Relevant bibliographies by topics / Arl15

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Academic literature on the topic 'Arl15'

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Published: 6 September 2023

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Journal articles on the topic "Arl15"

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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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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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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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Li, Yiping, Ying Yang, Yueting Yao, Xianli Li, Li Shi, Ying Zhang, Yuxin Xiong, Man Yan, Yufeng Yao, and Chunjie Xiao. "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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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 (April 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.06380.

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Richards, J. Brent, Dawn Waterworth, Stephen O'Rahilly, Marie-France Hivert, Ruth J. F. Loos, John R. B. Perry, Toshiko Tanaka, et al. "A Genome-Wide Association Study Reveals Variants in ARL15 that Influence Adiponectin Levels." PLoS Genetics 5, no. 12 (December 11, 2009): e1000768. http://dx.doi.org/10.1371/journal.pgen.1000768.

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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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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 (October 3, 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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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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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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Dissertations / Theses on the topic "Arl15"

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Panić, Bojana. "The small GTPases Arl1p/Arl1 and Arl3p/ARFRP1 act in a pathway for targeting proteins to the Golgi apparatus." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.616124.

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Lasić, Maja. "The yeast endosomal/TGN-localized Ysl2p-Arl1p-Neo1p network: search for novel interaction partners." [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:93-opus-34910.

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Ferreira, Cláudia Susana da Rosa. "Organelle-specific roles for the Arf-like G proteins Arl5 and Arl8." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609430.

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Man, Zhiqiu. "Localization and function of Arfaptins: Arl1-dependent trans-Golgi localization and induction of membrane deformation." 京都大学 (Kyoto University), 2012. http://hdl.handle.net/2433/157901.

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Ding, Jian. "Functional analysis of the extended N-terminus for the Drosophila Raf protein and initial characterization of the Arl1 gene." [Ames, Iowa : Iowa State University], 2010. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3403792.

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Sharma, Prerna. "Unravelling the functional role of Arf-like GTPases 14 and 15 in mammalian cells." Thesis, 2022. https://etd.iisc.ac.in/handle/2005/5831.

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Small G-proteins of Arf-like (Arl) GTPase subfamily are shown to regulate several cellular processes including intracellular trafficking, cytoskeletal organization, organelle biogenesis, cell adhesion and migration. Around 21 genes belong to this family have been identified in human. However, the critical function of Arl14 and Arl15 in cargo transport was unclear. In this study, we have attempted to characterize the role of Arl14 and Arl15 in multiple cellular processes, including intracellular trafficking using HeLa cells. Objective I: Elucidating the role of Arl15 in modulating cell adhesion, motility and filopodia biogenesis. Our study characterized the intracellular localization of Arl15 using epitope tagged Arl15-GFP in multiple mammalian types. We have observed that Arl15-GFP localizes to Golgi, plasma membrane (PM) including filopodia, and a cohort to recycling endosomes in HeLa, A549, neuro 2a, and primary keratinocytes. Additionally, we noticed the localization of Arl15 to long extracellular tube structures (resembling tunneling nanotubes, TNTs) connecting the Neuro 2a cells. The dual localization of Arl15 to Golgi and PM is independent of the actin cytoskeleton, but it is dependent on Golgi integrity. The dissociation of Golgi using small molecular inhibitors or the expression of Arf1 dominant-negative mutant completely mislocalizes Arl15 to the cytosol. We identified a novel V80A mutation in the GTP-binding domain that turns the Arl15 into a dominant-negative form and results in a reduced number of filopodia. Depletion of Arl15 in HeLa cells causes mislocalization of cargo such as caveolin-2, STX6, and ectopically expressed GFP-GPI from Golgi and accumulation of lipid droplets. Further, Arl15 knockdown cells display reduced filopodial number, dispersion of vinculin localization (focal adhesion kinase), and enhanced soluble and receptor-mediated cargo uptake without affecting the recycling kinetics. In addition, Arl15 knockdown decreases cell migration and increases cell adhesion, and displays enhanced cell spreading. Traction force microscopy studies revealed that Arl15 depleted cells exert higher traction force and generate multiple focal adhesion points. These studies demonstrated a function to Arl15 in Golgi, which regulates cargo transport to organize membrane domains at the cell surface to control cell migration, spreading and adhesion, including filopodial biogenesis. Objective II: Studying the role of Arl14 in vesicular trafficking Studies have suggested that Arl14 regulates the movement of MHC-II vesicles along the actin cytoskeleton in dendritic cells. We have studied the localization of Arl14 using epitope tagged Arl14-GFP in HeLa cells. Arl14 localizes to REs, late endosomes, and lysosomes. Expression of Arl14S27N-GFP showed no change in its localization, indicating that Arl14S27N-GFP is not acting as a dominant negative mutant while constitutive active mutant of Arl14 (Arl14Q68L-GFP) majorly localized as punctate structures that are clustered and positive for RFP-STX13 (represents endosomal structures). Depletion of Arl14 showed an enhanced number of LAMP-1-positive lysosomes without changing the localization of lysosome biogenesis transcription factors TFEB and TFE3. Immunoblotting analysis showed no change in Rab5, STX13, Rab11, annexinA2, LAMP-1, and LAMP-2 expression in siArl14 compared to siControl. Overall, these studies showed that Arl14 localizes to endo-lysosomal organelles, and its depletion altered the number of LAMP-1 positive compartments.
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Hsu, Hsin-Chia, and 許俽嘉. "Characterization of an Arl1p Guanine-Nucleotide Exchange Factor, Syt1p." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/04867349717273321965.

