Journal articles: 'Arl14'

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Brito, Cheila, Bruno Costa-Silva, Duarte C. Barral, and Marta Pojo. "Unraveling the Relevance of ARL GTPases in Cutaneous Melanoma Prognosis through Integrated Bioinformatics Analysis." International Journal of Molecular Sciences 22, no. 17 (August 26, 2021): 9260. http://dx.doi.org/10.3390/ijms22179260.

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Cutaneous melanoma (CM) is the deadliest skin cancer, whose molecular pathways underlying its malignancy remain unclear. Therefore, new information to guide evidence-based clinical decisions is required. Adenosine diphosphate (ADP)-ribosylation factor-like (ARL) proteins are membrane trafficking regulators whose biological relevance in CM is undetermined. Here, we investigated ARL expression and its impact on CM prognosis and immune microenvironment through integrated bioinformatics analysis. Our study found that all 22 ARLs are differentially expressed in CM. Specifically, ARL1 and ARL11 are upregulated and ARL15 is downregulated regardless of mutational frequency or copy number variations. According to TCGA data, ARL1 and ARL15 represent independent prognostic factors in CM as well as ARL11 based on GEPIA and OncoLnc. To investigate the mechanisms by which ARL1 and ARL11 increase patient survival while ARL15 reduces it, we evaluated their correlation with the immune microenvironment. CD4+ T cells and neutrophil infiltrates are significantly increased by ARL1 expression. Furthermore, ARL11 expression was correlated with 17 out of 21 immune infiltrates, including CD8+ T cells and M2 macrophages, described as having anti-tumoral activity. Likewise, ARL11 is interconnected with ZAP70, ADAM17, and P2RX7, which are implicated in immune cell activation. Collectively, this study provides the first evidence that ARL1, ARL11, and ARL15 may influence CM progression, prognosis, and immune microenvironment remodeling.

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Yang, Feng, Tiantian Li, Ziqing Peng, Yang Liu, and Yusong Guo. "The amphipathic helices of Arfrp1 and Arl14 are sufficient to determine subcellular localizations." Journal of Biological Chemistry 295, no. 49 (September 24, 2020): 16643–54. http://dx.doi.org/10.1074/jbc.ra120.014999.

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The subcellular localization of Arf family proteins is generally thought to be determined by their corresponding guanine nucleotide exchange factors. By promoting GTP binding, guanine nucleotide exchange factors induce conformational changes of Arf proteins exposing their N-terminal amphipathic helices, which then insert into the membranes to stabilize the membrane association process. Here, we found that the N-terminal amphipathic motifs of the Golgi-localized Arf family protein, Arfrp1, and the endosome- and plasma membrane–localized Arf family protein, Arl14, play critical roles in spatial determination. Exchanging the amphipathic helix motifs between these two Arf proteins causes the switch of their localizations. Moreover, the amphipathic helices of Arfrp1 and Arl14 are sufficient for cytosolic proteins to be localized into a specific cellular compartment. The spatial determination mediated by the Arfrp1 helix requires its binding partner Sys1. In addition, the residues that are required for the acetylation of the Arfrp1 helix and the myristoylation of the Arl14 helix are important for the specific subcellular localization. Interestingly, Arfrp1 and Arl14 are recruited to their specific cellular compartments independent of GTP binding. Our results demonstrate that the amphipathic motifs of Arfrp1 and Arl14 are sufficient for determining specific subcellular localizations in a GTP-independent manner, suggesting that the membrane association and activation of some Arf proteins are uncoupled.

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Zhang, Binbin, Aiqun Xu, Dong Wu, Wanli Xia, Pulin Li, Enze Wang, Rui Han, Peng Sun, Sijing Zhou, and Ran Wang. "ARL14 as a Prognostic Biomarker in Non-Small Cell Lung Cancer." Journal of Inflammation Research Volume 14 (December 2021): 6557–74. http://dx.doi.org/10.2147/jir.s340119.

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Yang, Yong-Kang, Hong Qu, Dong Gao, Wei Di, Hai-Wei Chen, Xin Guo, Zhong-He Zhai, and Dan-Ying Chen. "ARF-like Protein 16 (ARL16) Inhibits RIG-I by Binding with Its C-terminal Domain in a GTP-dependent Manner." Journal of Biological Chemistry 286, no. 12 (January 13, 2011): 10568–80. http://dx.doi.org/10.1074/jbc.m110.206896.

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Retinoic acid-inducible gene I (RIG-I) recognizes RNA virus-derived nucleic acids, which leads to the production of type I interferon (IFN) in most cell types. Tight regulation of RIG-I activity is important to prevent ultra-immune responses. In this study, we identified an ARF-like (ARL) family member, ARL16, as a protein that interacts with RIG-I. Overexpression of ARL16, but not its homologous proteins ARL1 and ARF1, inhibited RIG-I-mediated downstream signaling and antiviral activity. Knockdown of endogenous ARL16 by RNAi potentiated Sendai virus-induced IFN-β expression and vesicular stomatitis virus replication. ARL16 interacted with the C-terminal domain (CTD) of RIG-I to suppress the association between RIG-I and RNA. ARL16 (T37N) and ARL16Δ45–54, which were restricted to the GTP-disassociated form, did not interact with RIG-I and also lost the inhibitory function. Furthermore, we suggest that endogenous ARL16 changes to GTP binding status upon viral infection and binds with the RIG-I CTD to negatively control its signaling activity. These findings suggested a novel innate immune function for an ARL family member, and a GTP-dependent model in which RIG-I is regulated.

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Acosta-Herrera, Marialbert, Martin Kerick, David González-Serna, Cisca Wijmenga, Andre Franke, Peter K. Gregersen, Leonid Padyukov, et al. "Genome-wide meta-analysis reveals shared new loci in systemic seropositive rheumatic diseases." Annals of the Rheumatic Diseases 78, no. 3 (December 20, 2018): 311–19. http://dx.doi.org/10.1136/annrheumdis-2018-214127.

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ObjectiveImmune-mediated inflammatory diseases (IMIDs) are heterogeneous and complex conditions with overlapping clinical symptoms and elevated familial aggregation, which suggests the existence of a shared genetic component. In order to identify this genetic background in a systematic fashion, we performed the first cross-disease genome-wide meta-analysis in systemic seropositive rheumatic diseases, namely, systemic sclerosis, systemic lupus erythematosus, rheumatoid arthritis and idiopathic inflammatory myopathies.MethodsWe meta-analysed ~6.5 million single nucleotide polymorphisms in 11 678 cases and 19 704 non-affected controls of European descent populations. The functional roles of the associated variants were interrogated using publicly available databases.ResultsOur analysis revealed five shared genome-wide significant independent loci that had not been previously associated with these diseases: NAB1, KPNA4-ARL14, DGQK, LIMK1 and PRR12. All of these loci are related with immune processes such as interferon and epidermal growth factor signalling, response to methotrexate, cytoskeleton dynamics and coagulation cascade. Remarkably, several of the associated loci are known key players in autoimmunity, which supports the validity of our results. All the associated variants showed significant functional enrichment in DNase hypersensitivity sites, chromatin states and histone marks in relevant immune cells, including shared expression quantitative trait loci. Additionally, our results were significantly enriched in drugs that are being tested for the treatment of the diseases under study.ConclusionsWe have identified shared new risk loci with functional value across diseases and pinpoint new potential candidate loci that could be further investigated. Our results highlight the potential of drug repositioning among related systemic seropositive rheumatic IMIDs.

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Wicky, Sidonie, Heinz Schwarz, and Birgit Singer-Krüger. "Molecular Interactions of Yeast Neo1p, an Essential Member of the Drs2 Family of Aminophospholipid Translocases, and Its Role in Membrane Trafficking within the Endomembrane System." Molecular and Cellular Biology 24, no. 17 (September 1, 2004): 7402–18. http://dx.doi.org/10.1128/mcb.24.17.7402-7418.2004.

