Academic literature on the topic 'ATP2A1 gene'
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Journal articles on the topic "ATP2A1 gene"
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Christodoulou, Panayiota, Andreas Yiallouris, Artemis Michail, Maria-Ioanna Christodoulou, Panagiotis K. Politis, and Ioannis Patrikios. "Altered SERCA Expression in Breast Cancer." Medicina 57, no. 10 (October 8, 2021): 1074. http://dx.doi.org/10.3390/medicina57101074.
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Background and Objectives: Calcium (Ca2+) signaling is critical for the normal functioning of various cellular activities. However, abnormal changes in cellular Ca2+ can contribute to pathological conditions, including various types of cancer. The maintenance of intracellular Ca2+ levels is achieved through tightly regulated processes that help maintain Ca2+ homeostasis. Several types of regulatory proteins are involved in controlling intracellular Ca2+ levels, including the sarco/endoplasmic reticulum (SR/ER) Ca2+ ATPase pump (SERCA), which maintains Ca2+ levels released from the SR/ER. In total, three ATPase SR/ER Ca2+-transporting (ATP2A) 1-3 genes exist, which encode for several isoforms whose expression profiles are tissue-specific. Recently, it has become clear that abnormal SERCA expression and activity are associated with various types of cancer, including breast cancer. Breast carcinomas represent 40% of all cancer types that affect women, with a wide variety of pathological and clinical conditions. Materials and methods: Using cBioPortal breast cancer patient data, Kaplan–Meier plots demonstrated that high ATP2A1 and ATP2A3 expression was associated with reduced patient survival. Results: The present study found significantly different SERCA specific-type expressions in a series of breast cancer cell lines. Moreover, bioinformatics analysis indicated that ATP2A1 and ATP2A3 expression was highly altered in patients with breast cancer. Conclusion: Overall, the present data suggest that SERCA gene-specific expressioncan possibly be considered as a crucial target for the control of breast cancer development and progression.
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Li, Li, Huijuan Wu, Jialin Qian, Mingzhen Li, Yue Li, Baoming Li, Yu Han, et al. "Decreased Na+/K+ ATPase α1 (ATP1A1) gene expression in major depression patients’ peripheral blood." Open Life Sciences 8, no. 11 (November 1, 2013): 1077–82. http://dx.doi.org/10.2478/s11535-013-0207-8.
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AbstractMajor depression affects the central nervous system and thereafter the autonomic nervous system, immune system, and endocrine system. Na+/K+ ATPase, as a major mediator of cellular transmembrane ionic gradients, plays an important role in nervous signal transduction. Three types of Na+/K+ ATPase α subunit isoforms (ATP1A1, ATP1A2, and ATP1A3) are found in brain but vary in the type of cell and level of expression. It has been confirmed that reduced expression of ATP1A2 and ATP1A3 are related to depressive disorder. However, there is no reported correlation between ATP1A1 and major depression. This study investigated the potential correlation between ATP1A1 gene expression level and major depression. The expression levels of ATP1A1 gene in the peripheral circulation of both depressive patients and healthy human controls were quantified by using reverse transcripted quantitative polymerase chain reaction. Statistical analysis showed a significant decrease of ATP1A1 expression level in major depression patients when compared to that of healthy controls (P<0.01). The differences of gene nucleotide sequences and protein structures among ATP1A1, ATP1A2, and ATP1A3 were also illustrated. This study demonstrates, for the first time, that ATP1A1 gene expression level is significantly associated with major depression and suggests that ATP1A1 could be a significant molecular marker for diagnosis.
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Autry, Joseph M., Christine B. Karim, Sudeep Perumbakkam, Carrie J. Finno, Erica C. McKenzie, David D. Thomas, and Stephanie J. Valberg. "Sarcolipin Exhibits Abundant RNA Transcription and Minimal Protein Expression in Horse Gluteal Muscle." Veterinary Sciences 7, no. 4 (November 13, 2020): 178. http://dx.doi.org/10.3390/vetsci7040178.
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Ca2+ regulation in equine muscle is important for horse performance, yet little is known about this species-specific regulation. We reported recently that horse encode unique gene and protein sequences for the sarcoplasmic reticulum (SR) Ca2+-transporting ATPase (SERCA) and the regulatory subunit sarcolipin (SLN). Here we quantified gene transcription and protein expression of SERCA and its inhibitory peptides in horse gluteus, as compared to commonly-studied rabbit skeletal muscle. RNA sequencing and protein immunoblotting determined that horse gluteus expresses the ATP2A1 gene (SERCA1) as the predominant SR Ca2+-ATPase isoform and the SLN gene as the most-abundant SERCA inhibitory peptide, as also found in rabbit skeletal muscle. Equine muscle expresses an insignificant level of phospholamban (PLN), another key SERCA inhibitory peptide expressed commonly in a variety of mammalian striated muscles. Surprisingly in horse, the RNA transcript ratio of SLN-to-ATP2A1 is an order of magnitude higher than in rabbit, while the corresponding protein expression ratio is an order of magnitude lower than in rabbit. Thus, SLN is not efficiently translated or maintained as a stable protein in horse muscle, suggesting a non-coding role for supra-abundant SLN mRNA. We propose that the lack of SLN and PLN inhibition of SERCA activity in equine muscle is an evolutionary adaptation that potentiates Ca2+ cycling and muscle contractility in a prey species domestically selected for speed.
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Kong, Jie, Siming Sun, Fei Min, Xingli Hu, Yuan Zhang, Yan Cheng, Haiyan Li, Xiaojie Wang, and Xin Liu. "Integrating Network Pharmacology and Transcriptomic Strategies to Explore the Pharmacological Mechanism of Hydroxysafflor Yellow A in Delaying Liver Aging." International Journal of Molecular Sciences 23, no. 22 (November 18, 2022): 14281. http://dx.doi.org/10.3390/ijms232214281.
