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Journal articles on the topic 'Arl15'

Author: Grafiati
Published: 6 September 2023

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1

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 (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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2

Corre, Tanguy, Francisco J. Arjona, Caroline Hayward, et al. "Genome-Wide Meta-Analysis Unravels Interactions between Magnesium Homeostasis and Metabolic Phenotypes." Journal of the American Society of Nephrology 29, no. 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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Zolotarov, Yevgen, Chao Ma, Irene González-Recio, et al. "ARL15 modulates magnesium homeostasis through N-glycosylation of CNNMs." Cellular and Molecular Life Sciences 78, no. 13 (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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4

Li, Yiping, Ying Yang, Yueting Yao, et al. "Association Study of ARL15 and CDH13 with T2DM in a Han Chinese Population." International Journal of Medical Sciences 11, no. 5 (2014): 522–27. http://dx.doi.org/10.7150/ijms.8206.

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5

de Baaij, Jeroen H. F., Yevgen Zolotarov, Chao Ma, Gijs Franken, Michel L. Tremblay, and Joost Hoenderop. "ARL15 Regulates CNNM2‐dependent Mg 2+ Transport by Modulating its N‐linked Glycosylation." FASEB Journal 34, S1 (2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.06380.

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6

Richards, J. Brent, Dawn Waterworth, Stephen O'Rahilly, et al. "A Genome-Wide Association Study Reveals Variants in ARL15 that Influence Adiponectin Levels." PLoS Genetics 5, no. 12 (2009): e1000768. http://dx.doi.org/10.1371/journal.pgen.1000768.

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7

Yang, Yong-Kang, Hong Qu, Dong Gao, et al. "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 (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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8

Benabdelkamel, Hicham, Afshan Masood, Meshail Okla, Mohammed Y. Al-Naami, and Assim A. Alfadda. "A Proteomics-Based Approach Reveals Differential Regulation of Urine Proteins between Metabolically Healthy and Unhealthy Obese Patients." International Journal of Molecular Sciences 20, no. 19 (2019): 4905. http://dx.doi.org/10.3390/ijms20194905.

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Metabolic dysfunction associated with obesity threatens to inundate health care resources by increasing the incidences of obesity-related diseases. The aim of the present study was to investigate the changes in the urinary proteome of 18 individuals classified into metabolically healthy obese (MHO) and metabolically unhealthy obese (MUHO) patients. Proteome analysis was performed using the two-dimensional difference in gel electrophoresis (2D-DIGE) coupled with mass spectrometry (MS). Upon analysis, a total of 54 proteins were found to be affected with ≥1.5-fold change (ANOVA, p ≤ 0.05), of which 44 proteins were upregulated and 10 proteins were downregulated. These differentially abundant proteins were related to nuclear factor κB (NF-κB) and p38 mitogen-activated protein (MAP) kinase pathways and were involved in cellular compromise, inflammatory response, and cancer. Proteins involved in inflammation (fibrinogen alpha (FIBA), serotransferrin (TRFE, and kininogen-1 (KNG1)) and insulin resistance (ADP-ribosylation factor (ARF)-like protein 15 (ARL15) and retinol-binding protein 4 (RET4)) were found to be significantly increased in the urine samples of MUHO compared to MHO patients. Investigating the effects of obesity on urinary proteins can help in developing efficient diagnostic procedures for early detection and prevention of obesity-related complications.
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9

Shen, Jiayi, Miao Liu, Jing Xu, Bao Sun, Heng Xu, and Wei Zhang. "ARL15 overexpression attenuates high glucose-induced impairment of insulin signaling and oxidative stress in human umbilical vein endothelial cells." Life Sciences 220 (March 2019): 127–35. http://dx.doi.org/10.1016/j.lfs.2019.01.030.

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10

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 (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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11

Cui, Zhengwei, Tianxin Sheng, Yuping Wang, et al. "Association between single nucleotide polymorphisms (SNPs) in the gene of ADP-ribosylation factor-like 15 (ARL15) and type 2 diabetes (T2D) in Korean Chinese population in Yanbian, China." International Journal of Diabetes in Developing Countries 37, no. 2 (2015): 124–28. http://dx.doi.org/10.1007/s13410-015-0391-3.

