 SNPs, and 197 SNPs, respectively. Total of the identified SNPs within the the cattle, buffalo, and goat species CAPN1 gene comparison are 2050. This study can be used for the initial report in order to develop further research related to CAPN1 gene for the livestock ruminant.

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44

Zhou, Yu-Guang, Yong Xiong, Chao-Wu Yang, Xiao-Song Jiang, Jin-Shan Ran, Jie Jin, Ye Wang, et al. "Experimental Verification of CAPN1 and CAST Gene Polymorphisms in Different Generations of Da-Heng Broilers." BioMed Research International 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/7968450.

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The micromolar calcium activated neutral protease (CAPN1) and calpastatin (CAST) have been widely regarded as genes related to muscle growth and meat tenderness. The objective of this study was to verify the association of SNPs of CAPN1 and CAST genes with carcass and tenderness traits and search the possible change patterns of SNPs in CAPN1 and CAST genes in six generations of broiler breeding process for growth rate, efficiency, and reproduction, during the third generation and the ninth generation, respectively. We found that, for CAPN1, genetic effects between SNPs (G3535A, C7198A) and meat tenderness were similar in different generations, while SNP3 (G7324A) was a novel polymorphism and had significant association with carcass and tenderness traits (P<0.05) in this study. Furthermore, there was significant association between SNP4 (G9950A) and carcass indexes instead of tenderness traits (P<0.05) which was consistent in the two generations. Moreover, although SNP6 (G37868A) of CAST had no relevance to carcass traits or tenderness traits in the third generation, it showed significant association with LW and CW in the ninth generation (P<0.05).

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45

Desgarennes Alcalá, Carmen Monserrat, Sandra Del Moral Ventura, Victor Manuel Meza Villalvazo, Julián Mario Peña Castro, Juan Priciliano Zárate Martínez, and José Abad Zavaleta. "Estimación de las frecuencias alélicas y genotípicas de los genes CAPN1 Y CAST asociados a la calidad de la carne en bovinos de la Cuenca del Papaloapan." Nova Scientia 9, no. 19 (September 8, 2017): 211. http://dx.doi.org/10.21640/ns.v9i19.996.

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El ganado de doble propósito es aquel utilizado para producir carne y leche. Generalmente es el producto del cruce de razas de origen Cebú x europeas y/o Criollo. Este grupo genético se ha adaptado a las condiciones climáticas de temperatura, humedad, baja calidad de pastos y clases de parásitos que prevalecen en las regiones tropicales. En este trabajo, se realizó un escrutinio molecular para observar la frecuencia de dos polimorfismos del gen de la μ-calpaína (CAPN1-316, CAPN1-530) y uno del gen de la calpastatina (CAST), asociados a la suavidad de la carne en ganado bovino de doble propósito de la Cuenca del Papaloapan. Las pruebas se basaron en Reacción en Cadena de la Polimerasa (PCR) y Polimorfismos de la Longitud de Fragmentos de Restricción (RFLPs) con las enzimas de restricción Btg I, Ava II y Rsa I para los alelos C-G, A-G y C-G, respectivamente (n=331). Para CAPN1-316 las frecuencias genotípicas obtenidas fueron de 0.03 (AA), 0.86 (GG) y 0.11 (GA) y las frecuencias alélicas fueron 0.86 (G) y 0.14 (A). Para el marcador CAPN1-530 las frecuencias genotípicas fueron de 0.02 (CC), 0.85 (GG) y 0.13 (GC), con una frecuencia alélica de 0.85 para G y 0.15 para C. Las frecuencias genotípicas para el marcador CAST fueron de 0.32 (CC), 0.28 (GG) y 0.4 (GC), con una frecuencia alélica de 0.68 para el alelo G y 0.32 para el alelo C. La población en estudio no se encontró en equilibrio Hardy Weinberg y los valores de χ2P con dos grados de libertad fueron de 0.964, 0.985 y 0.9803 para CAPN1-316, CAPN1-530 y CAST, respectivamente. De acuerdo con el porcentaje de la genotipificación de los marcadores en los genes CAPN1 y CAST se concluye que la población analizada tiene bajos índices de marcadores para la suavidad o terneza de la carne, probablemente por las cruzas no dirigidas que se realizan habitualmente, de esta forma se propone, mejorar la calidad de la carne en base a programas de mejoramiento genético dirigido utilizando los animales genéticamente superiores resultantes de este estudio.

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46

Macqueen, Daniel J., and Alexander H. Wilcox. "Characterization of the definitive classical calpain family of vertebrates using phylogenetic, evolutionary and expression analyses." Open Biology 4, no. 4 (April 2014): 130219. http://dx.doi.org/10.1098/rsob.130219.