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碩士
臺灣大學
分子醫學研究所
98
ARF-like (ARL) proteins belong to ADP-ribosylation factor (ARF) GTPase family, which are involved in protein trafficking and cytoskeleton organization. Those small G proteins require guanine-nucleotide exchange factors (GEFs) to switch from GDP-bound to GTP-bound form and become active. Previous reports suggested that Syt1p is the GEF of Arf2p and is involved in vesicle trafficking. Recently, our studies showed that Syt1p also acted as a GEF for Arl1p. In this study, Syt1p was further characterized. Firstly, it has been shown that Syt1p belongs to BFA-resistant GEFs. Secondly, Syt1p can use multiple regions to interact with Arl1p. The N-terminus, Sec7 domain, and C-terminus of Syt1p can all interact with Arl1d17N form, whose N-terminal first 17 amino acids are deleted. The interactions between all of the three regions and Arl1d17N are stronger than the interaction between full-length Syt1p and Arl1pd17N. Therefore, it might hint that Syt1p is autoregulated as other GEFs of Small GTPases. Surprisingly, we next found that Syt1p has an intramolecular interaction between the C-terminal region and Sec7 domain and an intermolecular interaction between C-terminal regions, indicating that Syt1p could form dimers or oligomers and might be autoregulated. Syt1p dimerization or oligomerization is also supported by in vivo pull down results, which proved that Syt1p can interact with itself. Moreover, the N-terminus is important for the formation of dimers or oligomers. Yeast two-hybrid screen was also performed to search for putative regulators of Syt1p. However, those candidates remain to be elucidated. Besides, whether dimerization or oligomerization plays an important role in Syt1p activation or membrane tethering and whether autoinhibition truly exists in Syt1p in vivo require further investigation.
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LIn, Ching-Yi, and 林靜宜. "Functional Characterization of ADP-Ribosylation Factor-Like Proteins：ARL4 and ARL5." Thesis, 2001. http://ndltd.ncl.edu.tw/handle/37795439008511565193.