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12

Ishida, Morié, and Juan S. Bonifacino. "ARFRP1 functions upstream of ARL1 and ARL5 to coordinate recruitment of distinct tethering factors to the trans-Golgi network." Journal of Cell Biology 218, no. 11 (2019): 3681–96. http://dx.doi.org/10.1083/jcb.201905097.

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SNARE-mediated fusion of endosome-derived transport carriers with the trans-Golgi network (TGN) depends on the concerted action of two types of tethering factors: long coiled-coil tethers of the golgin family, and the heterotetrameric complex GARP. Whereas the golgins mediate long-distance capture of the carriers, GARP promotes assembly of the SNAREs. It remains to be determined, however, how the functions of these tethering factors are coordinated. Herein we report that the ARF-like (ARL) GTPase ARFRP1 functions upstream of two other ARL GTPases, ARL1 and ARL5, which in turn recruit golgins and GARP, respectively, to the TGN. We also show that this mechanism is essential for the delivery of retrograde cargos to the TGN. Our findings thus demonstrate that ARFRP1 is a master regulator of retrograde-carrier tethering to the TGN. The coordinated recruitment of distinct tethering factors by a bifurcated GTPase cascade may be paradigmatic of other vesicular fusion events within the cell.
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13

Hsu, Jia-Wei, Pei-Hua Tang, I.-Hao Wang, et al. "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 (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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14

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 (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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15

Ishida, Morié, and Juan S. Bonifacino. "Correction: ARFRP1 functions upstream of ARL1 and ARL5 to coordinate recruitment of tethering factors to the trans-Golgi network." Journal of Cell Biology 218, no. 11 (2019): 3880–81. http://dx.doi.org/10.1083/jcb.20190509710072019c.

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Xie, Ning, Qiuai Shu, Ziwei Wang, 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 (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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17

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 (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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18

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 (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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19

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 (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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20

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 (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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21

Rai, Amit, Vinit Raj, Ashok K. Singh, Amit K. Keshari, and Sudipta Saha. "A METHOD FOR DETERMINING 1,4-BENZOTHIAZINE DERIVATIVES IN RAT PLASMA BY HPLC AND ITS APPLICATION TO A PHARMACOKINETIC STUDY." International Journal of Pharmacy and Pharmaceutical Sciences 9, no. 12 (2017): 82. http://dx.doi.org/10.22159/ijpps.2017v9i12.19339.

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Objective: The objective of the study was to develop, optimize and validate of a new reverse-phase high-performance liquid chromatography (RP-HPLC) method for the determining 1,4-benzothiazine derivatives (AR13 and AR15) in a biological sample of rat plasma. The 1,4-benzothiazine derivatives are produced by the synthetic reactions.Methods: RP-HPLC separation was performed using an ODS-2 Hypersil column with gradient elution mobile phase consisting of water-acetonitrile for AR13 and AR15 (1:9 v/v, 3:7 v/v) at room temperature 1 ml/min flow rate, and interfaced with photodiode array detector (PDA) detector, 233 nm, 235 nm respectively.Results: A linear response was obtained between (range from 0.100-10.00 mg/ml) AR13 and (range from 0.096–9.88 mg/ml) AR15 with correlation coefficient 0.999 and 0.998. The linearity range of both AR13 and AR15 was 101.65±1.5 and 98.78±1.7.Conclusion: It was concluded that the method was simple, accurate, sensitive, accurate and reproducible and has been successfully applied to the pharmacokinetic study of AR13 and AR15 in rat plasma.
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22

Kim, Hyun Ji, Boram Kim, Hyung Jung Byun, et al. "Resolvin D1 Suppresses H2O2-Induced Senescence in Fibroblasts by Inducing Autophagy through the miR-1299/ARG2/ARL1 Axis." Antioxidants 10, no. 12 (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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Ghislain, Noumouha, Anguété Kouamé, Bouet Alphonse, Bahan Frank, N’Guetta Simon-Pierre, and Keli Zagbahi Jules. "New drought-tolerant rainfed upland rice (Oryza sp.) genotypes adapted to the west, centre-west, and centre regions of Côte d'Ivoire." Journal of Agricultural and Crop Research 8, no. 12 (2020): 289–96. http://dx.doi.org/10.33495/jacr_v8i12.20.202.