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ABSTRACT Neo1p is an essential yeast member of the highly conserved Drs2 family of P-type ATPases with proposed aminophospholipid translocase activity. Here we present evidence that Neo1p localizes to endosomes and Golgi elements. In agreement with that finding, the temperature-sensitive neo1-37 and neo1-69 mutants exhibit defects in receptor-mediated endocytosis, vacuole biogenesis, and vacuolar protein sorting. Furthermore, neo1 mutants accumulate aberrantly shaped membranous structures most likely derived from vacuoles and the endosomal/Golgi system. At permissive temperatures, HA-Neo1-69p, like wild-type Neo1p, is stable and associates with endosomes. In contrast, HA-Neo1-37p is rapidly degraded and is predominantly retained within the endoplasmic reticulum (ER). Thus, the two neo1 alleles affect the stability and localization of the mutant polypeptides in different ways. A C-terminally truncated and a C-terminally epitope-tagged version of Neo1p are nonfunctional and also mislocalize to the ER. In agreement with a role within the endomembrane system, Neo1p exhibits genetic and physical interactions with Ysl2p, a potential guanine nucleotide exchange factor for Arl1p. Interestingly, deletion of ARL1 rescues the temperature sensitivity of neo1-37 and neo1-69. We demonstrate that Arl1p in its myristoylated and GTP-bound form is responsible for the inhibitory effect. Thus, Neo1p, Ysl2p, and Arl1p represent three proteins that collaborate in membrane trafficking within the endosomal/Golgi system.

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Zolotarov, Yevgen, Chao Ma, Irene González-Recio, Serge Hardy, Gijs A. C. Franken, Noriko Uetani, Femke Latta, et al. "ARL15 modulates magnesium homeostasis through N-glycosylation of CNNMs." Cellular and Molecular Life Sciences 78, no. 13 (June 5, 2021): 5427–45. http://dx.doi.org/10.1007/s00018-021-03832-8.

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AbstractCyclin M (CNNM1-4) proteins maintain cellular and body magnesium (Mg2+) homeostasis. Using various biochemical approaches, we have identified members of the CNNM family as direct interacting partners of ADP-ribosylation factor-like GTPase 15 (ARL15), a small GTP-binding protein. ARL15 interacts with CNNMs at their carboxyl-terminal conserved cystathionine-β-synthase (CBS) domains. In silico modeling of the interaction between CNNM2 and ARL15 supports that the small GTPase specifically binds the CBS1 and CNBH domains. Immunocytochemical experiments demonstrate that CNNM2 and ARL15 co-localize in the kidney, with both proteins showing subcellular localization in the endoplasmic reticulum, Golgi apparatus and the plasma membrane. Most importantly, we found that ARL15 is required for forming complex N-glycosylation of CNNMs. Overexpression of ARL15 promotes complex N-glycosylation of CNNM3. Mg2+ uptake experiments with a stable isotope demonstrate that there is a significant increase of 25Mg2+ uptake upon knockdown of ARL15 in multiple kidney cancer cell lines. Altogether, our results establish ARL15 as a novel negative regulator of Mg2+ transport by promoting the complex N-glycosylation of CNNMs.

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Hsu, Jia-Wei, Pei-Hua Tang, I.-Hao Wang, Chia-Lun Liu, Wen-Hui Chen, Pei-Chin Tsai, Kuan-Yu Chen, Kuan-Jung Chen, Chia-Jung Yu, and Fang-Jen S. Lee. "Unfolded protein response regulates yeast small GTPase Arl1p activation at late Golgi via phosphorylation of Arf GEF Syt1p." Proceedings of the National Academy of Sciences 113, no. 12 (March 10, 2016): E1683—E1690. http://dx.doi.org/10.1073/pnas.1518260113.

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ADP ribosylation factor (Arf) GTPases are key regulators of membrane traffic at the Golgi complex. In yeast, Arf guanine nucleotide-exchange factor (GEF) Syt1p activates Arf-like protein Arl1p, which was accompanied by accumulation of golgin Imh1p at late Golgi, but whether and how this function of Syt1p is regulated remains unclear. Here, we report that the inositol-requiring kinase 1 (Ire1p)-mediated unfolded protein response (UPR) modulated Arl1p activation at late Golgi. Arl1p activation was dependent on both kinase and endo-RNase activities of Ire1p. Moreover, constitutively active transcription factor Hac1p restored the Golgi localization of Arl1p and Imh1p inIRE1-deleted cells. Elucidating the mechanism of Ire1p–Hac1p axis actions, we found that it regulated phosphorylation of Syt1p, which enhances Arl1p activation, recruitment of Imh1p to the Golgi, and Syt1p interaction with Arl1p. Consistent with these findings, the induction of UPR by tunicamycin treatment increases phosphorylation of Syt1p, resulting in Arl1p activation. Thus, these findings clarify how the UPR influences the roles of Syt1p, Arl1p, and Imh1p in Golgi transport.

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Liu, Ya-Wen, Chun-Fang Huang, Kai-Bin Huang, and Fang-Jen S. Lee. "Role for Gcs1p in Regulation of Arl1p atTrans-Golgi Compartments." Molecular Biology of the Cell 16, no. 9 (September 2005): 4024–33. http://dx.doi.org/10.1091/mbc.e05-01-0023.

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ADP-ribosylation factor (ARF) and ARF-like (ARL) proteins are members of the ARF family, which are critical components of several different vesicular trafficking pathways. ARFs have little or no detectable GTPase activity without the assistance of a GTPase-activating protein (GAP). Here, we demonstrate that yeast Gcs1p exhibits GAP activity toward Arl1p and Arf1p in vitro, and Arl1p can interact with Gcs1p in a GTP-dependent manner. Arl1p was observed both on trans-Golgi and in cytosol and was recruited from cytosol to membranes in a GTP-dependent manner. In gcs1 mutant cells, the fraction of Arl1p in cytosol relative to trans-Golgi was less than it was in wild-type cells. Increasing Gcs1p levels returned the distribution toward that of wild-type cells. Both Arl1p and Gcs1p influenced the distribution of Imh1p, an Arl1p effector. Our data are consistent with the conclusion that Arl1p moves in a dynamic equilibrium between trans-Golgi and cytosol, and the release of Arl1p from membranes in cells requires the hydrolysis of bound GTP, which is accelerated by Gcs1p.

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Xie, Ning, Qiuai Shu, Ziwei Wang, Xindi Huang, Yalan Wang, Bin Qin, Yan Chen, et al. "ARL11 correlates with the immunosuppression and poor prognosis in breast cancer: A comprehensive bioinformatics analysis of ARL family members." PLOS ONE 17, no. 11 (November 11, 2022): e0274757. http://dx.doi.org/10.1371/journal.pone.0274757.

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ADP-ribosylation factor-like protein (ARL) family members (ARLs) may regulate the malignant phenotypes of cancer cells. However, relevant studies on ARLs in breast cancer (BC) are limited. In this research, the expression profiles, genetic variations, and prognostic values of ARLs in BC have been systematically analyzed for the first time using various databases. We find that ARLs are significantly dysregulated in BC according to the TCGA database, which may result from DNA methylation and copy number alteration. Prognostic analysis suggests that ARL11 is the most significant prognostic indicator for BC, and higher ARL11 predicts worse clinical outcomes for BC patients. Further functional enrichment analysis demonstrates that ARL11 enhances the immunosuppression in BC, and dysregulation of ARL11 is significantly associated with immune infiltration in various types of cancer. Our results demonstrate the potential of ARL11 as an immune therapeutic target for BC.

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Schürmann, A., S. Koling, S. Jacobs, P. Saftig, S. Krauβ, G. Wennemuth, R. Kluge, and H. G. Joost. "Reduced Sperm Count and Normal Fertility in Male Mice with Targeted Disruption of the ADP-Ribosylation Factor-Like 4 (Arl4) Gene." Molecular and Cellular Biology 22, no. 8 (April 15, 2002): 2761–68. http://dx.doi.org/10.1128/mcb.22.8.2761-2768.2002.

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ABSTRACT The ADP-ribosylation factor-like protein 4 (ARL4) is a 22-kDa GTP-binding protein which is abundant in testes of pubertal and adult rodents but absent in testes from prepubertal animals. During testis development, ARL4 expression starts at day 16 when the spermatogenesis proceeds to the late pachytene. In the adult testis, the ARL4 protein was detected in pre- and postmeiotic cells, spermatocytes, and spermatides, but not in spermatogonia and mature spermatozoa. Mouse Arl4-null mutants generated by targeted disruption of the Arl4 gene were viable and grew normally; male as well as female Arl4−/− mice were fertile. However, inactivation of the Arl4 gene resulted in a significant reduction of testis weight and sperm count by 30 and 60%, respectively, without reduction of litter size or frequency. It is suggested that the disruption of Arl4 produces a moderate retardation of germ cell development, possibly at the stage of meiosis.