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Aging affects the structure and function of the liver. Hydroxysafflor yellow A (HSYA) effectively improves liver aging (LA) in mice, but the potential mechanisms require further exploration. In this study, an integrated approach combining network pharmacology and transcriptomics was used to elucidate the potential mechanisms of HSYA delay of LA. The targets of HSYA were predicted using the PharmMapper, SwissTargetPrediction, and CTD databases, and the targets of LA were collected from the GeneCards database. An ontology (GO) analysis and a Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotation of genes related to HSYA delay of LA were performed using the DAVID database, and Cytoscape software was used to construct an HSYA target pathway network. The BMKCloud platform was used to sequence mRNA from mouse liver tissue, screen differentially expressed genes (DEGs) that were altered by HSYA, and enrich their biological functions and signaling pathways through the OmicShare database. The results of the network pharmacology and transcriptomic analyses were combined. Then, quantitative real-time PCR (qRT-PCR) and Western blot experiments were used to further verify the prediction results. Finally, the interactions between HSYA and key targets were assessed by molecular docking. The results showed that 199 potentially targeted genes according to network pharmacology and 480 DEGs according to transcriptomics were involved in the effects of HSYA against LA. An integrated analysis revealed that four key targets, including HSP90AA1, ATP2A1, NOS1 and CRAT, as well as their three related pathways (the calcium signaling pathway, estrogen signaling pathway and cGMP–PKG signaling pathway), were closely related to the therapeutic effects of HSYA. A gene and protein expression analysis revealed that HSYA significantly inhibited the expressions of HSP90AA1, ATP2A1 and NOS1 in the liver tissue of aging mice. The molecular docking results showed that HSYA had high affinities with the HSP90AA1, ATP2A1 and NOS1 targets. Our data demonstrate that HSYA may delay LA in mice by inhibiting the expressions of HSP90AA1, ATP2A1 and NOS1 and regulating the calcium signaling pathway, the estrogen signaling pathway, and the cGMP–PKG signaling pathway.
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Sweadner, Kathleen J., Elena Arystarkhova, John T. Penniston, Kathryn J. Swoboda, Allison Brashear, and Laurie J. Ozelius. "Genotype-structure-phenotype relationships diverge in paralogs ATP1A1, ATP1A2, and ATP1A3." Neurology Genetics 5, no. 1 (February 2019): e303. http://dx.doi.org/10.1212/nxg.0000000000000303.
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ObjectiveWe tested the assumption that closely related genes should have similar pathogenic variants by analyzing >200 pathogenic variants in a gene family with high neurologic impact and high sequence identity, the Na,K-ATPases ATP1A1, ATP1A2, and ATP1A3.MethodsData sets of disease-associated variants were compared. Their equivalent positions in protein crystal structures were used for insights into pathogenicity and correlated with the phenotype and conservation of homology.ResultsRelatively few mutations affected the corresponding amino acids in 2 genes. In the membrane domain of ATP1A3 (primarily expressed in neurons), variants producing milder neurologic phenotypes had different structural positions than variants producing severe phenotypes. In ATP1A2 (primarily expressed in astrocytes), membrane domain variants characteristic of severe phenotypes in ATP1A3 were absent from patient data. The known variants in ATP1A1 fell into 2 distinct groups. Sequence conservation was an imperfect indicator: it varied among structural domains, and some variants with demonstrated pathogenicity were in low conservation sites.ConclusionsPathogenic variants varied between genes despite high sequence identity, and there is a genotype-structure-phenotype relationship in ATP1A3 that correlates with neurologic outcomes. The absence of “severe” pathogenic variants in ATP1A2 patients predicts that they will manifest either in a different tissue or by death in utero and that new ATP1A1 variants will produce additional phenotypes. It is important that some variants in poorly conserved amino acids are nonetheless pathogenic and could be incorrectly predicted to be benign.
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Molenaar, Joery P., Jamie I. Verhoeven, Richard J. Rodenburg, Erik J. Kamsteeg, Corrie E. Erasmus, Savine Vicart, Anthony Behin, et al. "Clinical, morphological and genetic characterization of Brody disease: an international study of 40 patients." Brain 143, no. 2 (February 1, 2020): 452–66. http://dx.doi.org/10.1093/brain/awz410.
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Abstract Brody disease is an autosomal recessive myopathy characterized by exercise-induced muscle stiffness due to mutations in the ATP2A1 gene. Almost 50 years after the initial case presentation, only 18 patients have been reported and many questions regarding the clinical phenotype and results of ancillary investigations remain unanswered, likely leading to incomplete recognition and consequently under-diagnosis. Additionally, little is known about the natural history of the disorder, genotype-phenotype correlations, and the effects of symptomatic treatment. We studied the largest cohort of Brody disease patients to date (n = 40), consisting of 22 new patients (19 novel mutations) and all 18 previously published patients. This observational study shows that the main feature of Brody disease is an exercise-induced muscle stiffness of the limbs, and often of the eyelids. Onset begins in childhood and there was no or only mild progression of symptoms over time. Four patients had episodes resembling malignant hyperthermia. The key finding at physical examination was delayed relaxation after repetitive contractions. Additionally, no atrophy was seen, muscle strength was generally preserved, and some patients had a remarkable athletic build. Symptomatic treatment was mostly ineffective or produced unacceptable side effects. EMG showed silent contractures in approximately half of the patients and no myotonia. Creatine kinase was normal or mildly elevated, and muscle biopsy showed mild myopathic changes with selective type II atrophy. Sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) activity was reduced and western blot analysis showed decreased or absent SERCA1 protein. Based on this cohort, we conclude that Brody disease should be considered in cases of exercise-induced muscle stiffness. When physical examination shows delayed relaxation, and there are no myotonic discharges at electromyography, we recommend direct sequencing of the ATP2A1 gene or next generation sequencing with a myopathy panel. Aside from clinical features, SERCA activity measurement and SERCA1 western blot can assist in proving the pathogenicity of novel ATP2A1 mutations. Finally, patients with Brody disease may be at risk for malignant hyperthermia-like episodes, and therefore appropriate perioperative measures are recommended. This study will help improve understanding and recognition of Brody disease as a distinct myopathy in the broader field of calcium-related myopathies.
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Tao, Rong, Chu-Pak Lau, and Gui-Rong Li. "Inositol 1,4,5-Trisphosphate Receptors Mediating Spontaneous Ca2+ Oscillation Favors Proliferation in Human Mesenchymal Stem Cells from Bone Marrow." Blood 108, no. 11 (November 16, 2006): 2572. http://dx.doi.org/10.1182/blood.v108.11.2572.2572.