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The calpains are a superfamily of proteases with extensive relevance to human health and welfare. Vast research attention is given to the vertebrate ‘classical’ subfamily, making it surprising that the evolutionary origins, distribution and relationships of these genes is poorly characterized. Consequently, there exists uncertainty about the conservation of gene family structure, function and expression that has been principally defined from work with mammals. Here, more than 200 vertebrate classical calpains were incorporated in phylogenetic analyses spanning an unprecedented range of taxa, including jawless and cartilaginous fish. We demonstrate that the common vertebrate ancestor had at least six classical calpains, including a single gene that gave rise to CAPN11 , 1 , 2 and 8 in the early jawed fish lineage, plus CAPN3 , 9 , 12 , 13 and a novel calpain gene, hereafter named CAPN17 . We reveal that while all vertebrate classical calpains have been subject to persistent purifying selection during evolution, the degree and nature of selective pressure has often been lineage-dependent. The tissue expression of the complete classic calpain family was assessed in representative teleost fish, amphibians, reptiles and mammals. This highlighted systematic divergence in expression across vertebrate taxa, with most classic calpain genes from fish and amphibians having more extensive tissue distribution than in amniotes. Our data suggest that classical calpain functions have frequently diverged during vertebrate evolution and challenge the ongoing value of the established system of classifying calpains by expression.

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47

Garcia-Berlanga, Jesus Eduardo, Mariana Moscovich, Isaac Jair Palacios, Alejandro Banegas-Lagos, Augusto Rojas-Martinez, and Daniel Martinez-Ramirez. "CAPN1 Variants as Cause of Hereditary Spastic Paraplegia Type 76." Case Reports in Neurological Medicine 2019 (July 1, 2019): 1–5. http://dx.doi.org/10.1155/2019/7615605.

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Background. Autosomal recessive hereditary spastic paraplegias (HSP) are a rare group of hereditary neurodegenerative disorders characterized by spasticity with or without other symptoms. SPG11 gene is the most common cause of autosomal recessive HSP. We report a case of autosomal recessive spastic paraplegia type 76 due to heterozygous variants of CAPN1 in an Argentinean subject. Case Presentation. A 38-year-old Argentinean female presented with progressive gait problems and instability of 15-year duration. Oculomotor abnormalities, ataxia, bradykinesia, cervical dystonia, and lower limb pyramidal signs were observed. Brain MRI was unremarkable. Whole-exome sequencing analysis identified two heterozygous variants in CAPN1. Conclusions. Clinicians should screen for CAPN1 mutation in a young female patient without significant family history with a spastic paraplegia syndrome associated with other symptoms.

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48

Macqueen, Daniel J., Lara Meischke, Sujatha Manthri, Attia Anwar, Christel Solberg, and Ian A. Johnston. "Characterisation of capn1, capn2-like, capn3 and capn11 genes in Atlantic halibut (Hippoglossus hippoglossus L.): Transcriptional regulation across tissues and in skeletal muscle at distinct nutritional states." Gene 453, no. 1-2 (March 2010): 45–58. http://dx.doi.org/10.1016/j.gene.2010.01.002.

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49

Saifullah, Abusayeed, Sriram Sankar, Jie Liu, Chenyang Lu, Ranveer Chandra, and Bodhi Priyantha. "CapNet." ACM Transactions on Sensor Networks 15, no. 1 (February 21, 2019): 1–34. http://dx.doi.org/10.1145/3278624.

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50

Zhou, Jun, Xuanqing Wang, Lulu Zhang, Xuan Zhou, Siqi Jing, and Guangchuan Liang. "An Improved Genetic Algorithm for the Uncapacitated Facility Location Problem and Applications in Oil and Gas Fields." Journal of Physics: Conference Series 2224, no. 1 (April 1, 2022): 012134. http://dx.doi.org/10.1088/1742-6596/2224/1/012134.

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Abstract Uncapacitated Facility Location Problem (UFLP) is a NP-hard Problem that to determine the optimal Location of facilities. In this paper, the general Genetic Algorithm (gGA) is first introduced and adopted to solve a small case of UFLP (case1). Then an improved genetic algorithm (iGA) based on real coding is proposed to solve the UFLP problem. This paper mainly makes appropriate adjustments in the selection of fitness function, crossover operator and mutation operator to be more suitable for UFLP. Facilities thus can be roughly allocated according to the cost of facilities and the demands of customers. Case2 was calculated by several CAP data (CAP101, CAP103, CAP104, CAP131, CAP133, CAPB and CAPC) in OR-LIBRORY. The results proved that the iGA is feasible and effective, and it is found that 80% of the results obtained by the iGA are within 0.05% of the optimal solutions. Compared with several other common algorithms, the advantages of iGA increase as the scale of calculation increases. Finally, applying iGA to an on-site oilfield pipeline network, it was found that it can find the optimal solution in a short time.

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