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81por Galindo, Antonio, Soler, Nicolas, McLaughlin, Stephen H., Yu, Minmin, Williams, Roger L., Munro, Sean“…The trans-Golgi-specific targeting of BIG1 and BIG2 depends on the Arf-like GTPase Arl1. We find that Arl1 binds to the dimerization and cyclophilin binding (DCB) domain in BIG1 and report a crystal structure of human Arl1 bound to this domain. …”
Publicado 2016
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82“…Here we demonstrate that 2 monomeric GTP-binding proteins in Saccharomyces cerevisiae, Arl1 and Ypt6, which belong to the Arf/Arl/Sar protein family and the Rab family, respectively, and control endosome-trans-Golgi traffic, are also necessary for starvation-induced autophagy under high temperature stress. …”
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84por Fiorentino, Alessia, Yu, Jing, Arno, Gavin, Pontikos, Nikolas, Halford, Stephanie, Broadgate, Suzanne, Michaelides, Michel, Carss, Keren J., Raymond, F. Lucy, Cheetham, Michael E., Webster, Andrew R., Downes, Susan M., Hardcastle, Alison J.“…RESULTS: Homozygous variants in ARL2BP (NM_012106.3) were identified in two unrelated individuals with RP. …”
Publicado 2018
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85por Zhang, Yiliu, Huang, Yameng, Srivathsan, Amrita, Lim, Teck Kwang, Lin, Qingsong, He, Cynthia Y.“…The small GTPase Arl13b is one of the most conserved and ancient ciliary proteins. …”
Publicado 2018
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86por Shi, Meng, Chen, Bing, Mahajan, Divyanshu, Boh, Boon Kim, Zhou, Yan, Dutta, Bamaprasad, Tie, Hieng Chiong, Sze, Siu Kwan, Wu, Geng, Lu, Lei“…By testing components of the AA-stimulated mTORC1 signaling pathway, we demonstrate that SLC38A9, v-ATPase and Ragulator, but not Rag GTPases and mTORC1, are essential for the AA-stimulated trafficking. Arl5, an ARF-like family small GTPase, interacts with Ragulator in an AA-regulated manner and both Arl5 and its effector, the Golgi-associated retrograde protein complex (GARP), are required for the AA-stimulated trafficking. …”
Publicado 2018
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87por Kwiecinski, Jakub M., Crosby, Heidi A., Valotteau, Claire, Hippensteel, Joseph A., Nayak, Manasa K., Chauhan, Anil K., Schmidt, Eric P., Dufrêne, Yves F., Horswill, Alexander R.“…Finally, we demonstrated that the ArlRS—MgrA regulatory cascade is a druggable target through the identification of a small-molecule inhibitor of ArlRS signaling. …”
Publicado 2019
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88“…Here we demonstrate that ELMOD2, an ARL2 GTPase-activating protein (GAP), is necessary for ARL2 to promote mitochondrial elongation. …”
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89por Kimura, Kenji, Matsumoto, Shinji, Harada, Takeshi, Morii, Eiichi, Nagatomo, Izumi, Shintani, Yasushi, Kikuchi, Akira“…In this study, the involvement of ADP‐ribosylation factor (ARF)‐like (ARL) 4C (ARL4C), a member of the small GTP‐binding protein family, in the progression of lung adenocarcinoma and the possibility of ARL4C as a molecular target for lung cancer therapy were explored. …”
Publicado 2020
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90por Powell, L., Barroso-Gil, M., Clowry, G. J., Devlin, L. A., Molinari, E., Ramsbottom, S. A., Miles, C. G., Sayer, J. A.“…There are a growing number of genetic causes for these rare syndromes, including the recently described genes ARL3 and CEP120. METHODS: We sought to explore the developmental expression patterns of ARL3 and CEP120 in humans to gain additional understanding of these genetic conditions. …”
Publicado 2020
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91“…Mechanistically, miR-145 inhibited mitochondrial function by targeting ARL5B directly. Futhermore, miR-145 overexpression decreased ARL5B expression in ovarian cancer tissue subcutaneous tumors of nude mice. …”
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92“…However, the biological function of ARL2 in CRC remains unclear. The present study was performed to identify the expression level and functional role of ARL2 in CRC. …”
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93“…Purpose: ARL3 (ADP-ribosylation factor-like 3) variants cause autosomal dominant retinitis pigmentosa (RP) or autosomal recessive Joubert syndrome. …”
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94por Villanueva, Maite, Roch, Melanie, Lasa, Iñigo, Renzoni, Adriana, Kelley, William L.“…We discovered a role for both ArlRS and VraSR TCS as determinants responsible for MW2 survival in the presence of sub-MIC ceftaroline. …”
Publicado 2021
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95por Keren-Kaplan, Tal, Sarić, Amra, Ghosh, Saikat, Williamson, Chad D., Jia, Rui, Li, Yan, Bonifacino, Juan S.“…These studies thus identify RUFY3 and RUFY4 as ARL8-dependent, dynein-dynactin adaptors or regulators, and highlight the role of ARL8 in the control of both anterograde and retrograde endolysosome transport.…”
Publicado 2022
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96“…Our study demonstrates that the BORC-ARL8-HOPS ensemble is required for cholesterol egress from lysosomes by enabling CI–MPR-dependent trafficking of NPC2 to the endosomal-lysosomal system.…”
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97por Mahbub, Luba, Kozlov, Guennadi, Zong, Pengyu, Tetteh, Sandra, Nethramangalath, Thushara, Knorn, Caroline, Jiang, Jianning, Shahsavan, Ashkan, Lee, Emma, Yue, Lixia, Runnels, Loren W., Gehring, Kalle“…The crystal structure of the complex between ARL15 GTPase domain and CNNM2 CBS-pair domain reveals the molecular determinants of the interaction and allowed the identification of mutations in ARL15 and CNNM2 mutations that abrogate binding. …”
Publicado 2023
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99por Mahbub, Luba, Kozlov, Guennadi, Zong, Pengyu, Lee, Emma L, Tetteh, Sandra, Nethramangalath, Thushara, Knorn, Caroline, Jiang, Jianning, Shahsavan, Ashkan, Yue, Lixia, Runnels, Loren, Gehring, Kalle“…Here, we characterize ARL15 as a GTP and CNNM-binding protein and demonstrate that ARL15 also inhibits CNNM2 Mg(2+) efflux. …”
Publicado 2023
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100por Lin, Shin-Jin, Lin, Ming-Chieh, Liu, Tsai-Jung, Tsai, Yueh-Tso, Tsai, Ming-Ting, Lee, Fang-Jen S.“…Impaired Arl4A-VPS36 interaction enhances EGFR degradation and clearance of EGFR ubiquitinylation. …”
Publicado 2023
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