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Abstract Although human mesenchymal stem cells (hMSCs) constitute a very small population of cells in bone marrow, they play an important role in the regulation of hematopoietic microenvironment. The self-renew and/or proliferation of hMSCs is believed to be particularly important in maintaining bone marrow niche; however, the regulation of this process is not fully understood. The present study was designed to investigate whether spontaneous Ca2+ oscillation mediated by inositol 1,4,5-trisphosphate (IP3) receptors participates in the proliferation regulation in cultured hMSCs from bone marrow using RT-PCR, cell proliferation assay, Western-blotting analysis. It was found that no gene expression for ryanodine-sensitive receptors was detected in undifferentiated hMSCs, while three subtypes of IP3 receptor genes (i.e. IP3R1, IP3R2, and IP3R3), and genes for sarco/endoplasmic reticulum Ca2+ ATPases (SERCA) (ATP2A1, ATP2A2, and ATP2A3) were expressed in these cells. The proliferation of hMSCs was reduced by inhibiting Ca2+ oscillation with the IP3 receptor antagonist 2-aminoethyl diphenylborinate (2-APB) or the SERCA inhibitor cyclopiazonic acid (CPA). In addition, inhibition of Mek/Erk and PI-3K/Akt signaling also decreased hMSCs proliferation. The relation of Ca2+ oscillation to the activity of these kinases was revealed by Western blotting analysis. Erk1/2 (Thr185/Tyr187) phosphorylation level was found to be reduced by directly inhibiting Ca2+ oscillation with 2-APB or CPA either in the presence or absence of serum. However, Akt (Thr308) phosphorylation was decreased only in the presence of serum, and serum-free starvation (2 h) eliminated Akt (Thr308) phosphorylation. Finally the calmodulin inhibitors W-7 and SKF-7171A were employed to further investigate whether this ubiquitous Ca2+ sensor is involved in the Ca2+ signal-mediated effect. Similarly, the phosphorylation level of Erk1/2 (Thr185/Tyr187) and Akt (Thr308) reduced upon the inhibition of calmodulin. In conclusion, our results demonstrate that IP3 receptors-mediated spontaneous Ca2+ oscillation and/or Ca2+/calmodulin signaling play(s) a crucial role in the regulation of cell proliferation mediated by multiple pro-proliferation signaling pathways (e.g. Mek/Erk and PI-3K/Akt). Importantly, Erk1/2 phosphorylation is sensitive to spontaneous Ca2+ oscillation, and therefore is responsible for the proliferation induced by Ca2+ oscillation in hMSCs.
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Kim, Kyunam, Hee Eun Kang, Jong In Yook, Hyung-Seog Yu, Euiseong Kim, Jung-Yul Cha, and Yoon Jeong Choi. "Transcriptional Expression in Human Periodontal Ligament Cells Subjected to Orthodontic Force: An RNA-Sequencing Study." Journal of Clinical Medicine 9, no. 2 (January 28, 2020): 358. http://dx.doi.org/10.3390/jcm9020358.
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This study was performed to investigate the changes in gene expression in periodontal ligament (PDL) cells following mechanical stimulus through RNA sequencing. In this study, premolars extracted for orthodontic treatment were used. To stimulate the PDL cells, an orthodontic force of 100× g was applied to the premolar (experimental group; n = 11), whereas the tooth on the other side was left untreated (control group; n = 11). After the PDL cells were isolated from the extracted teeth, gene set enrichment analysis (GSEA), differentially expressed gene (DEG) analysis, and real-time PCR were performed to compare the two groups. GSEA demonstrated that gene sets related to the cell cycle pathway were upregulated in PDL. Thirteen upregulated and twenty downregulated genes were found through DEG analysis. Real-time PCR results confirmed that five upregulated genes (CC2D1B, CPNE3, OPHN1, TANGO2, and UAP-1) and six downregulated genes (MYOM2, PPM1F, PCDP1, ATP2A1, GPR171, and RP1-34H18.1-1) were consistent with RNA sequencing results. We suggest that, from among these eleven genes, two upregulated genes, CPNE3 and OPHN1, and one downregulated gene, PPM1F, play an important role in PDL regeneration in humans when orthodontic force is applied.
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Dohrn, Maike F., Adriana P. Rebelo, Siddharth Srivastava, Gerarda Cappuccio, Robert Smigiel, Alka Malhotra, Donald Basel, et al. "De Novo ATP1A1 Variants in an Early-Onset Complex Neurodevelopmental Syndrome." Neurology 98, no. 11 (February 2, 2022): 440–45. http://dx.doi.org/10.1212/wnl.0000000000013276.
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ATP1A1 encodes the α1 subunit of the sodium-potassium ATPase, an electrogenic cation pump highly expressed in the nervous system. Pathogenic variants in other subunits of the same ATPase, encoded by ATP1A2 or ATP1A3, are associated with syndromes such as hemiplegic migraine, dystonia, or cerebellar ataxia. Worldwide, only 16 families have been reported carrying pathogenic ATP1A1 variants to date. Associated phenotypes are axonal neuropathies, spastic paraplegia, and hypomagnesemia with seizures and intellectual disability. By whole exome or genome sequencing, we identified 5 heterozygous ATP1A1 variants, c.674A>G;p.Gln225Arg, c.1003G>T;p.Gly335Cys, c.1526G>A;p.Gly509Asp, c.2152G>A;p.Gly718Ser, and c.2768T>A;p.Phe923Tyr, in 5 unrelated children with intellectual disability, spasticity, and peripheral, motor predominant neuropathy. Additional features were sensory loss, sleep disturbances, and seizures. All variants occurred de novo and are absent from control populations (MAF GnomAD = 0). Affecting conserved amino acid residues and constrained regions, all variants have high pathogenicity in silico prediction scores. In HEK cells transfected with ouabain-insensitive ATP1A1 constructs, cell viability was significantly decreased in mutants after 72h treatment with the ATPase inhibitor ouabain, demonstrating loss of ATPase function. Replicating the haploinsufficiency mechanism of disease with a gene-specific assay provides pathogenicity information and increases certainty in variant interpretation. This study further expands the genotype-phenotype spectrum of ATP1A1.
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Åkerström, Tobias, Holger Sven Willenberg, Kenko Cupisti, Julian Ip, Samuel Backman, Ana Moser, Rajani Maharjan, et al. "Novel somatic mutations and distinct molecular signature in aldosterone-producing adenomas." Endocrine-Related Cancer 22, no. 5 (October 2015): 735–44. http://dx.doi.org/10.1530/erc-15-0321.
