RB1CC1
ظاهر
پروتئین ۱ خمشدۀ خمیدۀ القاشونده توسط آربی۱ (انگلیسی: RB1-inducible coiled-coil protein 1) یک پروتئین است که در انسان توسط ژن «RB1CC1» کُدگذاری میشود.[۴][۵][۶][۷]
این پروتئین با مولکول های PTK2B،[۸] ASK1[۹] و PTK2 تعامل پروتئین-پروتئین دارد.[۸]
منابع
[ویرایش]- ↑ ۱٫۰ ۱٫۱ ۱٫۲ GRCm38: Ensembl release 89: ENSMUSG00000025907 - Ensembl, May 2017
- ↑ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ↑ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ↑ Chano T, Ikegawa S, Kontani K, Okabe H, Baldini N, Saeki Y (Feb 2002). "Identification of RB1CC1, a novel human gene that can induce RB1 in various human cells". Oncogene. 21 (8): 1295–8. doi:10.1038/sj.onc.1205171. PMID 11850849. S2CID 1446211.
- ↑ Maucuer A, Camonis JH, Sobel A (Apr 1995). "Stathmin interaction with a putative kinase and coiled-coil-forming protein domains". Proceedings of the National Academy of Sciences of the United States of America. 92 (8): 3100–4. doi:10.1073/pnas.92.8.3100. PMC 42112. PMID 7724523.
- ↑ Hara T, Takamura A, Kishi C, Iemura S, Natsume T, Guan JL, Mizushima N (May 2008). "FIP200, a ULK-interacting protein, is required for autophagosome formation in mammalian cells". The Journal of Cell Biology. 181 (3): 497–510. doi:10.1083/jcb.200712064. PMC 2364687. PMID 18443221.
- ↑ "Entrez Gene: RB1CC1 RB1-inducible coiled-coil 1".
- ↑ ۸٫۰ ۸٫۱ Ueda H, Abbi S, Zheng C, Guan JL (Apr 2000). "Suppression of Pyk2 kinase and cellular activities by FIP200". The Journal of Cell Biology. 149 (2): 423–30. doi:10.1083/jcb.149.2.423. PMC 2175150. PMID 10769033.
- ↑ Gan B, Peng X, Nagy T, Alcaraz A, Gu H, Guan JL (Oct 2006). "Role of FIP200 in cardiac and liver development and its regulation of TNFalpha and TSC-mTOR signaling pathways". The Journal of Cell Biology. 175 (1): 121–33. doi:10.1083/jcb.200604129. PMC 2064504. PMID 17015619.
- مشارکتکنندگان ویکیپدیا. «RB1CC1». در دانشنامهٔ ویکیپدیای انگلیسی، بازبینیشده در ۱۴ اکتبر ۲۰۲۲.
برای مطالعهٔ بیشتر
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