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Lu, Lei, and Wanjin Hong. "Interaction of Arl1-GTP with GRIP Domains Recruits Autoantigens Golgin-97 and Golgin-245/p230 onto the Golgi." Molecular Biology of the Cell 14, no. 9 (September 2003): 3767–81. http://dx.doi.org/10.1091/mbc.e03-01-0864.

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A cellular role and the mechanism of action for small GTPase Arl1 have been defined. Arl1-GTP interacts with the GRIP domains of Golgin-97 and Golgin-245, a process dependent on conserved residues of the GRIP domains that are important for Golgi targeting. The switch II region of Arl1 confers the specificity of this interaction. Arl1-GTP mediates Golgi recruitment of Golgin-97 in a switch II-dependent manner, whereas tethering Arl1-GTP onto endosomes can mediate endosomal targeting of Golgin-97. Golgin-97 and Golgin-245 are dissociated from the Golgi when Arl1 is knocked-down by its siRNA. Arl1-GTP thus functions to recruit Golgin-97 and Golgin-245 onto the Golgi via interacting with their GRIP domains.

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Lu, Lei, Heinz Horstmann, Cheepeng Ng, and Wanjin Hong. "Regulation of Golgi structure and function by ARF-like protein 1 (Arl1)." Journal of Cell Science 114, no. 24 (December 15, 2001): 4543–55. http://dx.doi.org/10.1242/jcs.114.24.4543.

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Arl1 is a member of the ARF-like protein (Arl) subfamily of small GTPases. Nothing is known about the function of Arl1 except for the fact that it is essential for normal development in Drosophila and that it is associated with the Golgi apparatus. In this study, we first demonstrate that Arl1 is enriched at the trans side of the Golgi, marked by AP-1. Association of Arl1 with the Golgi is saturable in intact cells and depends on N-terminal myristoylation. Over-expression of Arl1(T31N), which is expected to be restricted to the GDP-bound form and thus function as a dominant-negative mutant, causes the disappearance of the Golgi apparatus (marked by Golgi SNARE GS28), suggesting that Arl1 is necessary for maintaining normal Golgi structure. Overexpression of Arl1(Q71L), a mutant restricted primarily to the activated GTP-bound form, causes an expansion of the Golgi apparatus with massive and stable Golgi association of COPI and AP-1 coats. Interestingly, Golgi ARFs also become stably associated with the expanded Golgi. Transport of the envelope protein of vesicular stomatitis virus (VSV-G) along the secretory pathway is arrested at the expanded Golgi upon expression of Arl1(Q71L). The structure of stacked cisternae of the Golgi is disrupted in cells expressing Arl1(Q71L), resulting in the transformation of the Golgi into an extensive vesicule-tubule network. In addition, the GTP form of Arl1 interacts with arfaptin-2/POR1 but not GGA1, both of which interact with GTP-restricted ARF1, suggesting that Arl1 and ARF1 share some common effectors in regulating cellular events. On the basis of these observations, we propose that one of the mechanisms for the cell to regulate the structure and function of the Golgi apparatus is through the action of Arl1.

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Benjamin, Jeremy J. R., Pak P. Poon, John D. Drysdale, Xiangmin Wang, Richard A. Singer, and Gerald C. Johnston. "Dysregulated Arl1, a regulator of post-Golgi vesicle tethering, can inhibit endosomal transport and cell proliferation in yeast." Molecular Biology of the Cell 22, no. 13 (July 2011): 2337–47. http://dx.doi.org/10.1091/mbc.e10-09-0765.

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Small monomeric G proteins regulated in part by GTPase-activating proteins (GAPs) are molecular switches for several aspects of vesicular transport. The yeast Gcs1 protein is a dual-specificity GAP for ADP-ribosylation factor (Arf) and Arf-like (Arl)1 G proteins, and also has GAP-independent activities. The absence of Gcs1 imposes cold sensitivity for growth and endosomal transport; here we present evidence that dysregulated Arl1 may cause these impairments. We show that gene deletions affecting the Arl1 or Ypt6 vesicle-tethering pathways prevent Arl1 activation and membrane localization, and restore growth and trafficking in the absence of Gcs1. A mutant version of Gcs1 deficient for both ArfGAP and Arl1GAP activity in vitro still allows growth and endosomal transport, suggesting that the function of Gcs1 that is required for these processes is independent of GAP activity. We propose that, in the absence of this GAP-independent regulation by Gcs1, the resulting dysregulated Arl1 prevents growth and impairs endosomal transport at low temperatures. In cells with dysregulated Arl1, an increased abundance of the Arl1 effector Imh1 restores growth and trafficking, and does so through Arl1 binding. Protein sequestration at the trans-Golgi membrane by dysregulated, active Arl1 may therefore be the mechanism of inhibition.

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JACOBS, Stephan, Annette SCHÜRMANN, Walter BECKER, Tobias M. BÖCKERS, Neal G. COPELAND, Nancy A. JENKINS, and Hans-Georg JOOST. "The mouse ADP-ribosylation factor-like 4 gene: two separate promoters direct specific transcription in tissues and testicular germ cell." Biochemical Journal 335, no. 2 (October 15, 1998): 259–65. http://dx.doi.org/10.1042/bj3350259.

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ADP-ribosylation factor-like protein 4 (ARL4) is a Ras-related GTPase that has been cloned from the 3T3-L1 preadipocyte cell line as an adipocyte-specific cDNA [Schürmann, Breiner, Becker, Huppertz, Kainulainen, Kentrup and Joost (1994) J. Biol. Chem. 269, 15683–15688]. The Arl4 gene maps to the proximal region of mouse chromosome 12 linked to Lamb1-1, Hfhbf1 and Sos2. Compared with all other known genes of Ras-related GTPases, the genomic organization of Arl4 is unusual in that its entire coding region, the 3´ untranslated region (UTR) and most of the 5´ UTR are located on a single exon. This structure suggests that Arl4 has evolved by retroposition of an Arf (ADP-ribosylation factor) or Arf-like gene. Isolation of the 5´ UTR by rapid amplification of cDNA ends (RACE)-PCR revealed heterogeneous transcription initiation sites in alternative exons 1. Both 5´-flanking regions exhibited promoter activity when expressed in COS-7 cells, indicating that the expression of Arl4 is directed by two separate promoters. mRNA transcribed under the control of the downstream promoter was isolated by RACE-PCR from all investigated tissues. In contrast, the upstream promoter seems to drive specifically the expression of Arl4 in adult testis. Hybridization of rat testis in situ indicated that Arl4 is expressed in germ cells of puberal and adult testis, but not in prepuberal testis, suggesting that Arl4 is involved in sperm production.

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Widersten, M., R. H. Kolm, R. Björnestedt, and B. Mannervik. "Contribution of five amino acid residues in the glutathione-binding site to the function of human glutathione transferase P1-1." Biochemical Journal 285, no. 2 (July 15, 1992): 377–81. http://dx.doi.org/10.1042/bj2850377.

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Five amino acids in proximity to GSH bound in the active-site cavity of human Class Pi glutathione transferase (GST) P1-1 were mutated by oligonucleotide-directed site-specific mutagenesis. The following mutations gave catalytically active mutant proteins with the proper dimeric structure: Arg14----Ala, Lys45----Ala, Gln52----Ala, Gln65----His and Asp99----Asn. The mutation Gln65----Ala was also made, but the protein was not characterized because of its poor catalytic activity. Residues Arg14, Lys45, Gln52 and Gln65 all contribute to binding of glutathione, and the substitutions caused an approx. 10-fold decrease in affinity, corresponding to 5 kJ/mol, except for Arg14, for which the effect was larger. In addition, Arg14 appears to have an important structure role, since the Arg14----Ala mutant demonstrated a significantly lower stability as compared with the wild-type and the other mutant enzymes. Asp99 primarily contributes to catalysis rather than to binding. The kcat./Km-versus-pH profile for the Asp99----Asn mutant is shifted by 0.5 pH unit in the alkaline direction, and it is proposed that Asp99 may participate in proton transfer in the catalytic mechanism. The possibility of redesigning the substrate specificity for GSTs was shown by the fact that the mutant Lys45----Ala displayed a higher catalytic efficiency with GSH monoethyl ester than with its natural substrate, GSH.