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Aldosterone-producing adenomas (APAs) are found in 1.5–3.0% of hypertensive patients in primary care and can be cured by surgery. Elucidation of genetic events may improve our understanding of these tumors and ultimately improve patient care. Approximately 40% of APAs harbor a missense mutation in the KCNJ5 gene. More recently, somatic mutations in CACNA1D, ATP1A1 and ATP2B3, also important for membrane potential/intracellular Ca2+ regulation, were observed in APAs. In this study, we analyzed 165 APAs for mutations in selected regions of these genes. We then correlated mutational findings with clinical and molecular phenotype using transcriptome analysis, immunohistochemistry and semiquantitative PCR. Somatic mutations in CACNA1D in 3.0% (one novel mutation), ATP1A1 in 6.1% (six novel mutations) and ATP2B3 in 3.0% (two novel mutations) were detected. All observed mutations were located in previously described hotspot regions. Patients with tumors harboring mutations in CACNA1D, ATP1A1 and ATP2B3 were operated at an older age, were more often male and had tumors that were smaller than those in patients with KCNJ5 mutated tumors. Microarray transcriptome analysis segregated KCNJ5 mutated tumors from ATP1A1/ATP2B3 mutated tumors and those without mutation. We observed significant transcription upregulation of CYP11B2, as well as the previously described glomerulosa-specific gene NPNT, in ATP1A1/ATP2B3 mutated tumors compared to KCNJ5 mutated tumors. In summary, we describe novel somatic mutations in proteins regulating the membrane potential/intracellular Ca2+ levels, and also a distinct mRNA and clinical signature, dependent on genetic alteration.
Dissertations / Theses on the topic "ATP2A1 gene"
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Silverstein, Robert S. "Regulation of the Atp2b2 gene /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/10656.
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Cardin, V. "MECCANISMI PATOGENETICI NELLA EMICRANIA EMIPLEGICA FAMILIARE E SPORADICA:DESCRIZIONE DI TRE NUOVE MUTAZIONI DEL GENE ATP1A2." Doctoral thesis, Università degli Studi di Milano, 2010. http://hdl.handle.net/2434/150074.
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Familial hemiplegic migraine (FHM) is a rare, autosomal-dominant, form of migraine with aura. Sporadic hemiplegic migraine (SHM) is a heterogeneous disorder, where some patients may have a pathophysiology identical to FHM, with a mutation in one of the FHM genes (CACNA1A, ATP1A2, SCN1A), but others, possibly the majority, may have a different pathophysiologic background. In our study we have described 24 patients (13 FHM and 11 SHM) and their genetic screenings, positive for mutations only in 3 cases, 2 of them in apparently sporadic cases. All the mutations, 2 missense and 1 nonsense, are in ATP1A2 gene. Our results confirm a more frequent involvement of the ATP1A2 gene in the sporadic cases and, in our opinion, an identical pathogenesis of the Familial and the Sporadic forms. Moreover, the absence of mutations in the HM genes in the other 12 familial cases is probably the result of the involvement of many other genes and it underlines the crucial role of a biobank like this one.
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Singh, Prashant. "Regulation of the Menkes Protein in neuroendocrine Cells in Response to Copper." Bowling Green State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1237841061.
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Liu, Li. "Roles of PMCA Isoforms in Ca2+-Homeostasis and Contractility of Bladder Smooth Muscle: Evidence from PMCA Gene-Ablated Mice." Cincinnati, Ohio : University of Cincinnati, 2007. http://rave.ohiolink.edu/etdc/view.cgi?acc_num=ucin1178307168.
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Thesis (Ph.D.)--University of Cincinnati, 2007.Advisor: Richard J. Paul. Title from electronic thesis title page (viewed Apr. 4, 2009). Keywords: PMCA (human gene symbols; ATP2B); SERCA2 (human gene symbols; ATP2A2); NCX; bladder smooth muscle; Ca²⁺ homeostasis; gene-altered mice. Ca²⁺ waves; Ca²⁺ sparks; Fura-PE3; Fluo-4; Indo-1; multi-photon microscopy. Includes abstract. Includes bibliographical references.
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Lefebvre, Valerie. "Identification of Novel Parkinson’s Disease Genes Involved in Parkin Mediated Mitophagy." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/30222.
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Mitochondrial dysfunction has been implicated as one of the primary causes of Parkinson's disease (PD). The proteins PINK1, a serine-threonine kinase, and Parkin, an E3 ubiquitin ligase, are mutated in many genetic cases of PD. In healthy individuals, Parkin is recruited to damaged mitochondria and leads to autophagic degradation of mitochondria in a process termed mitophagy. Following depolarization of the mitochondrial membrane, PINK1 is stabilized on the outer mitochondrial membrane, and triggers Parkin translocation from the cytosol to mitochondria. Precisely how this phenomenon is regulated is still unclear. We employed RNA interference (RNAi) technology in a 384-well format to identify novel genes that are required for Parkin recruitment to mitochondria. We identified ATPase inhibitory factor 1 (IF1) as the strongest hit required for Parkin recruitment following treatment with the protonophore CCCP. We show that IF1 is upstream of PINK1 and Parkin, and required to sense mitochondrial damage by allowing the loss of membrane potential. In cells treated with CCCP, the absence of IF1 permits the ATP synthase to run freely in reverse, consuming ATP to maintain potential across the inner mitochondrial membrane, thus blocking PINK1 and Parkin activation. Interestingly, Rho0 cells, that lack mitochondrial DNA, have downregulated endogenous expression of IF1 in order to maintain mitochondrial function. Overexpression of IF1 in Rho0 cells results in the depletion of mitochondrial membrane potential and the initiation of mitophagy. These data demonstrate a unique role for IF1 in the regulation of mitochondrial quality control that has not been explored in the etiology of PD.
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Trivilin, Ana Paula. "Superexpressão do gene codificante do peptídeo AtPep1 em A.Thaliana visando a obtenção de resistência à isolados de diferentes espécies do gênero Pythium." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2008. http://hdl.handle.net/10183/15865.