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博士
國立臺灣大學
分子醫學研究所
89
ADP-ribosylation factors (ARFs) Ras-related small GTP-binding proteins (~20 kDa), were originally identified as protein cofactors for the cholera toxin-catalyzed ADP-ribosylation of GS, the stimulatory subunit for adenylate cyclase. Their cofactor activity depends on GTP-binding－ regulated by interactions with ARF-specific guanine nucleotide exchange factors (GEFs) or ARF-specific GTPase activating proteins (GAPs). Today, at least six mammalian ARF members have been identified and grouped into three classes. ARFs have been found in different subcellular localizations, and regulate several different vesicle transport steps in the exocytic and endocytic pathways－ including budding from the endoplasmic reticulum and fusion to the Golgi stacks, endosomes, and nuclear vesicles. ARF-like (ARL) proteins, which belong to another subfamily of ARFs, have been cloned recently from Drosophila, rat, human and yeast. Although ARLs and ARFs have very similar amino acid sequences, ARLs lack cofactor activity for the cholera toxin-catalyzed ADP-ribosylation. dARL1 is essential in Drosophila, while disruption of yeast ARL1 gene is not lethal. ARL1 from yeast and human were reported to localize at the Golgi complex. In this thesis, we report the biochemical characterization and subcellular localizations of two ARLs－ ARL4 and ARL5. We first cloned mouse and human ARL4 (mARL4 and hARL4) cDNA, respectively. Mice ARL4 is abundant in testis and has developmental stages-specific expression pattern. The appearance of mARL4 mRNA during embryonic development coincides with the sequential formation of somites and the establishment of brain compartmentation. Using ARL4-specific antibody in immuno-fluorescence microscopy, we found that endogenous mARL4 in cultured Sertoli and neuroblastoma cells was mainly concentrated in nuclei. When ectopically expressed in COS7 cells, ARL4-T34N mutant (predicted to be the GDP-bound form) was concentrated in nucleoli. Yeast two-hybrid screen and in vitro protein-interaction assays showed that hARL4 interacts with importin-a－required its C-terminal NLS region, and the interaction is nucleotide-independent. Like ARL2 and ARL3, recombinant hARL4 does not enhance cholera toxin-catalyzed auto-ADP-ribosylation. Its binding with GTPγS could be affected by phospholipid, and the N-terminus of hARL4, like that of ARF, is myristoylated. Our findings suggest that ARL4－ with its distinctive nuclear/nucleolar localization and developmentally regulated expression pattern－may play a unique role(s) in neurogenesis and somitogenesis during embryonic development, and in the early stages of spermatogenesis in adults, respectively. Mouse and human ARL5 (mARL5 and hARL5) were also cloned, and the hARL5 mRNA is ubiquitously expressed in many tissues and considerably abundant in liver. mARL5 mRNA is mainly present at day 7 mouse embryos, then disappears at day 11. Our findings suggest that ARL5 may have an important role(s) in the early events of embryonic development. Immunostaining of COS7 cells transfected with Myc-tagged hARL5-WT, hARL5-T35N, hARL5-Q80L, and hARL5-dC constructs provide direct evidence for its subcellular localization in the cell. Interestingly, hARL5-T35N mutant, the predicted GDP-bound form, was most concentrated in nucleoli, but sometimes present in cytosol. By yeast two-hybrid screen, hARL5 interacts with NLS-receptor, importin-a, through the putative bipartite NLS in its C-terminal region. When NLS is removed from hARL5, hARL5-dC is colocalized with mitochondria; hARL5-T35N has the same pattern when it appears in the cytosol. In addition, yeast two-hybrid screen and in vitro protein-interaction assays showed that hARL5-WT, hARL5-Q80L can interact with HP1a, and the interaction is nucleotide-dependent. The interaction was further confirmed by in vivo protein-interaction assays. hARL5 contains MIR homology sequence－ VPVLVL (residue 128~133)－ that is crucial for hARL5 binding to HP1a. As ARL2, 3, and 4, recombinant hARL5 did not enhance the cholera toxin-catalyzed auto-ADP-ribosylation. Its intrinsic GTPgS-binding activity was low. The N-terminus of hARL5 is myristoylated as are ARFs. Based on these results, we have demonstrated that hARL5, like hARL4, with its specific interaction proteins and distinctive nuclear/nucleolar localizations may have important biological functions.
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Diamantino, João Marques da Cunha dos Santos. "The role of Arl17 in healthy and influenza A virus infected cells." Master's thesis, 2019. http://hdl.handle.net/10362/89281.