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Corre, Tanguy, Francisco J. Arjona, Caroline Hayward, Sonia Youhanna, Jeroen H. F. de Baaij, Hendrica Belge, Nadine Nägele, et al. "Genome-Wide Meta-Analysis Unravels Interactions between Magnesium Homeostasis and Metabolic Phenotypes." Journal of the American Society of Nephrology 29, no. 1 (November 1, 2017): 335–48. http://dx.doi.org/10.1681/asn.2017030267.

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Magnesium (Mg2+) homeostasis is critical for metabolism. However, the genetic determinants of the renal handling of Mg2+, which is crucial for Mg2+ homeostasis, and the potential influence on metabolic traits in the general population are unknown. We obtained plasma and urine parameters from 9099 individuals from seven cohorts, and conducted a genome-wide meta-analysis of Mg2+ homeostasis. We identified two loci associated with urinary magnesium (uMg), rs3824347 (P=4.4×10−13) near TRPM6, which encodes an epithelial Mg2+ channel, and rs35929 (P=2.1×10−11), a variant of ARL15, which encodes a GTP-binding protein. Together, these loci account for 2.3% of the variation in 24-hour uMg excretion. In human kidney cells, ARL15 regulated TRPM6-mediated currents. In zebrafish, dietary Mg2+ regulated the expression of the highly conserved ARL15 ortholog arl15b, and arl15b knockdown resulted in renal Mg2+ wasting and metabolic disturbances. Finally, ARL15 rs35929 modified the association of uMg with fasting insulin and fat mass in a general population. In conclusion, this combined observational and experimental approach uncovered a gene–environment interaction linking Mg2+ deficiency to insulin resistance and obesity.

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Kaykioglu, Gul, and Elcin Gunes. "Comparison of Acid Red 114 Dye Adsorption by Fe3O4and Fe3O4Impregnated Rice Husk Ash." Journal of Nanomaterials 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/6304096.

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The removal of Acid Red 114 (AR114) dye by adsorption process, using the magnetic nanoparticle (RHA-MNP) which is produced from rice husk ash burned at 300°C and the magnetic nanoparticle (MNP, Fe3O4), was studied. Batch processes were used under different test parameters: pH (2, 4, 6, and 10) and without pH, initial dye concentration (20, 40, 60, 80, and 100 mg/L), and contact time (0, 1, 5, 10, 15, 30, 45, 60, 90, and 150 min). Optimum conditions for AR114 removal were found to be at natural pH (pH without correction) for both adsorbents. Freundlich isotherm was found to be more consistent for MNP and Langmuir isotherm was found to be more consistent for RHA-MNP. The maximum adsorption capacities of MNP and RHA-MNP adsorbents for AR114 dye were equal to 111 mg/g. The kinetic experimental data fitted the pseudo-second-order model for both MNP and RHA-MNP. It can be concluded that RHA-MNP which is a waste could be used as low-cost adsorbent to remove AR114 from aqueous solution.

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Jensen, J. G., and A. J. Popay. "Reductions in root aphid populations by non-toxic endophyte strains in tall fescue." NZGA: Research and Practice Series 13 (January 1, 2007): 341–44. http://dx.doi.org/10.33584/rps.13.2006.3160.

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In two separate pot trials, tall fescue plants infected with the endophyte strain AR542, which is non-toxic to livestock, were shown to have lower numbers of root aphid per plant compared with uninfected plants, but more aphids than plants infected with other non-toxic endophytes (AR502, AR510 and AR514). These differences were not always significant when aphid numbers per gram of root were analysed. A Petri dish trial investigated the mechanism of resistance. Aphid survival was lower on endophyte-free fescue than on AR514- and AR542-infected fescue. Compared with endophyte-free, fewer aphids on roots of AR514- and AR542-infected tall fescue showed signs of feeding, as measured by production of wax and honey dew, and more were mobile on and around roots. Keywords: Aploneura lentisci, Festuca arundinacea, Neotyphodium

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Fu, Yun-Chang, Hongshen Jiang, and Paul Bishop. "An Inhibition Study of the Effect of Azo Dyes on Bioactivity of Biofilms." Water Science and Technology 29, no. 7 (April 1, 1994): 365–72. http://dx.doi.org/10.2166/wst.1994.0363.

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An inhibition study showed that toxic compounds caused two responses when present at low concentration. One is stimulation of the biomass by simply serving as an energy source; this caused an increase in the total respiration rate. The other is inhibition of the reaction. AR14 was more toxic than AO7 for biofilm from reactors fed with a primary substrate. However, AO7 demonstrated inhibition for biofilm from reactors fed with AR14 and primary substrate, and AR14 could serve as a carbon source for the same film.

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Kim, Hyun Ji, Boram Kim, Hyung Jung Byun, Lu Yu, Tuan Minh Nguyen, Thi Ha Nguyen, Phuong Anh Do, et al. "Resolvin D1 Suppresses H2O2-Induced Senescence in Fibroblasts by Inducing Autophagy through the miR-1299/ARG2/ARL1 Axis." Antioxidants 10, no. 12 (November 30, 2021): 1924. http://dx.doi.org/10.3390/antiox10121924.

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ARG2 has been reported to inhibit autophagy in vascular endothelial cells and keratinocytes. However, studies of its mechanism of action, its role in skin fibroblasts, and the possibility of promoting autophagy and inhibiting cellular senescence through ARG2 inhibition are lacking. We induced cellular senescence in dermal fibroblasts by using H2O2. H2O2-induced fibroblast senescence was inhibited upon ARG2 knockdown and promoted upon ARG2 overexpression. The microRNA miR-1299 suppressed ARG2 expression, thereby inhibiting fibroblast senescence, and miR-1299 inhibitors promoted dermal fibroblast senescence by upregulating ARG2. Using yeast two-hybrid assay, we found that ARG2 binds to ARL1. ARL1 knockdown inhibited autophagy and ARL1 overexpression promoted it. Resolvin D1 (RvD1) suppressed ARG2 expression and cellular senescence. These data indicate that ARG2 stimulates dermal fibroblast cell senescence by inhibiting autophagy after interacting with ARL1. In addition, RvD1 appears to promote autophagy and inhibit dermal fibroblast senescence by inhibiting ARG2 expression. Taken together, the miR-1299/ARG2/ARL1 axis emerges as a novel mechanism of the ARG2-induced inhibition of autophagy. Furthermore, these results indicate that miR-1299 and pro-resolving lipids, including RvD1, are likely involved in inhibiting cellular senescence by inducing autophagy.

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Garg, Alok, Gaganpreet Kaur, Vikas K. Sangal, Pramod K. Bajpai, and Sushant Upadhyay. "Optimization methodology based on neural networks and box-behnken design applied to photocatalysis of acid red 114 dye." Environmental Engineering Research 25, no. 5 (October 22, 2019): 753–62. http://dx.doi.org/10.4491/eer.2019.246.

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The present work deals with the modeling and optimization of photocatalytic degradation (UV/TiO2) of aqueous solution of Acid Red 114 (AR114) dye using Artificial Neural Networks (ANN) and RSM. Photocatalytic treatment of AR114 has been executed using suspension TiO2catalyst for commercial applications exposed to ultraviolet irradiation in a shallow pond reactor. ANN optimization has been applied to for predicting the behavior of photocatalysis. The input parameters used for analysis of aqueous dye solution are - TiO2 dose, pH of the dye solution, initial dye concentration, UV light intensity, time and area/volume, and time whereas the outputs are evaluated in form of degradation and decolorization efficiency of AR114. The outcomes of ANN optimization have been experimentally validated. Results achieved establish ANN modeling as a good predictive model. Parameteric optimization using multi-parameter optimization has been employed with desirability function approach. Results obtained from RSM are in line as per the results of ANN modeling as well as experimental. First order kinetics is use to effectively express degradation and decolorization of AR114 dyes. Total organic carbon (TOC) removal and GC-MS study of the dye shows the total mineralization and formation of non-toxic intermediate products.

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Sheppard, Ryan L., Espen E. Spangenburg, Eva R. Chin, and Stephen M. Roth. "Androgen receptor polyglutamine repeat length affects receptor activity and C2C12 cell development." Physiological Genomics 43, no. 20 (October 2011): 1135–43. http://dx.doi.org/10.1152/physiolgenomics.00049.2011.