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To select new rainfed upland rice genotypes, adapted to the West, Centre-West, and Centre regions of Côte d'Ivoire, a study was conducted in research stations. Six genotypes (ART15-11-8-5-2-B-1, WAB891-SG12, WAB1092-B-40AB.1, ARCC3Fa3L10P1-1-B-1, and ART15-16-12 -3-1-B-1-B-3-1) including the control IDSA 10, widely cultivated across the country, were evaluated on three research stations of the National Center of Agricultural Research (CNRA), during the wet seasons of the year 2016 and 2017. These stations are located at the West, Center, and West-Center of Côte d'Ivoire. The trial was set up in a randomised complete block design with four replications. The agromorphological traits such as tillering ability, sowing-50% heading cycle, plant height, percentage of productive tillers, sowing-maturity cycle, and paddy yield were collected for each genotype. In all the environments evaluated, the genotypes ART15-11-8-5-2-B-1, WAB891-SG12, ARCC3Fa3L10P1-1-B-1, and ART15-16-12-3-1-B-1-B -3-1 were characterised by high percentages of productive tillers (87 to 91%), intermediate plant heights (114 to 121 cm), and high average paddy yields (2,601 to 2,810 kg/ha). Yield gains of these genotypes compared to the control ranged from 16 to 25%. The Genotype × Environment interaction (G × E) was highly significant for paddy yield (p < 0.001). The study of the interaction based on the first two principal components analysis of the GGE biplot, explained a 97% of the main effect of the Genotype and the G × E interaction. The polygon tool of the biplot suggested the existence of a single complex mega-environment. Visualizing the mean and stability of genotypes' paddy yield in the biplot indicated that genotypes ART15-11-8-5-2-B-1, WAB891-SG12, ARCC3Fa3L10P1-1-B-1, and ART15-16-12-3-1-B-1-B- 3-1 were more adapted to upland rice-growing regions of the West, Center-West, and Center of Côte d'Ivoire. These genotypes can be released for large scale rice production in these regions. Keywords: Rainfed upland rice, G × E interaction, GGE biplot analysis
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Chen, Yan-Ting, I.-Hao Wang, Yi-Hsun Wang, et al. "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 (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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25

Scott, CF, HR Wenzel, HR Tschesche, and RW Colman. "Kinetics of inhibition of human plasma kallikrein by a site-specific modified inhibitor Arg15-aprotinin: evaluation using a microplate system and comparison with other proteases." Blood 69, no. 5 (1987): 1431–36. http://dx.doi.org/10.1182/blood.v69.5.1431.1431.

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Abstract Human plasma kallikrein, a product of contact-activated plasma proteolysis, is moderately inhibited by aprotinin, a small polypeptide from bovine lung that has been used as an experimental drug in human disease states. Aprotinin has a Lys residue in the P1 (reactive center) position occupying residue 15. Since kallikrein is an arginine-directed serine protease, we hypothesized that an altered form of aprotinin, Arg15-aprotinin, might be a better inhibitor. Kinetic evaluations were performed in 96-well microplates. We found that the KL (loose or Michaelis-Menten complex) was unchanged by the modification. However, the association rate constant was increased from 1.14 X 10(4) (mol/L)- 1s-1 to 1.5 X 10(5) (mol/L)-1s1, thus indicating that the inhibition rate was increased 14-fold for the modified protein. The Ki (at equilibrium) was decreased from 3.2 X 10(-7) mol/L to 1.5 X 10(-8) mol/L after substituting Arg for Lys in the P1 position. Therefore, the modified inhibitor binds to plasma kallikrein more tightly than the natural protein. We also investigated the effect of Arg15-aprotinin on tissue kallikrein, plasmin, factor XIIa, factor XIa, and thrombin and found that the Ki slightly decreased from 5.1 X 10(-7) mol/L to 1.2 X 10(-7) mol/L for tissue kallikrein and slightly decreased from 2 X 10(- 8) mol/L to 1 X 10(-8) mol/L for plasmin. Arg15-aprotinin did not inhibit thrombin or factor XIIa, even though both enzymes are arginine- directed serine proteases. However, factor XIa, although it was not inhibited by aprotinin, had a Ki of 3.4 X 10(-8) mol/L for Arg15- aprotinin. Therefore, Arg15-aprotinin is a more effective inhibitor of plasma kallikrein as well as factor XIa but shows minimal preference for plasmin and tissue kallikrein. This study also indicates that it is possible and practical to perform kinetic analyses directly in microplates.
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26

Scott, CF, HR Wenzel, HR Tschesche, and RW Colman. "Kinetics of inhibition of human plasma kallikrein by a site-specific modified inhibitor Arg15-aprotinin: evaluation using a microplate system and comparison with other proteases." Blood 69, no. 5 (1987): 1431–36. http://dx.doi.org/10.1182/blood.v69.5.1431.bloodjournal6951431.