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Influenza A virus (IAV) is an important human pathogen that causes epidemic and pandemic events of flu. The study of the viral life cycle and its interactions with the infected host is crucial for the development of novel therapeutic strategies. IAV has an eight-part segmented RNA genome organized in viral ribonucleoprotein complexes (vRNP), which are replicated in the nucleus of the cell. De novo synthesized vRNPs need to leave the nucleus to reach the cytosol for viral assembly, budding and release. Several pathways have been implicated in nuclear export of vRNPs, including CRM1, apoptosis activation and extracellular signal-regulated kinase 1 and 2 (ERK1/2) signaling cascade. Mitochondria are crucial organelles for the maintenance of cellular homeostasis, since they are responsible for the regulation of metabolism, apoptosis, calcium homeostasis and innate immunity. Their functions are tightly regulated by dynamic changes in mitochondrial morphology. Given their importance, many viruses modulate mitochondria to promote cellular environments favoring their proliferation. IAV has been shown to fragment mitochondria to decrease the antiviral immune response. Our lab identified a candidate modulator of mitochondrial morphology and IAV infection: the host GTPase Arl17. Our work demonstrated that depletion of Arl17 leads to a reduction in viral titers and promotes mitochondrial fragmentation, regardless of infection. Interestingly, this phenotype was not accompanied by alterations in IFNβ1 expression and mitochondrial unfolded protein response activation (UPRmt). However, ATP levels were significantly reduced in the absence of Arl17. Additionally, we showed that Arl17 is required for regular vRNP nuclear export. In its absence, we observed a delay in vRNPs nuclear export that was CRM1- and ERK1/2-independent. Therefore, influence of Arl17 on the induction of apoptosis should be further investigated as its inhibition could explain vRNPs nuclear export delay and it could be the element that links mitochondria and vRNPs nuclear export.
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Wu, Tsung-Shung. "Functional characterization of Arf-like protein, ARL5 and its interacting protein EB1." 2005. http://www.cetd.com.tw/ec/thesisdetail.aspx?etdun=U0001-0908200521130700.

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Books on the topic "Arl15"

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Build Your Own AR15 Rifle. Createspace, 2010.

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Zediker, Glen D. America's Gun: The Practical AR15. Primedia eLaunch LLC, 2018.

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Gun Digest Shooters Guide To The Ar15. F+W Media Inc, 2014.

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The Competitive AR15; The Mouse That Roared. Zediker Publishing, 1998.

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Bartocci, Christopher. Armorer's Manual AR15/M16/M4 Family of Weapons. Independently published, 2017.

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Gun Digest Book of the AR15 Volume 4. Gun Digest Books, 2012.

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The M16/AR15 Rifle (A Shooter's and Collector's Guide). 3rd ed. North Cape Publications Inc, 2007.

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Luggage, Handbags, Saddlery & Harness (UK Markets: Annual Reports 1993: AR15). The Stationery Office Books (Agencies), 1994.

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Luggage, Handbags, Saddlery and Harness (UK Markets: Annual Reports 1994: AR15). The Stationery Office Books (Agencies), 1995.

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LINDA. 2nd Amendment for Men 556 2A AR15 Accessories Pro Gun Rights Meme. Independently Published, 2022.

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Book chapters on the topic "Arl15"

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Schrapper, Christian. "Sozialpädagogische Diagnosen und sozialpädagogisches Fallverstehen." In Handbuch Allgemeiner Sozialer Dienst (ASD), 3. aktual. u. erw. Auflage. München: Ernst Reinhardt Verlag, 2019. http://dx.doi.org/10.2378/asda3.art15.

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Cross, Eric, and Helen Pickering. "La contribution de l'enseignement supérieur au développement culturel régional dans le Nord-Est de l'Angleterre." In Politiques et gestion de l'enseignement supérieur, Volume 20 Numéro 2, 1–15. OECD, 2008. http://dx.doi.org/10.1787/hemp-v20-art15-fr.

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Pacheco-Rodriguez, Gustavo, Joel Moss, and Martha Vaughan. "[44] Preparation and assay of recombinant ADP-ribosylation factor-like protein-1 (ARL1)." In Methods in Enzymology, 424–28. Elsevier, 2001. http://dx.doi.org/10.1016/s0076-6879(01)29103-4.