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Testosterone (T) has an anabolic effect on skeletal muscle and is believed to exert its local effects via the androgen receptor (AR). The AR harbors a polymorphic stretch of glutamine repeats demonstrated to inversely affect receptor transcriptional activity in prostate and kidney cells. The effects of AR glutamine repeat length on skeletal muscle are unknown. In this study we examined the effect of AR CAG repeat length on AR function in C2C12 cells. AR expression vectors harboring 14, 24, and 33 CAG repeats were used to assess AR transcriptional activity. C2C12 cell proliferation, differentiation, gene expression, myotube formation, and myonuclear fusion index were assessed. Transcriptional activity increased with increasing repeat length and in response to testosterone (AR14 = 3.91 ± 0.26, AR24 = 25.21 ± 1.72, AR33 = 36.08 ± 3.22 relative light units; P < 0.001). Ligand activation was increased for AR33 (2.10 ± 0.04) compared with AR14 (1.54 ± 0.09) and AR24 (1.57 ± 0.05, P < 0.001). AR mRNA expression was elevated in each stably transfected line. AR33 cell proliferation (20,512.3 ± 1,024.0) was decreased vs. AR14 (27,604.17 ± 1,425.3; P < 0.001) after 72 h. Decreased CK activity in AR14 cells (54.9 ± 2.9 units/μg protein) in comparison to AR33 (70.8 ± 8.1) ( P < 0.05) was noted. The myonuclear fusion index was lower for AR14 (15.21 ± 3.24%) and AR33 (9.97 ± 3.14%) in comparison to WT (35.07 ± 5.60%, P < 0.001). AR14 and AR33 cells also displayed atypical myotube morphology. RT-PCR revealed genotype differences in myostatin and myogenin expression. We conclude that AR polyglutamine repeat length is directly associated with transcriptional activity and alters the growth and development of C2C12 cells. This polymorphism may contribute to the heritability of muscle mass in humans.

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Chen, Yan-Ting, I.-Hao Wang, Yi-Hsun Wang, Wan-Yun Chiu, Jen-Hao Hu, Wen-Hui Chen, and Fang-Jen S. Lee. "Action of Arl1 GTPase and golgin Imh1 in Ypt6-independent retrograde transport from endosomes to the trans-Golgi network." Molecular Biology of the Cell 30, no. 8 (April 2019): 1008–19. http://dx.doi.org/10.1091/mbc.e18-09-0579.

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The Arf and Rab/Ypt GTPases coordinately regulate membrane traffic and organelle structure by regulating vesicle formation and fusion. Ample evidence has indicated that proteins in these two families may function in parallel or complementarily; however, the manner in which Arf and Rab/Ypt proteins perform interchangeable functions remains unclear. In this study, we report that a Golgi-localized Arf, Arl1, could suppress Ypt6 dysfunction via its effector golgin, Imh1, but not via the lipid flippase Drs2. Ypt6 is critical for the retrograde transport of vesicles from endosomes to the trans-Golgi network (TGN), and its mutation leads to severe protein mislocalization and growth defects. We first overexpress the components of the Arl3-Syt1-Arl1-Imh1 cascade and show that only Arl1 and Imh1 can restore endosome-to-TGN trafficking in ypt6-deleted cells. Interestingly, increased abundance of Arl1 or Imh1 restores localization of the tethering factor Golgi associated retrograde–protein (GARP) complex to the TGN in the absence of Ypt6. We further show that the N-terminal domain of Imh1 is critical for restoring GARP localization and endosome-to-TGN transport in ypt6-deleted cells. Together, our results reveal the mechanism by which Arl1-Imh1 facilitates the recruitment of GARP to the TGN and compensates for the endosome-to-TGN trafficking defects in dysfunctional Ypt6 conditions.

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Al-Hawary, Sulieman Ibraheem Shelash, Razzagh Rahimpoor, Abdolrasoul Rahmani, Rosario Mireya Romero-Parra, Andrés Alexis Ramírez-Coronel, Firas Rahi Alhachami, Nezamaddin Mengelizadeh, and Davoud Balarak. "Enhanced Sonophotocatalytic Degradation of Acid Red 14 Using Fe3O4@SiO2/PAEDTC@MIL-101 (Fe) Based on Metal-Organic Framework." Catalysts 13, no. 2 (February 15, 2023): 411. http://dx.doi.org/10.3390/catal13020411.

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Here, the magnetic Fe3O4@SiO2/PAEDTC@MIL-101 (Fe) with a new core-shell structure was synthesized, and its sonophotocatalytic properties were evaluated for acid red 14 (AR14) degradation. Particle characterizations were determined by scanning electron microscope (SEM), transmission electron microscopy (TEM), X-ray powder diffraction (XRD), and vibrating-sample magnetometer (VSM), and the analysis results offered an excellent synthesis of mesoporous particles. Fe3O4@SiO2/PAEDTC@MIL-101 (Fe)/UV/US showed high degradation kinetics rate (0.0327 min−1) compared to sonocatalytic processes (0.0181 min−1), photocatalytic (0218 min−1), sonolysis (0.008 min−1), and photolysis (0.005 min−1). Maximum removal efficiencies of AR14 (100%) and total organic carbon (69.96%) were obtained at pH of 5, catalyst mass of 0.5 g/L, initial AR14 concentration of 50 mg/L, and ultrasound power of 36 W. Evaluation of BOD5/COD ratio during dye treatment confirmed that the sonophotocatalysis process can be useful for converting major contaminant molecules into biodegradable compounds. After recycling eight times, the prepared composite still has sonophotocatalytic degradation stability above 90% for AR14. Scavenging tests confirmed that holes (h+) and hydroxyl (•OH) were the pivotal agents in the decomposition system. Based on the results, the synthesized sample can be suggested as an excellent and promising sonophotocatalyst for the degradation of AR14 dye and its conversion into biodegradable compounds.

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Shojaat, Rahim, Afzal Karimi, Naghi Saadatjoo, and Soheil Aber. "Dye removal from artificial wastewater using heterogeneous bio-fenton system." Chemical Industry and Chemical Engineering Quarterly 23, no. 4 (2017): 447–56. http://dx.doi.org/10.2298/ciceq160621058s.

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In the present study, GOx/MnFe2O4/calcium alginate nano-composite was prepared by the trapping enzyme/nanoparticles in calcium alginate. The prepared absorbent was applied for decolorization of artificial dye wastewater of acid red 14 (AR14) by heterogeneous bio-Fenton system. Kinetic and isotherm studies were carried out. The decolorization of acid red 14 followed the Michaelis- Menten, pseudo-first order and pseudo-second order kinetic models. Good correlation coefficients were obtained by fitting the experimental data to Michaelis- Menten and pseudo-second order kinetic models. The adsorption isotherms were described by Langmuir, Freundlich and Temkin isotherms. Among the three isotherm models, the Freundlich model was fitted with the equilibrium data obtained from adsorption of AR14 onto MnFe2O4/calcium alginate; while Temkin isotherm gave the best correlation for adsorption on MnFe2O4 nanoparticles. The effect of various parameters such as initial pH of solution, initial dye concentration, and contact time on the adsorption of AR14 on MnFe2O4 and MnFe2O4/ /calcium alginate as well as dye enzymatic decomposition was studied. The decolorization of AR14 with initial concentration of 10 mg.L?1 by using GOx/ /MnFe2O4/calcium alginate was 60.17%.

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Rotevatn, T. A., Vilde Bergstad Larsen, Tone Bjordal Johansen, Elisabeth Astrup, Pål Surén, Margrethe Greve-Isdahl, and Kjetil Elias Telle. "Transmission of SARS-CoV-2 in Norwegian schools during academic year 2020-21: population wide, register based cohort study." BMJ Medicine 1, no. 1 (August 2022): e000026. http://dx.doi.org/10.1136/bmjmed-2021-000026.