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Human plasma kallikrein, a product of contact-activated plasma proteolysis, is moderately inhibited by aprotinin, a small polypeptide from bovine lung that has been used as an experimental drug in human disease states. Aprotinin has a Lys residue in the P1 (reactive center) position occupying residue 15. Since kallikrein is an arginine-directed serine protease, we hypothesized that an altered form of aprotinin, Arg15-aprotinin, might be a better inhibitor. Kinetic evaluations were performed in 96-well microplates. We found that the KL (loose or Michaelis-Menten complex) was unchanged by the modification. However, the association rate constant was increased from 1.14 X 10(4) (mol/L)- 1s-1 to 1.5 X 10(5) (mol/L)-1s1, thus indicating that the inhibition rate was increased 14-fold for the modified protein. The Ki (at equilibrium) was decreased from 3.2 X 10(-7) mol/L to 1.5 X 10(-8) mol/L after substituting Arg for Lys in the P1 position. Therefore, the modified inhibitor binds to plasma kallikrein more tightly than the natural protein. We also investigated the effect of Arg15-aprotinin on tissue kallikrein, plasmin, factor XIIa, factor XIa, and thrombin and found that the Ki slightly decreased from 5.1 X 10(-7) mol/L to 1.2 X 10(-7) mol/L for tissue kallikrein and slightly decreased from 2 X 10(- 8) mol/L to 1 X 10(-8) mol/L for plasmin. Arg15-aprotinin did not inhibit thrombin or factor XIIa, even though both enzymes are arginine- directed serine proteases. However, factor XIa, although it was not inhibited by aprotinin, had a Ki of 3.4 X 10(-8) mol/L for Arg15- aprotinin. Therefore, Arg15-aprotinin is a more effective inhibitor of plasma kallikrein as well as factor XIa but shows minimal preference for plasmin and tissue kallikrein. This study also indicates that it is possible and practical to perform kinetic analyses directly in microplates.
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27

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 (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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28

Wang, Yueying, Mengting Qin, JinPing Liu, Xiaobo Chen, Jia Xue, and Sheng Guo. "Abstract 2053: Structural variants detected by optical genome mapping in acute lymphoblastic leukemia patient-derived xenografts models." Cancer Research 83, no. 7_Supplement (2023): 2053. http://dx.doi.org/10.1158/1538-7445.am2023-2053.

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Abstract Background: The established classification of acute lymphoblastic leukemia (ALL) does not cover all high-risk patients because of the difficulty in detecting novel or rare structural variants (SVs). Furthermore, many SVs and formed gene fusions have adverse prognostic effects on hematological malignancies. This study aims to investigate SVs in 22 patient-derived xenografts (PDX) of ALL and to assess rare SVs and chromosomal aberrations, particularly hematological malignancy genes and gene fusions in different individuals detected by optical genome mapping (OGM). Methods: Leukemia cells from 16 patients with B-cell precursor acute lymphoblastic leukemia (B-ALL) and 6 patients with T-cell acute lymphoblastic leukemia (T-ALL) were inoculated into immuno-deficient mice, growth curves were monitored, and leukemia cells were collected after human CD45 was more than 80%. OGM (Bionano Genomics), RNA sequencing (RNA-seq) and whole genome sequencing (WGS) techniques were used to detect SVs and gene fusions. In validation, polymerase chain reaction (PCR) and fluorescence in situ hybridization (FISH) tests were performed to identify specific SVs. Results: On average, each model detected 42 rare SVs with known overlapping genes in different types by OGM: 12 insertions, 25 deletions, 1 inversion, 3 duplications, 2 inter-chromosomal translocations and 1 intra-chromosomal translocation. 5 rare SVs were found in multiple models (>=5), and two of them were never reported in B-ALL and T-ALL. Gene fusions were detected in all ALL models by OGM, and 17% were novel fusions. At the mRNA level, gene fusions were detected only in 19 models, and 24% of the predicted gene fusions by OGM were identical to the results of RNA-seq (high confidence results including pseudogenes). These two technologies could detect different fusion partners. For example, MLLT1 was seen at the mRNA level, and ACER1 was detected at the DNA level in the same KMT2A rearrangement model. Of the 16 B-ALL models, 6 were p190 BCR-ABL1 (a fusion of BCR exon 1 and ABL1 exon 2), 1 was p210 BCR-ABL1 (a fusion of BCR exon 13 and ABL1 exon 2) and 5 of 7 had IKZF1 gene deletions. 2 p190 BCR-ABL1 models were insensitive to imatinib and 2 p190 BCR-ABL1 models as well as the model with IKZF1 exons 4-7 deletion were sensitive to imatinib when treatment was initiated early in the disease. A novel ARL15-IKZF1 fusion was identified in one of the sensitive models. Deletion of the PRKAR2B gene was another rare SV in both models sensitive to imatinib besides the IKZF1 deletion. Conclusion: OGM assays were more comprehensive, and novel rare SVs were identified in ALL. Combining the results of gene fusions between different technologies will provide more accurate predictions for ALL classifications. The combination of aberrant SVs may synergize to influence the efficacy of imatinib, which warrants further investigations. Citation Format: Yueying Wang, Mengting Qin, JinPing Liu, Xiaobo Chen, Jia Xue, Sheng Guo. Structural variants detected by optical genome mapping in acute lymphoblastic leukemia patient-derived xenografts models [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2053.
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29