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As plantas estão expostas a uma gama de patógenos que utilizam diversas estratégias para infectar seus hospedeiros. Em resposta, as plantas expressam diferentes mecanismos de defesa, onde ocorre o reconhecimento de moléculas conservadas do patógeno por receptores específicos das plantas, desencadeando as respostas de defesa. A descoberta de sinais endógenos e exógenos que regulam a expressão de genes de defesa em Arabidopsis thaliana tem auxiliado a compreensão dos mecanismos de defesa. O desenvolvimento de uma estratégia de superexpressão para avaliação do papel do peptídeo endógeno AtPep1 na resistência a isolados de diferentes espécies do gênero Pythium é importante para a compreensão do mecanismo de defesa e a futura utilização do mesmo em cultivares resistentes ao patógeno. Nesse sentido, foram realizados experimentos que consistiram da inoculação de A. thaliana com isolados das espécies de P. graminicola, P. inflatum, P. deliense e P. ultimum. As plantas foram avaliadas quanto à presença de sintomas da doença. Paralelamente, o gene codificante do peptídeo AtPep1, PROPEP1, foi isolado de A. thaliana, ligado nos vetores binários pGSA1427 ou pEGAD, e transformados em Agrobacterium tumefaciens. Células de A. tumefaciens contendo os plasmídeos com e sem PROPEP1 foram usadas para transformação floral de A. thaliana. As plantas transformadas foram selecionadas pela presença do gene que confere tolerância ao herbicida glufosinato de amônio e, no caso da planta transformada com o vetor pEGAD, também pela presença da GFP (proteína verde fluorescente). A presença dos genes inseridos foi confirmada por PCR seguido de seqüenciamento. As plantas transformadas foram avaliadas quanto ao acúmulo de mRNA de PROPEP1 e a resistência aos isolados do gênero Pythium. Os resultados indicam que plantas tipo selvagem de A. thaliana são suscetíveis aos isolados das diferentes espécies do gênero Pythium. As plantas pEGAD-AtPep apresentaram um aumento na expressão relativa de PROPEP1 de até 4.000 vezes a encontrada nas plantas controle. Este alto acúmulo de PROPEP1 nas plantas pEGAD-AtPep e pGSAAtPep revelou ser importante na resistência ao isolado de P. deliense. As evidências suportam o papel do peptídeo AtPep1 como um elicitor endógeno que é gerado em resposta aos patógenos e suas PAMPs.Plants are exposed to a range of pathogens that use several strategies to infect their host. In response, the plants express different mechanisms of defense, in which the recognition of conserved pathogen molecules by plant specific receptors triggers the defence responses. The discovery of exogenous and endogenous signals that regulate the expression of defense genes in Arabidopsis thaliana has helped the understanding of the mechanisms of defense. The development of a strategy of overexpression for evaluating the role of endogenous peptide AtPep1 in resistance to isolates of different species of the genus Pythium is important for understanding the mechanism of defense and its future use in resistant cultivars to the pathogen. Therefore, experiments that were performed consisted in the inoculation of A. thaliana with isolates of the of P. graminicola, P.inflatum, P. deliense, and P. ultimum species. The plants were evaluated for the presence of disease symptoms. In addition to that, the gene coding the peptide AtPep1, PROPEP1 was isolated from A. thaliana, ligated in the binary vectors pGSA1427 or pEGAD, and transformed in Agrobacterium tumefaciens. Cells of A. tumefaciens containing the plasmids with or without PROPEP1 were used to floral transformation of A. thaliana. The transformed plants were selected for the presence of the gene that confers tolerance to the herbicide ammonium glufosinate and, in the case of plants transformed with the vector pEGAD, they were also selected for the presence of GFP (green fluorescent protein). The presence of the inserted gene was confirmed by PCR followed by sequencing. The transformed plants were evaluated on the accumulation of mRNA from PROPEP1 and resistance to isolates of the genus Pythium. The results indicate that A. thaliana wild type plants are susceptible to isolates from various species of the genus Pythium. The pEGAD-AtPep plants showed an increase in the expression of PROPEP1 of up to 4.000 times more than that was found in control plants. Such high accumulation of PROPEP1 in pEGAD-AtPep and pGSA-AtPep plants was shown to be important in resistance to the isolate of P. deliense. The evidences support the role of the peptide AtPep1 as an endogenous elicitor that is generated in response to pathogens and their PAMPs.
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Minghetti, Matteo. "Characterisation and expression of copper homeostasis genes in sea bream (Sparus aurata)." Thesis, University of Stirling, 2009. http://hdl.handle.net/1893/1113.