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ObjectiveTo assess the risk of transmission of SARS-CoV-2 in schools in Norway mainly kept open during the covid-19 pandemic in the academic year 2020-21.DesignPopulation wide, register based cohort study.SettingPrimary and lower secondary schools in Norway open during the academic year 2020-21, with strict infection prevention and control measures in place, such as organisation of students into smaller cohorts. Contact tracing, quarantine, and isolation were also implemented, and testing of students and staff identified as close contacts.ParticipantsAll students and educational staff in primary and lower secondary schools in Norway, from August 2020 to June 2021.Main outcome measuresOverall attack rate of SARS-CoV-2 transmission (AR14) was defined as the number of individuals (among students, staff, or both) in the school with covid-19, detected within 14 days of the index case, divided by the number of students and staff members in the school. AR14 to students (attack rates from all index cases to students only) and AR14 to school staff (attack rates from all index cases to staff members only) were also calculated. These measures for student and school staff index cases were also calculated separately to explore variation in AR14 based on the characteristics of the index case.ResultsFrom August 2020 to June 2021, 4078 index cases were identified; 3220 (79%) students and 858 (21%) school staff. In most (2230 (55%)) schools with an index case, no subsequent individuals with covid-19 were found within 14 days; in 631 (16%) schools, only one more individual with covid-19 within 14 days was found. Overall, AR14 was 0.33% (95% confidence interval 0.32% to 0.33%). When restricting index cases and subsequent individuals with covid-19 to students born in the same year, AR14 to students (0.56-0.78%) was slightly higher.ConclusionsRegarding the number of people infected with SARS-CoV-2 among students and staff, these results suggest that schools were not an important setting for transmission of the virus in Norway during the covid-19 pandemic in the academic year 2020-21.

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Lu, Lei, Guihua Tai, and Wanjin Hong. "Autoantigen Golgin-97, an Effector of Arl1 GTPase, Participates in Traffic from the Endosome to the Trans-Golgi Network." Molecular Biology of the Cell 15, no. 10 (October 2004): 4426–43. http://dx.doi.org/10.1091/mbc.e03-12-0872.

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The precise cellular function of Arl1 and its effectors, the GRIP domain Golgins, is not resolved, despite our recent understanding that Arl1 regulates the membrane recruitment of these Golgins. In this report, we describe our functional study of Golgin-97. Using a Shiga toxin B fragment (STxB)-based in vitro transport assay, we demonstrated that Golgin-97 plays a role in transport from the endosome to the trans-Golgi network (TGN). The recombinant GRIP domain of Golgin-97 as well as antibodies against Golgin-97 inhibited the transport of STxB in vitro. Membrane-associated Golgin-97, but not its cytosolic pool, was required in the in vitro transport assay. The kinetic characterization of inhibition by anti-Golgin-97 antibody in comparison with anti-Syntaxin 16 antibody established that Golgin-97 acts before Syntaxin 16 in endosome-to-TGN transport. Knock down of Golgin-97 or Arl1 by their respective small interference RNAs (siRNAs) also significantly inhibited the transport of STxB to the Golgi in vivo. In siRNA-treated cells with reduced levels of Arl1, internalized STxB was instead distributed peripherally. Microinjection of Golgin-97 antibody led to the fragmentation of Golgi apparatus and the arrested transport to the Golgi of internalized Cholera toxin B fragment. We suggest that Golgin-97 may function as a tethering molecule in endosome-to-TGN retrograde traffic.

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Price, H. P., D. Goulding, and D. F. Smith. "ARL1 has an essential role in Trypanosoma brucei." Biochemical Society Transactions 33, no. 4 (August 1, 2005): 643–45. http://dx.doi.org/10.1042/bst0330643.

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Myristoyl-CoA protein:NMT (N-myristoyl transferase) catalyses the N-myristoylation of cellular proteins with a range of functions and is essential for viability in the protozoan parasites, Leishmania major and Trypanosoma brucei. In our investigations to define the essential downstream targets of NMT, we have focused on the ARF (ADP-ribosylation factor) family of proteins, as growth arrest in Saccharomyces cerevisiae mutants with reduced NMT activity correlates with decreased modification of members of this group of proteins. We have identified nine ARF/ARLs (where ARL stands for ARF-like) encoded in the T. brucei and T. cruzi genomes and ten in L. major. The T. brucei ARL1 protein is expressed only in the mammalian bloodstream form of the parasite, in which it is localized to the Golgi apparatus. RNAi (RNA interference) has been used to demonstrate that ARL1 is essential for viability in these infective cells. Before cell death, depletion of ARL1 protein results in disintegration of the Golgi structure and a delay in exocytosis of the abundant GPI (glycosylphosphatidylinositol)-anchored VSG (variant surface glycoprotein) to the parasite surface.

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Young, Howard S., Delaine K. Ceholski, and Catharine A. Trieber. "Deception in simplicity: Hereditary phospholamban mutations in dilated cardiomyopathy." Biochemistry and Cell Biology 93, no. 1 (February 2015): 1–7. http://dx.doi.org/10.1139/bcb-2014-0080.

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The sarcoplasmic reticulum (SR) calcium pump (SERCA) and its regulator phospholamban are required for cardiovascular function. Phospholamban alters the apparent calcium affinity of SERCA in a process that is modulated by phosphorylation via the β-adrenergic pathway. This regulatory axis allows for the dynamic control of SR calcium stores and cardiac contractility. Herein we focus on hereditary mutants of phospholamban that are associated with heart failure, such as Arg9-Cys, Arg9-Leu, Arg9-His, and Arg14-deletion. Each mutant has a distinct effect on PLN function and SR calcium homeostasis. Arg9-Cys and Arg9-Leu do not inhibit SERCA, Arg14-deletion is a partial inhibitor, and Arg9-His is comparable to wild-type. While the mutants have distinct functional effects on SERCA, they have in common that they cannot be phosphorylated by protein kinase A (PKA). Arg9 and Arg14 are required for PKA recognition and phosphorylation of PLN. Thus, mutations at these positions eliminate β-adrenergic control and dynamic cardiac contractility. Hydrophobic mutations of Arg9 cause more complex changes in function, including loss of PLN function and dominant negative interaction with SERCA in heterozygous individuals. In addition, aberrant interaction with PKA may prevent phosphorylation of wild-type PLN and sequester PKA from other local subcellular targets. Herein we consider what is known about each mutant and how the synergistic changes in SR calcium homeostasis lead to impaired cardiac contractility and dilated cardiomyopathy.

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Munro, S. "The Arf-like GTPase Arl1 and its role in membrane traffic." Biochemical Society Transactions 33, no. 4 (August 1, 2005): 601–5. http://dx.doi.org/10.1042/bst0330601.

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Small GTP-binding proteins of the Rab and Arf (ADP-ribosylation factor) families play a central role in the membrane trafficking pathways of eukaryotic cells. The prototypical members of the Arf family are Arf1–Arf6 and Sar1, which have well-characterized roles in membrane traffic or cytoskeletal reorganization. However, eukaryotic genomes encode additional proteins, which share the characteristic structural features of the Arf family, but the role of these ‘Arf-like’ (Arl) proteins is less well understood. This review discusses Arl1, a GTPase that is widely conserved in evolution, and which is localized to the Golgi in all species so far examined. The best-characterized effectors of Arl1 are coiled-coil proteins which share a C-terminal GRIP domain, but other apparent effectors include the GARP (Golgi-associated retrograde protein)/VFT (Vps fifty-three) vesicle-tethering complex and Arfaptin 2. As least some of these proteins are believed to have a role in membrane traffic. Genetic analysis in a number of species has shown that Arl1 is not essential for exocytosis, but rather suggest that it is required for traffic from endosomes to the Golgi.

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Christis, Chantal, and Sean Munro. "The small G protein Arl1 directs the trans-Golgi–specific targeting of the Arf1 exchange factors BIG1 and BIG2." Journal of Cell Biology 196, no. 3 (January 30, 2012): 327–35. http://dx.doi.org/10.1083/jcb.201107115.

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The small G protein Arf1 regulates Golgi traffic and is activated by two related types of guanine nucleotide exchange factor (GEF). GBF1 acts at the cis-Golgi, whereas BIG1 and its close paralog BIG2 act at the trans-Golgi. Peripheral membrane proteins such as these GEFs are often recruited to membranes by small G proteins, but the basis for specific recruitment of Arf GEFs, and hence Arfs, to Golgi membranes is not understood. In this paper, we report a liposome-based affinity purification method to identify effectors for small G proteins of the Arf family. We validate this with the Drosophila melanogaster Arf1 orthologue (Arf79F) and the related class II Arf (Arf102F), which showed a similar pattern of effector binding. Applying the method to the Arf-like G protein Arl1, we found that it binds directly to Sec71, the Drosophila ortholog of BIG1 and BIG2, via an N-terminal region. We show that in mammalian cells, Arl1 is necessary for Golgi recruitment of BIG1 and BIG2 but not GBF1. Thus, Arl1 acts to direct a trans-Golgi–specific Arf1 GEF, and hence active Arf1, to the trans side of the Golgi.