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Tai, Guihua, Lei Lu, Ludger Johannes, and Wanjin Hong. "Functional Analysis of Arl1 and Golgin‐97 in Endosome‐to‐TGN Transport Using Recombinant Shiga Toxin B Fragment." In Methods in Enzymology, 442–53. Elsevier, 2005. http://dx.doi.org/10.1016/s0076-6879(05)04039-5.

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Lu, Lei, Guihua Tai, and Wanjin Hong. "Interaction of Arl1 GTPase with the GRIP Domain of Golgin‐245 as Assessed by GST (Glutathione‐S‐transferase) Pull‐Down Experiments." In Methods in Enzymology, 432–41. Elsevier, 2005. http://dx.doi.org/10.1016/s0076-6879(05)04038-3.

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Conference papers on the topic "Arl15"

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Silva, Daniel Campos, Leonardo Paes Rangel, Marcone Lima Sobreira, Natan Padoin, and Cíntia Soares. "COMPUTATIONAL SIMULATION OF ABDOMINAL AORTIC ANEURISM AND ITS ASSESSMENT TO MEDICAL TREATMENT." In Simpósio Paranaense de Modelagem, Simulação e Controle de Processos. Departamento de Engenharia Química UFPR, 2020. http://dx.doi.org/10.5380/simproc4.2019.art15.

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Lepre, Priscilla. "DO TANGÍVEL AO INTANGÍVEL NO DESIGN DE S.PSS - REFLEXÕES SOBRE A POSSE E O VALOR." In Simpósio de Design Sustentável. Departamento de Design da UFPR, 2021. http://dx.doi.org/10.5380/8sds2021.art15.

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Schennach, S., A. Müller, A. Frank, J. Haselbauer, W. Spies, O. Uwira, M. Wagner, et al. "Dielectronic recombination of Ar15+ ions involving Δn=0 and Δn=1 transitions." In 6th International conference on the physics of highly charged ions. AIP, 1993. http://dx.doi.org/10.1063/1.43658.

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Lee, Sooyong, Sangkyou Lee, Jolanta Bondaruk, Hua Wang, Shizhen Zhang, Menashe Bar-Eli, Peter Black, et al. "Abstract 3065: Loss of ARL11 function promotes growth ofin situneoplasia by activating the ras pathway." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3065.

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Moazzen-Ahmadi, Nasser, A. R. W. McKellar, and A. Barclay. "COMPLETION OF THE FIRST SOLVATION SHELL OF CARBON DIOXIDE IN ARGON: ROTATIONALLY RESOLVED INFRARED SPECTRA OF CO2-AR15 AND CO2-AR17." In 2022 International Symposium on Molecular Spectroscopy. Urbana, Illinois: University of Illinois at Urbana-Champaign, 2022. http://dx.doi.org/10.15278/isms.2022.ri09.

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"ПРАКТИКА ОКАЗАНИЯ ПСИХОЛОГО-ПЕДАГОГИЧЕСКОЙ ПОМОЩИ И СОПРОВОЖДЕНИЯ ДЕТЕЙ С РАССТРОЙСТВАМИ АУТИСТИЧЕСКОГО СПЕКТРА В Г. МАГАДАНЕ." In НА ПЕРЕКРЕСТКЕ СЕВЕРА И ВОСТОКА (МЕТОДОЛОГИИ И ПРАКТИКИ РЕГИОНАЛЬНОГО РАЗВИТИЯ). Science and Innovation Center Publishing House, 2023. http://dx.doi.org/10.12731/978-5-907608-10-8-art15.

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Reports on the topic "Arl15"

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Sweeney, Steven, L. D. Stephenson, Ralph Eichlin, and Robert Weber. Demonstration and validation of stainless steel materials for critical above-grade piping in highly corrosive locations : final report on Project F07-AR15. Construction Engineering Research Laboratory (U.S.), May 2017. http://dx.doi.org/10.21079/11681/22548.

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