Price, H. P., D. Goulding, and D. F. Smith. "ARL1 has an essential role in Trypanosoma brucei." Biochemical Society Transactions 33, no. 4 (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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30

Munro, S. "The Arf-like GTPase Arl1 and its role in membrane traffic." Biochemical Society Transactions 33, no. 4 (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 (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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32

Martino, Bruno, Claudia Labate, Caterina Alati, et al. "A Genetic Risk Score for Insulin Resistance Identify Patients with Chronic Myeloid Leukemia, Treated with Nilotinib, Developing Diabetes." Blood 128, no. 22 (2016): 3098. http://dx.doi.org/10.1182/blood.v128.22.3098.3098.

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Abstract BACKGROUD: Nilotinib, a potent 2nd generation tyrosin kinase inhibitor, is efficacious in the treatment of chronic myelogenous leukemia (CML). Impaired glucose metabolism represents one of the most frequently observed adverse events and several clinical trials, reported a high diabetes incidence during treatment with this drug. The mechanism of this side effect is poorly understood, but recently has been hypothesized an increased postreceptorial insulin resistence. Moreover, "in vitro"results indicated that c-ABL is involved in the insulin receptor signaling pathway. A large number of genetic variants associated with Type 2 diabetes (T2D) are implicated in beta-cell function but the role of common genetic variants associated with insulin resistance in the etiology of T2D, remains poorly documented. Scott R. and al. (Diabetes 2014) recently identified 10 multiple single nucleotide polymorphisms (SNPs) associated with insulin resistance and created a genetic risk scores (uGRS) as complementary tool to for insulin resistance. AIM of the study was to identify whether this uGRS could be a valid prognostic tool in identifying patients developing diabetes during Nilotinib therapy PATIENTS AND METHODS:45 patients (19 males) were included in the study. Twenty-four were treated with Nilotinib in first-line and 21 as second line (10 for resistance, 8 intolerance and 3 for other reasons). None of the subjects studied had abnormal blood glucose or took any antidiabetic drug before Nilotinib treatment. We genotyped all patients with the GRS created by Scott R. including those in, or near, the IRS1, GRB14, ARL15, PPARG, PEPD, ANKRD55/MAP3K1, PDGFC, LYPLAL1, RSPO3, and FAM13A1 genes that have primary effects on subcutaneous adipocyte function. Also we added 2 new variants, one for TCF7L2 gene, associated with insulin secretion and another in FTO gene, whose effect on insulin levels is mediated by BMI. The uGRS was calculated, as previously reported, by summing the number of risk alleles across the 12 variants (0 for risk allele absent, 1 for heterozygosity and 2 for homozygosity for risk allele). A cut-off point for uGRS, maximizing predictivity and sensitivity of the score was calculated using Youden's index. Diabetes and impaired fasting Glycaemia were defined using the American Diabetes association (ADA) criteria. Data were reported as median and range, RESULTS:Age at diagnosis was 45(18-82) years, the Sokal was low in 16 (42%), intermediate in 12 (26%) and high in 17 (32%) patients. During treatment and subsequent follow up of 45(7-127) months, 28 patients remained euglycemic, 5 (2 treated in the first line) developed diabetes after 14(1-32) months and 12 (6 treated as first line) developed IFG in 6 (1-12) months. No IFG patients developed an overt diabetes in the subsequent follow-up of 60.3 (33-102) months. We calculated a cut-off point of 12 for uGRS. When the 28 euglycemic patient were compared with 5 patients becoming diabetics after Nilotinib, uGRS showed a sensibility of 100% and a specificity of 46% in predicting diabetes. Consequently, the positive predictive valuewas 25% where the negative predictive values 100%. When the 28 euglycemic patients were compared with the 12 patients developing IFG after Nilotinib, the sensibility and specificity of uGRS was low: 50% and 46% respectively. CONCLUSIONS: A Genetic risk score for insulin resistance showed high specificity and a strong negative predictive values when used to identify CML patients treated with Nilotinib developing an overt diabetes. Further studies in lager populations are needed to confirm this predictivity that can be used in clinical practice to tailor the best anti TKI therapy. Disclosures No relevant conflicts of interest to declare.
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33