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Amor, J. Carlos, John R. Horton, Xinjun Zhu, Yi Wang, Cameron Sullards, Dagmar Ringe, Xiaodong Cheng, and Richard A. Kahn. "Structures of Yeast ARF2 and ARL1." Journal of Biological Chemistry 276, no. 45 (September 4, 2001): 42477–84. http://dx.doi.org/10.1074/jbc.m106660200.

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Rosenwald, Anne G., Mary Ann Rhodes, Hillary Van Valkenburgh, Vikram Palanivel, George Chapman, Annette Boman, Chun-jiang Zhang, and Richard A. Kahn. "ARL1 and membrane traffic inSaccharomyces cerevisiae." Yeast 19, no. 12 (2002): 1039–56. http://dx.doi.org/10.1002/yea.897.

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Tiplica, Teodor. "ARL1 of the Attribute c Control Chart with Estimated Parameter." International Journal of Reliability, Quality and Safety Engineering 22, no. 02 (April 2015): 1550009. http://dx.doi.org/10.1142/s0218539315500096.

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In this paper, the out of control average run length (ARL1) of the c control chart with estimated parameter is computed for various shifts in the average number of nonconformities. In spite of the discrete nature of this chart, it is proved that a target in-control average run length (ARL0) can be obtained when the average number of nonconformities is estimated. This is a good starting point for comparing the performances of the c control chart with those of other attribute control charts with estimated parameters. Based on the computational results obtained, it is showed that the ARL1 of the c control chart with estimated parameter can be approximated by using a polynomial expression.

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Ma, Qing, Lingping Kong, and Diansheng Zhong. "Abstract 5231: Case report: dramatic response to Crizotinib in a patient with synchronous multiple primary lung cancer positive for a novel ARL1-MET fusion." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5231. http://dx.doi.org/10.1158/1538-7445.am2022-5231.

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Abstract Background: With the use of high-resolution chest imaging system, an increasing number of lung cancer patients are being diagnosed with multiple primary lung cancer (MPLC). Although surgery is considered as the first choice of treatment for early MPLC, targeted therapy is essential in the management of unresectable MPLC. To date, the driver oncogenes reported in the patients with MPLC are limited, and MET fusion has not yet been reported in MPLC. Case presentation: In this case, we reported a female patient with simultaneous MPLC (sMPLC). A novel ARL1-MET fusion was detected in her right lung tumor tissues using next-generation sequencing (NGS). The patient achieved about 5-month progressive-free survival (PFS) after receiving Crizotinib for the unresectable right lung malignancies. Conclusion: To the best of our knowledge, this case provided the first clinical evidence that the novel ARL1-MET fusion might be an actionable mutation in sMPLC. Citation Format: Qing Ma, Lingping Kong, Diansheng Zhong. Case report: dramatic response to Crizotinib in a patient with synchronous multiple primary lung cancer positive for a novel ARL1-MET fusion [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5231.

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Abiko, T., and S. Nakatsubo. "Synthesis of [ARG14 17 19 20jdeacetyl-thymosin a1 and its immunological effect on the impaired T lymphocytes of uremic patients." Protein & Peptide Letters 7, no. 6 (December 2000): 373–79. http://dx.doi.org/10.2174/092986650706221207161638.

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Abstract: A deacetyl-thymosin cx1analogue containing four arginines at positions 14, 17, 19, and 20, instead of four lysines was synthesized by the manual solid-phase method. The synthetic [Arg14 17 19 20 deacetyl-thymosin cx1 and deacetyl-thymosin cx1 were tested for the effect on impaired T-lymphocyte transformation by phytohemagglutinin in uremic patients suffering from recurrent infectious diseases. The restoring activity on the impaired phytohemagglutinin stimulation of T-lymphocytes was obtained after incubation of peripheral lymphocytes isolated from uremic patients with the synthetic [Arg14•17•19•20] deacetyl-thymosin cx1. This analogue exhibited a far stronger restoring effect than that of our synthetic deacetyl-thymosin ex1. Abbreviations used: Obzl, benzyl estrer; Bzl, benzyl; Boe, tert-butoxycarbonyl; Mts, mesitylene-2-sulfonyl; DCC, N, N' -dicyclohexylcarbodiimide; HOBT, 1-hydro-xybenzotriazole; DMF, dimethylformamide; Et3N, triethylamine; AcOH, acetic acid; TFA, trifluoroacetic acid; TLC, thin-layer chromatography; HPLC, high performance liquid chromatography; PHA, phytohemagglutinin; SDS, sodium dodecyl sulfate; PBS, phosphate buffered saline; RPMI, Rosewell Park Memorial Institute; FCS, fetal calf serum; E-rosette, a rosette with sheep erythrocytes.

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Jochum, Alexandra, David Jackson, Heinz Schwarz, Rüdiger Pipkorn, and Birgit Singer-Krüger. "Yeast Ysl2p, Homologous to Sec7 Domain Guanine Nucleotide Exchange Factors, Functions in Endocytosis and Maintenance of Vacuole Integrity and Interacts with the Arf-Like Small GTPase Arl1p." Molecular and Cellular Biology 22, no. 13 (July 1, 2002): 4914–28. http://dx.doi.org/10.1128/mcb.22.13.4914-4928.2002.

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ABSTRACT We previously described the isolation of ysl2-1 due to its genetic interaction with Δypt51/vps21, a mutant with a deletion of the coding sequence for the yeast Rab5 homolog, which regulates endocytic traffic between early and late endosomes. Here we report that Ysl2p is a novel 186.8-kDa peripheral membrane protein homologous to members of the Sec7 family. We provide multiple genetic and biochemical evidence for an interaction between Ysl12p and the Arf-like protein Arl1p, consistent with a potential function as an Arf guanine nucleotide exchange factor (GEF). The temperature-sensitive alleles ysl2-307 and ysl2-316 are specifically defective in ligand-induced degradation of Ste2p and α-factor and exhibit vacuole fragmentation directly upon a shift to 37°C. In living cells, green fluorescent protein (GFP)-Ysl2p colocalizes with endocytic elements that accumulate FM4-64. The GFP-Ysl2p staining is sensitive to a mutation in VPS27 resulting in the formation of an aberrant class E compartment, but it is not affected by a sec7 mutation. Consistent with the idea that Ysl2p and Arl1p have closely related functions, Δarl1 cells are defective in endocytic transport and in vacuolar protein sorting.

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Ireland, Stephen C., Haoran Huang, Jianchao Zhang, Jie Li, and Yanzhuang Wang. "Hydrogen peroxide induces Arl1 degradation and impairs Golgi-mediated trafficking." Molecular Biology of the Cell 31, no. 17 (August 1, 2020): 1931–42. http://dx.doi.org/10.1091/mbc.e20-01-0063.

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H2O2 treatment induces the degradation of Golgi structural proteins in the trans-Golgi, including Arl1, Golgin-97, and Golgin-245, and thereby impairs membrane trafficking. This study revealed the trans-Golgi and trafficking at the trans-Golgi as novel targets of ROS in cells.

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Zaman, Bisma, Syed Muhammad Muslim Raza, Javed Iqbal, Naima Shehzadi, Muhammad Moeen Butt, and Muhammad Riaz. "Efficient control charting methodology based on Distance Weighted Mean for normal distribution." Natural and Applied Sciences International Journal (NASIJ) 4, no. 1 (May 21, 2023): 1–16. http://dx.doi.org/10.47264/idea.nasij/4.1.1.

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This research suggests a Distance Weighted Mean (DWM) based control chart under normal distribution implementing Simple Random Sampling (SRS). The control limits are calculated using the quantile point method. The control chart's performance is assessed using the Average Run Length (ARL) statistic. The numerical findings are illustrated using samples of sizes 3 and 5. The ARL1 values are determined using Monte Carlo Simulation for increasing and decreasing shifts in the location parameter ranging from 5% to 30%. Using the ARL1 measurement, the proposed DWM control charts are compared to the existing Shewhart control charts. According to the comparison analysis, the suggested DWM control chart surpasses the competing Shewhart control chart. The real-life application of the proposed DWM control chart is also shown by using the lifetime of the light bulb (in hours). The results suggest that the proposed DWM control chart can be a useful tool for monitoring process mean shifts, especially when the sample size is large, and the magnitude of the shift is significant.