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The redox properties of Copper (Cu) make it both an ideal cofactor for many enzymes, and, in its free form, a highly toxic molecule capable of stimulating production of reactive oxygen species or binding to protein thiol groups. Therefore, living organisms have evolved homeostatic systems to “handle” Cu avoiding dangerous and wasteful aspecific interactions. These systems comprise uptake, carrier, storage and excretion proteins. The importance of Cu-homeostatic systems was initially discovered in humans where alterations of Cu-excretory proteins were shown to be responsible for two lethal genetic disorders; the Wilson and Menkes diseases. The levels of bioavailable Cu in the aquatic environment is important because concentrations in oceanic waters tend to be minute, whilst in some fresh and coastal waters, particularly around areas of mineral extraction, viniculture and farming operations, concentrations can be excessive. In contrast to terrestrial vertebrates, fish are not only exposed to dietary sources of copper but are also exposed to dissolved ionic copper that may enter via the skin and gills. Indeed, the latter route is important in fish and it has been demonstrated in physiological studies that under conditions of dietary deficiency, fish can satisfy their own body requirements by uptake from water. Therefore, fish must have systems relating to both gill and gut to enable maintenance of body homeostasis of this essential, yet toxic, metal. In an attempt to understand the mechanisms of Cu homeostasis in fish, whether under conditions of deficiency, adequacy or excess, it is essential to consider the expression of known Cu-homeostasis proteins. Thus, cDNAs for sea bream (Sparus aurata) homologues of copper transporter 1 (Ctr1), antioxidant protein 1 (Atox1), Menkes protein (ATP7A), Wilson protein (ATP7B), and metallothionein (MT), which are responsible for the uptake, delivery to the secretory pathway and scavenging of intracellular Cu, were cloned and their mRNA tissue expression levels measured. To investigate the molecular basis of the different homeostatic and toxic responses to waterborne or dietary Cu, sea bream were exposed to sub-toxic levels of Cu in the diet (130 mg/Kg of dry diet) or water (0.3 mg/L) and tissue mRNA and Cu levels were measured. Moreover, to discriminate between the effect of different metals on the transcriptional regulation of Cu homeostasis genes in fish, Sparus aurata fibroblast (SAF1) cells were exposed to sub-toxic levels of Cu (25 μM), Zn (100 μM) and Cd (10 μM). In addition, a microarray was used to gain a broader overview of the transcriptional response of SAF1 cells to Cu (25 μM). Waterborne or dietary Cu resulted in distinct expression profiles of Cu-homeostasis genes and markers of oxidative stress. After dietary exposure, Cu increased in intestine and liver, whilst after waterborne exposure Cu increased in gill and liver. Exposure to dietary Cu resulted in decreases in Ctr1 and ATP7A mRNA in both liver and intestine. Renal Ctr1 levels remained unchanged, whilst ATP7A mRNA decreased. In contrast, waterborne Cu exposure increased intestinal Ctr1 and ATP7A mRNA, and increased renal Ctr1 and decreased renal ATP7A mRNA. Both dietary and waterborne Cu increased ATP7B mRNA in liver. Metallothionein (MT) mRNA increased in liver and gill after waterborne Cu. Glutathione reductase (GR), a marker of oxidative stress, increased expression in liver and gill after waterborne Cu exposure, but decreased in intestine. Thus, exposure to Cu via water or diet has different, often opposite effects on Cu-homeostasis genes. The decrease in expression of both Cu-transport genes in intestine after dietary exposure may indicate a defensive mechanism to limit uptake of Cu. The opposite effects in intestine after waterborne exposure are more difficult to explain, but again may reflect a defence mechanism against excess bloodborne Cu coming from the gill. Since both dietary and waterborne Cu increased Cu levels in liver and increased hepatic ATP7B it is likely that well-characterised mammalian route of Cu excretion to bile is active in sea bream. However, only hepatic Cu derived from gill increased the expression of the stress markers MT and GR. This suggests that Cu is delivered to liver in a different form from gill as that from intestine, the intestinally derived pool being less toxic. Thus the increase in copper transport gene expression in intestine after gill exposure might be a mechanism to enable incorporation of excess bloodborne Cu into the intestinal pathway of Cu delivery to liver, thus minimizing toxicity. The in vitro exposure of SAF1 cells to Cu showed a similar response to liver of fish exposed to waterborne Cu indicating similar Cu availability and complexation. ATP7A mRNA levels were induced by Cu but not by Zn or Cd suggesting Cu-specific regulation. Conversely, MT and GR were induced by all metals tested. The transcriptomic analysis highlighted that the biological processes most significantly affected by Cu were secretion, protein trafficking and stress. Overall, these results show that in fish copper has distinct effects on tissue Cu transporter genes and oxidative stress depending on whether it is taken up via the gill or gut and that intestinal absorption may be required for normal uptake and metabolism of Cu, regardless of the route of uptake. Moreover, changes in mRNA levels indicate that Cu homeostasis genes, at least in fish, may be regulated at the transcriptional level. Although more work needs to be done to identify genes that are robust predictors of Cu toxicity, the microarray results presented here show a clear transcriptional fingerprint which may characterize Cu toxicity in fish.
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Drager, Robert Gray. "Structure and transcript processing of a Euglena gracilis chloroplast operon encoding genes rps2, atpI, atpH, atpF, atpA and rps18." Diss., The University of Arizona, 1993. http://hdl.handle.net/10150/186334.
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A 9.8 kbp region of the Euglena gracilis chloroplast genome has been cloned, sequenced and analyzed. This region contains six genes, rps2, rps18, atpI, atpH, atpF and atpA which encode ribosomal proteins S2 and S18 and ATP synthase subunits CFₒIV, CFₒIII, CFₒI and CF₁α, respectively. The linear order of these genes, 5'-rps2-atpI-atpH-atpF-atpA-rps18-3', is similar to that of land plant chloroplasts. These six genes are co-transcribed with two tRNA genes which are 5' to rps2. A fully spliced, 5.5 kb transcript containing all six genes accumulates. The spliced hexa-cistronic transcript is processed by intercistronic cleavage to mono-cistronic mRNAs. The 5' ends of the accumulated mono-cistronic transcripts map to single-stranded regions of the most stable secondary structure for each intercistronic sequence. There is no evidence for initiation of transcription in this region of the Euglena gracilis chloroplast genome. This Euglena chloroplast operon is interrupted by 17 introns. Nine of the introns are group III and seven are group II. All of the group III introns have potential secondary structures near their 3' ends which resemble domain VI of group II introns. The remaining intron is a complex twintron excised as four group III introns. This intron is comprised of two group III introns within the internal intron of a group III twintron. Two of the internal introns are excised from multiple splice sites. Two of the internal introns interrupt the domain VI-like structure of the host group III intron. The 16S rRNA sequence of Euglena chloroplasts is phylogenetically related to the 16S rRNA sequence of chromophyte chloroplasts, while the Euglena derived atpA amino acid sequence is more closely related to atpA sequences of chlorophyte chloroplasts than to atpA sequences of chromophyte chloroplasts. Too few chloroplast ribosomal protein sequences are available in the databases to perform meaningful phylogenetic analysis of rps2 or rps18. Although clustering of rps2 with the ATP synthase genes in chloroplasts of chlorophytes, rhodophytes, chromophytes and euglenophytes, but not prokaryotes, is evidence that chloroplasts are of mono-phyletic origin.
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Höhn, Stephanie [Verfasser], Wolfgang [Akademischer Betreuer] Kreis, and Wolfgang [Gutachter] Kreis. "21-Hydroxypregnan-21O-Malonyltransferasen aus Arabidopsis thaliana und Erysimum crepidifolium: Teilreinigung und Charakterisierung sowie rekombinante Expression des AtPMaT1 Gens / Stephanie Höhn ; Gutachter: Wolfgang Kreis ; Betreuer: Wolfgang Kreis." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2018. http://d-nb.info/1163455792/34.
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RIMBAULT, BLANDINE. "Etude de l'expression des genes chloroplastiques atpa et atpb, codant pour les sous unites et de l'atp synthetase, dans l'algue verte c. Reinhardtii." Paris 11, 2001. http://www.theses.fr/2001PA112043.