Schennach, S., A. M�ller, O. Uwira, et al. "Dielectronic recombination of lithium-like Ar15+." Zeitschrift f�r Physik D Atoms, Molecules and Clusters 30, no. 4 (1994): 291–306. http://dx.doi.org/10.1007/bf01426394.

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34

Amor, J. Carlos, John R. Horton, Xinjun Zhu, et al. "Structures of Yeast ARF2 and ARL1." Journal of Biological Chemistry 276, no. 45 (2001): 42477–84. http://dx.doi.org/10.1074/jbc.m106660200.

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35

Rosenwald, Anne G., Mary Ann Rhodes, Hillary Van Valkenburgh, et al. "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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36

Tiplica, Teodor. "ARL1 of the Attribute c Control Chart with Estimated Parameter." International Journal of Reliability, Quality and Safety Engineering 22, no. 02 (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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37

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 (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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38

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 (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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39

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 (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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40

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 (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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41

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 (2015): e0118743. http://dx.doi.org/10.1371/journal.pone.0118743.

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42

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

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43

Lu, W., W. Zhang, S. S. Molloy, et al. "Arg15-Lys17-Arg18 turkey ovomucoid third domain inhibits human furin." Journal of Biological Chemistry 268, no. 20 (1993): 14583–85. http://dx.doi.org/10.1016/s0021-9258(18)82370-5.

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44

Knoop, S., D. Fischer, Y. Xue, et al. "Single-electron capture in keV Ar15+…18++He collisions." Journal of Physics B: Atomic, Molecular and Optical Physics 41, no. 19 (2008): 195203. http://dx.doi.org/10.1088/0953-4075/41/19/195203.

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45

Zhang, Binbin, Aiqun Xu, Dong Wu, et al. "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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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 (2017): 1691–99. http://dx.doi.org/10.1242/jcs.201319.

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Chen, K. Y., P. C. Tsai, J. W. Hsu, et al. "Syt1p promotes activation of Arl1p at the late Golgi to recruit Imh1p." Journal of Cell Science 123, no. 20 (2010): 3478–89. http://dx.doi.org/10.1242/jcs.074237.

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Nogales Rincón, David. "Maribel Fierro y Alejandro García Sanjuán (eds.), Hispania, al-Ándalus y España. Identidad y nacionalismo en la Historia." Conceφtos, no. 1 (December 21, 2020): 259–62. http://dx.doi.org/10.46608/conceptos2020a/art15.

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Martínez López, Diego. "Modernidad y guerra total: los primeros pasos del orden antiaéreo republicano durante la Guerra Civil española (1936-1937)." Conceφtos, no. 2 (December 31, 2020): 243–57. http://dx.doi.org/10.46608/conceptos2020b/art15.

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GAFFIN, RICHARD B. "The Reformed Dogmatics of Geerhardus Vos." Unio Cum Christo 4, no. 1 (2018): 127. http://dx.doi.org/10.35285/ucc4.1.2018.art15.

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