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Huang, Lien-Hung, Wei-Chung Lee, Shu-Ting You, Chia-Chen Cheng, and Chia-Jung Yu. "Arfaptin-1 Negatively Regulates Arl1-Mediated Retrograde Transport." PLOS ONE 10, no. 3 (March 19, 2015): e0118743. http://dx.doi.org/10.1371/journal.pone.0118743.

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Munson, A. M. "Yeast ARL1 encodes a regulator of K+ influx." Journal of Cell Science 117, no. 11 (May 1, 2004): 2309–20. http://dx.doi.org/10.1242/jcs.01050.

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Giridhar, Karthik, Carlos Sosa, David W. Hillman, Cristobal T. Sanhueza, Liguo Wang, John C. Cheville, Scott Dehm, and Manish Kohli. "Whole blood androgen receptor (AR) variant (ARV12, ARV14) expression and overall survival (OS) in metastatic castrate resistant prostate cancer (mCRPC)." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): 5058. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.5058.

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5058 Background: The detection of full length AR (AR-FL) or AR variants (AR-Vs) in blood and association with outcomes in mCRPC is unknown. We compared whole blood mRNA expression of AR-FL and AR-Vs to circulating tumor cells (CTCs) for predicting OS and time to treatment failure (TTF). Methods: We isolated RNA from whole blood collected in PAXgene RNA tubes and concurrent metastatic tissue biopsy from 51 men with mCRPC prior to initiation of abiraterone acetate in a prospective clinical trial (NCT#01953640). Whole transcriptome sequencing (RNAseq) was performed on blood samples and paired biopsies to detect AR-FL, ARV1, ARV3, ARV7, ARV8, AR12, ARV14, and ARV45. Reads were aligned to the GRCh38 reference genome with the spliced-alignment TopHat2 package. The Pearson correlation coefficient was calculated between AR-FL in blood and matched bone biopsy. CTCs were determined using the CELLSEARCH assay. Cox proportional hazard regression analysis was performed on AR-FL, each AR-V, and CTCs for association with OS and TTF. We compared the area under the curve (AUC) using CTCs alone to a multivariable model that included AR-Vs for predicting OS. Results: The median follow up was 3.0 years, (range 0.3-3.5); the median CTC count was 3 (range 0-372); 34/53 men were deceased. Blood based AR-FL or AR-Vs were detected in 50/53 patients with following distribution: AR-FL (41/53), ARV3 (9/53), ARV45 (8/53), ARV12 (4/53), ARV14 (4/53), ARV7 (2/53), and ARV8 (2/53). Whole blood AR-FL transcripts were highly correlated to paired bone biopsy (r2= 0.76). Elevated transcripts of either ARV12 or ARV14 were associated with decreased OS [hazard ratio (HR) 3.46, p = 0.006]. CTC count ≥5 was associated with poorer OS [HR 3.42, p = 0.02] and shorter TTF [HR 3.52, p = < 0.001]. Adjusting for CTC counts, in a multivariate model, blood AR12 expression was associated with poor OS [HR = 6.33, p = 0.009]. AR12 and CTCs trended toward improved AUC compared to CTC alone (0.78 vs 0.71, p = 0.07). Conclusions: AR-FL and AR-Vs are detectable in whole blood and are highly correlated with metastatic bone AR-FL expression. AR-Vs may add to prognostication in mCRPC and further validation is needed. Clinical trial information: NCT#01953640.

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McKay, Gordon, Mohammed El-Geundi, and Mamdouh M. Nassar. "Adsorption Model for the Removal of Acid Dyes from Effluent by Bagasse Pith Using a Simplified Isotherm." Adsorption Science & Technology 15, no. 10 (November 1997): 737–52. http://dx.doi.org/10.1177/026361749701501002.

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The adsorption of two acid dyes, viz. Acid Red AR114 and Acid Blue AB25, on to bagasse pith, a waste material from the sugar cane industry, has been studied. Equilibrium isotherms and agitated batch contact time studies have been carried out. A mass-transfer model has been used based on a Langmuir-type isotherm at maximum saturation. This simple or pseudo-irreversible isotherm and the assumption of pore diffusion enables a pore diffusion mass-transfer model to theoretically predict the experimental concentration decay curves very rapidly.

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Sarker, Souvic, Young Ha Woo, and Un Taek Lim. "Laboratory Evaluation of Beauveria bassiana ARP14 Against Grapholita molesta (Lepidoptera: Tortricidae)." Current Microbiology 77, no. 9 (May 4, 2020): 2365–73. http://dx.doi.org/10.1007/s00284-020-02012-4.

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Menzel, Julia, Daniel Kownatzki-Danger, Sergiy Tokar, Alice Ballone, Kirsten Unthan-Fechner, Markus Kilisch, Christof Lenz, et al. "14-3-3 binding creates a memory of kinase action by stabilizing the modified state of phospholamban." Science Signaling 13, no. 647 (September 1, 2020): eaaz1436. http://dx.doi.org/10.1126/scisignal.aaz1436.

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The cardiac membrane protein phospholamban (PLN) is targeted by protein kinase A (PKA) at Ser16 and by Ca2+/calmodulin-dependent protein kinase II (CaMKII) at Thr17. β-Adrenergic stimulation and PKA-dependent phosphorylation of Ser16 acutely stimulate the sarcoplasmic reticulum calcium pump (SERCA) by relieving its inhibition by PLN. CaMKII-dependent phosphorylation may lead to longer-lasting SERCA stimulation and may sustain maladaptive Ca2+ handling. Here, we demonstrated that phosphorylation at either Ser16 or Thr17 converted PLN into a target for the phosphoadaptor protein 14-3-3 with different affinities. 14-3-3 proteins were localized within nanometers of PLN and endogenous 14-3-3 coimmunoprecipitated with pentameric PLN from cardiac membranes. Molecular dynamics simulations predicted different molecular contacts for peptides phosphorylated at Ser16 or Thr17 with the binding groove of 14-3-3, resulting in varied binding affinities. 14-3-3 binding protected either PLN phosphosite from dephosphorylation. β-Adrenergic stimulation of isolated adult cardiomyocytes resulted in the membrane recruitment of endogenous 14-3-3. The exogenous addition of 14-3-3 to β-adrenergic–stimulated cardiomyocytes led to prolonged SERCA activation, presumably because 14-3-3 protected PLN pentamers from dephosphorylation. Phosphorylation of Ser16 was disrupted by the cardiomyopathy-associated ∆Arg14 mutation, implying that phosphorylation of Thr17 by CaMKII may become crucial for 14-3-3 recruitment to ∆Arg14 PLN. Consistent with PLN acting as a dynamic hub in the control of Ca2+ handling, our results identify 14-3-3 binding to PLN as a contractility-augmenting mechanism.

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Hamasha, Safeia M., and Yasmeen Abu-Nassar. "Theoretical spectral analysis of Ar ions from Ar9+ to Ar14+." Journal of Quantitative Spectroscopy and Radiative Transfer 266 (May 2021): 107567. http://dx.doi.org/10.1016/j.jqsrt.2021.107567.

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Yu, Chia-Jung, and Fang-Jen S. Lee. "Multiple activities of Arl1 GTPase in the trans-Golgi network." Journal of Cell Science 130, no. 10 (May 3, 2017): 1691–99. http://dx.doi.org/10.1242/jcs.201319.

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Chen, K. Y., P. C. Tsai, J. W. Hsu, H. C. Hsu, C. Y. Fang, L. C. Chang, Y. T. Tsai, C. J. Yu, and F. J. S. Lee. "Syt1p promotes activation of Arl1p at the late Golgi to recruit Imh1p." Journal of Cell Science 123, no. 20 (September 14, 2010): 3478–89. http://dx.doi.org/10.1242/jcs.074237.

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Peng, Ya-li, Min Chang, Shou-liang Dong, Wei Li, Ren-wen Han, Guo-xing Fu, Qiang Chen, and Rui Wang. "Novel potent agonist [(pF)Phe4,Aib7,Aib11,Arg14,Lys15]N/OFQ-NH2 and antagonist [Nphe1,(pF)Phe4,Aib7,Aib11,Arg14,Lys15]N/OFQ-NH2 of nociceptin/orphanin FQ receptor." Regulatory Peptides 134, no. 2-3 (May 2006): 75–81. http://dx.doi.org/10.1016/j.regpep.2006.01.003.

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Journal articles on the topic 'Arl14'

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