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L'origine endosymbiotique des chloroplastes se manifeste par le transfert de nombreux genes, a partir de l'ancetre procaryote, dans le genome nucleaire. L'existence, pour chaque complexe de l'appareil photosynthetique, de sous unites codees par le genome nucleaire et d'autres codees par le chloroplaste implique une regulation de l'expression des genes, afin que les sous unites soient produites dans les proportions requises pour leur assemblage. Les travaux presentes dans notre these concernent la regulation de l'expression de deux genes chloroplastiques de l'algue verte c. Reinhardtii, atpa et atpb, codant pour les sous unites et du complexe de l'atp synthetase. La majeure partie des genes chloroplastiques sont transcrits separement et de maniere independante. Le gene atpa fait cependant partie d'une des rares unites de transcription qui comprend trois autres genes : psbl cema et atph. Huit transcrits sont accumules. Le gene atpa occupe une position privilegiee, en tant que gene situe le plus en amont de l'unite de transcription. L'efficacite de sa traduction ne depend ni de la nature, mono ou polycistronique des transcrits contenant la phase codante de atpa, ni de leur accumulation. Le gene atpb est plus representatif de l'ensemble des genes demeures dans le chloroplaste. Un facteur nucleaire specifique, mdb1p, agit au niveau de la stabilite du transcrit. Ce facteur agit en stabilisant le transcrit, peut-etre en le rendant competent pour la traduction. Le transcrit subit de plus une maturation de la region 5 qui depend de la nature, chloroplastique ou bacterienne, de sa phase codante. Meme si le transcrit atpb possede trois codons d'initiation possibles, la traduction s'effectue a partir d'un seul aug : c'est uniquement la position du codon qui determine la traduction. Enfin nous avons mis en evidence que la traduction de atpa et atpb est coordonnee en fonction de l'assemblage de l'enzyme. L'absence d'une sous-unite du couple perturbe la synthese de l'autre sous unite: nous avons montre que des intermediaires dans la voie de biogenese de l'atp synthetase regulent negativement la synthese des deux sous unites.
Books on the topic "ATP2A1 gene"
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Trocello, Jean-Marc, and France Woimant. Disorders of Copper and Iron Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0044.
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Both copper and iron are essential metals that have a critical function in a series of biochemical pathways. This chapter describes the disorders associated with genetic abnormalities in copper and iron metabolic pathways and their manifestations in adult patients. Mutations in the genes of the copper transporting P-type ATPases, ATP7A and ATP7B are associated with Wilson disease, Menkes disease, occipital horn syndrome and ATP7A-related distal motor neuropathy. Neurodegeneration with brain iron accumulation (NBIA) is a group of disorders characterized by excess iron deposition in globus pallidus, substantia nigra pars reticulata, striata and cerebellar dentate nuclei. Several genes associated with NBIA have been identified.
Book chapters on the topic "ATP2A1 gene"
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Tümer, Zeynep, Lisbeth Birk Møller, and Nina Horn. "Mutation Spectrum of ATP7A, the Gene Defective in Menkes Disease." In Copper Transport and Its Disorders, 83–95. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4859-1_7.
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Bizec, C. Le, S. Nicole, E. Panagiotakaki, N. Seta, and S. Vuillaumier-Barrot. "No Mutation in the SLC2A3 Gene in Cohorts of GLUT1 Deficiency Syndrome–Like Patients Negative for SLC2A1 and in Patients with AHC Negative for ATP1A3." In JIMD Reports, 115–20. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/8904_2013_253.
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Bortolozzi, Mario. "Defects in the Atp2b2 Gene Causing Hereditary Hearing and Balance Loss in Mice and Humans: A Biophysical Study of Normal and Mutated PMCA2 Pump Function." In Biophotonics: Spectroscopy, Imaging, Sensing, and Manipulation, 371. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9977-8_23.
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"ATP2A1-3 (Human Genes for SERCA1-3)." In Encyclopedia of Metalloproteins, 201. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1533-6_100146.
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Kaler, Stephen G., and Courtney S. Holmes. "Catecholamine Metabolites Affected by the Copper-Dependent Enzyme Dopamine-Beta-Hydroxylase Provide Sensitive Biomarkers for Early Diagnosis of Menkes Disease and Viral-Mediated ATP7A Gene Therapy." In A New Era of Catecholamines in the Laboratory and Clinic, 223–33. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-411512-5.00011-7.
Full textConference papers on the topic "ATP2A1 gene"
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Rombouts, T., T. Druet, J. L. Gualdrón Duarte, N. Ahariz, K. Karim, W. Coppieters, S. D. Smet, M. Georges, and C. Charlier. "634. A hypomorphic mutation in the ATP2A1 gene increases muscle mass yet compromises meat quality of Belgian Blue cattle." In World Congress on Genetics Applied to Livestock Production. The Netherlands: Wageningen Academic Publishers, 2022. http://dx.doi.org/10.3920/978-90-8686-940-4_634.
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Nussa, H. T., S. B. Aritonang, S. A. Puteri, A. F. Rahmani, A. Bowolaksono, and R. Lestari. "Thermal stress effect on ATP1A1 gene expression in Bali cattle (Bos sondaicus) in Barru district, South Sulawesi." In PROCEEDINGS OF THE 3RD INTERNATIONAL SYMPOSIUM ON CURRENT PROGRESS IN MATHEMATICS AND SCIENCES 2017 (ISCPMS2017). Author(s), 2018. http://dx.doi.org/10.1063/1.5064149.
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Resende, Ana Flávia Morais, Guilherme Rabelo Nasuk, Bruna Calixto de Jesus, Allan Luis Barboza Atum, and José Antônio Silva Júnior. "EXPRESSÃO MIOCÁRDICA RELACIONADA À CINÉTICA DO CÁLCIO EM ANIMAIS COM EXPOSIÇÃO PRÉ-NATAL AO ÁLCOOL." In Congresso Médico Acadêmico da Universidade Nove de Julho. Universidade Nove de Julho, 2022. http://dx.doi.org/10.5585/comamedvg.2022.16.
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Introdução: A exposição alcoólica pré-natal (E.P.A.) é considerada uma das principais responsáveis pelas alterações congênitas humanas. No sistema cardiovascular, a E.P.A. pode levar a alterações na expressão de genes relacionados à homeostase cardiovascular. Estudos têm mostrado que miócitos cardíacos expostos ao etanol durante a embriogênese não amadurecem morfológica ou funcionalmente, bem como apresentam alterações no transporte e captação/ligação de Ca2+ pelo retículo sarcoplasmático (SR). Uma diminuição da concentração citosólica de Ca2+ resultante do um efeito inibitório do álcool nas proteínas reguladoras desse íon pode resultar em diminuição do volume sistólico e alterações na frequência cardíaca. Objetivo: Analisar o impacto da E.P.A. na ativação da via de transdução de sinal da cinética do cálcio pela análise da expressão de RNA mensageiro de componentes desta via. Materiais e Métodos: O estudo foi aprovado pelo Comitê de Ética no Uso de Animais (CEUA = 9355120319 ID 000115). Foram utilizados camundongos isogênicos da linhagem C57Bl/6. As fêmeas progenitoras foram separadas e randomizadas no grupo controle (n=4) e no grupo de exposição ao álcool (n=11). O protocolo do grupo E.P.A. durante a gestação, foi a exposição do álcool na proporção de 10% (v/v) diluídos em água de consumo. Após 45 dias, 10 filhotes de cada grupo (n=20) foram anestesiados com isoflurano (<20 seg.) e decapitados. O ventrículo esquerdo (VE) foi coletado e tratado. A expressão relativa foi obtida por técnica RT-qPCR utilizando placas customizadas TaqMan®, sendo utilizado como controle endógeno o gene rRNA 18S. A estatística foi calculada com a aplicação IBM SPSS Statistics for Windows, Version 25.0. (Armonk, NY: IBM Corp., 2017); A normalidade foi testada através do teste de Shapiro-Wilk e os dados representados por média ± EPM. Comparação entre grupos: Teste T para amostras independentes sendo considerado o valor de significância p ≤0,05. Resultados: No grupo E.P.A, houve redução de 65,51% (p<0,001) e 60,17% (p<0,001) na expressão dos genes Calsequestrina 2 (Casq2) e Família de trocadores de soluto (Na-Ca) 8, membro A1 (Slc8a1), respectivamente, quando comparados ao grupo Controle. Por sua vez, o grupo E.P.A. apresentou aumento de 254,86% (p<0,001), 231,70% (p<0,001) e 183,37% (p<0,001) na expressão dos genes ATPase, transporte de Ca ++, músculo cardíaco, contração lenta 2 (Atp2a2), Receptor 2 de Rianodina, Cardíaco (RyR-2) e Fosfolamban (Pln) nessa ordem, quando comparado ao grupo Controle. Conclusão: Concluímos que a agressão mediada pelo álcool no miocárdio pode modular a via de cinética de cálcio. Estes resultados indicam que o insulto gerado pelo álcool, por meio de EPA e dependendo da concentração e/ou duração do estímulo, pode comprometer a expressão proteica de componentes da cinética do cálcio em favor de uma disfunção cardíaca. Palavras-chave: Álcool; cálcio; genes.
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Flodby, Per, Zea Borok, Danping Gao, Yong-Ho Kim, Agnes Banfalvi, Kwang-Jin Kim, and Edward D. Crandall. "AT1 Cell-Specific Knockout Of The Sodium Pump B1 Subunit Gene (ATP1B1) Results In Impaired Alveolar Fluid Clearance." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4230.
Full textReports on the topic "ATP2A1 gene"
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Izhar, Shamay, Maureen Hanson, and Nurit Firon. Expression of the Mitochondrial Locus Associated with Cytoplasmic Male Sterility in Petunia. United States Department of Agriculture, February 1996. http://dx.doi.org/10.32747/1996.7604933.bard.
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The main goal of the proposed research was to continue the mutual investigations into the molecular basis of CMS and male fertility restoration [MRF], with the ultimate goal of understanding these phenomena in higher plants. The experiments focused on: (1) dissecting apart the complex CMS - specific mitochondrial S-Pcf locus, in order to distinguish its essential parts which cause sterility from other parts and study its molecular evolution. (2) Studying the expression of the various regions of the S-Pcf locus in fertile and sterile lines and comparing the structure and ultrastructure of sterile and fertile tissues. (3) Determine whether alteration in respiration is genetically associated with CMS. Our mutual investigations further substantiated the association between the S-Pcf locus and CMS by the findings that the fertile phenotype of a population of unstable petunia somatic hybrids which contain the S-Pcf locus, is due to the presence of multiple muclear fertility restoration genes in this group of progenies. The information obtained by our studies indicate that homologous recombination played a major role in the molecular evolution of the S-Pcf locus and the CMS trait and in the generation of mitochondrial mutations in general. Our data suggest that the CMS cytoplasm evolved by introduction of a urs-s containing sublimon into the main mitochondrial genome via homologous recombination. We have also found that the first mutation detected so far in S-Pcf is a consequence of a homologous recombination mechanism involving part of the cox2 coding sequence. In all the cases studied by us, at the molecular level, we found that fusion of two different cells caused mitochondrial DNA recombination followed by sorting out of a specific mtDNA population or sequences. This sequence of events suggested as a mechanism for the generation of novel mitochondrial genomes and the creation of new traits. The present research also provides data concerning the expression of the recombined and complex CMS-specific S-Pcf locus as compared with the expression of additional mitochondrial proteins as well as comparative histological and ultrastructural studies of CMS and fertile Petunia. Evidence is provided for differential localization of mitochondrially encoded proteins in situ at the tissue level. The similar localization patterns of Pcf and atpA may indicate that Pcf product could interfere with the functioning of the mitochondrial ATPase in a tissue undergoing meiosis and microsporogenesis. Studies of respiration in CMS and fertile Petunia lines indicate that they differe in the partitioning of electron transport through the cytochrome oxidase and alternative oxidase pathways. The data indicate that the electron flux through the two oxidase pathways differs between mitochondria from fertile and sterile Petunia lines at certain redox states of the ubiquinone pool. In summary, extensive data concerning the CMS-specific S-Pcf locus of Petunia at the DNA and protein levels as well as information concerning different biochemical activity in CMS as compared to male fertile lines have been accumulated during the three years of this project. In addition, the involvement of the homologous recombination mechanism in the evolution of mt encoded traits is emphasized.