BNIP3

BNIP3
ساختارهای موجود
PDB	جستجوی هم‌ساخت‌شناسی: PDBe RCSB
فهرست شناسه‌های PDB
	2J5D, 2KA1, 2KA2
معین‌کننده‌ها
نام‌های دیگر	BNIP3, NIP3, BCL2/adenovirus E1B 19kDa interacting protein 3, BCL2 interacting protein 3, HABON
شناسه‌های بیرونی	OMIM: 603293 MGI: 109326 HomoloGene: 2990 GeneCards: BNIP3
موقعیت ژن (موش)
کروموزوم	کروموزوم ۷ (موش)
پایان	138,511,248 bp
الگوی گسترش RNA
	; ;
	More reference expression data
هستی‌شناسی ژن
عملکرد ملکولی	• protein homodimerization activity; • GO:0001948، GO:0016582 پیوند پروتئینی; • identical protein binding; • protein heterodimerization activity; • GTPase binding;
ترکیبات سلولی	• سیتوپلاسم; • integral component of membrane; • nuclear envelope; • mitochondrial membranes; • membrane; • integral component of mitochondrial outer membrane; • نوکلئوپلاسم; • mitochondrial outer membrane; • دندریت; • شبکه آندوپلاسمی; • میتوکندری; • mitochondrial envelope; • هسته یاخته; • GO:0097483، GO:0097481 postsynaptic density;
فرایند زیستی	• neuron apoptotic process; • regulation of aerobic respiration; • mitochondrial fragmentation involved in apoptotic process; • positive regulation of mitochondrial fission; • response to hypoxia; • positive regulation of autophagy; • regulation of mitochondrion organization; • response to hyperoxia; • positive regulation of cardiac muscle cell apoptotic process; • مرگ یاخته; • negative regulation of apoptotic process; • positive regulation of programmed cell death; • negative regulation of cell death; • toxin transport; • negative regulation of membrane potential; • reactive oxygen species metabolic process; • intrinsic apoptotic signaling pathway; • positive regulation of macroautophagy; • positive regulation of protein-containing complex disassembly; • cellular response to mechanical stimulus; • cellular response to cobalt ion; • regulation of mitochondrial membrane permeability; • میتوفاژی; • defense response to virus; • intrinsic apoptotic signaling pathway in response to hypoxia; • brown fat cell differentiation; • positive regulation of apoptotic process; • positive regulation of release of cytochrome c from mitochondria; • negative regulation of reactive oxygen species metabolic process; • GO:0022415 viral process; • negative regulation of mitochondrial fusion; • granzyme-mediated apoptotic signaling pathway; • mitochondrial outer membrane permeabilization; • mitochondrial protein catabolic process; • autophagic cell death; • cellular response to hydrogen peroxide; • GO:0097285 مرگ برنامه‌ریزی‌شده یاخته; • cardiac muscle cell apoptotic process; • negative regulation of mitochondrial membrane potential; • positive regulation of necrotic cell death; • cerebral cortex development; • oligodendrocyte differentiation; • positive regulation of mitochondrial calcium ion concentration; • cellular response to hypoxia; • negative regulation of mitochondrial membrane permeability involved in apoptotic process; • positive regulation of autophagy of mitochondrion; • response to bacterium;
	منابع: آمیگو / کوئیک‌گو
هم‌ساخت‌شناسی
	664
	12176
	ENSG00000176171
	ENSMUSG00000078566
	Q12983
	O55003
	NM_004052
	NM_009760
	NP_004043
	NP_033890
	ویکی‌داده
مشاهده/ویرایش انسان	مشاهده/ویرایش موش

پروتئین ۳ واکنش‌دهنده با پروتئین ۱۹ کیلو دالتونی E1B 19 آدنوویروس/E1B 19 (انگلیسی: BCL2/adenovirus E1B 19 kDa protein-interacting protein 3) یک پروتئین است که در انسان توسط ژن «BNIP3» کُدگذاری می‌شود.^[۴]

این پروتئین عضوی از خانوادهٔ Bcl-2 است و در آپوپتوز نقش مهمی دارد و نفوذپذیری غشاء خارجی میتوکندری را با تشکیل هومو- و هترواولیگومرهایی در درون غشاء کنترل می‌کند.^[۵] افزایش این پروتئین سبب کاهش پتانسیل الکتریکی میتوکندری، افزایش رادیکال‌های آزاد اکسیژن، تورم و شکافتگی در میتوکندری و مرگ آنها از طریق خودخواری می‌گردد.^[۶]

منابع

1 2 3 GRCm38: Ensembl release 89: ENSMUSG00000078566 - 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.
↑ Boyd JM, Malstrom S, Subramanian T, Venkatesh LK, Schaeper U, Elangovan B, et al. (October 1994). "Adenovirus E1B 19 kDa and Bcl-2 proteins interact with a common set of cellular proteins". Cell. 79 (2): 341–51. doi:10.1016/0092-8674(94)90202-X. PMID 7954800. S2CID 38609845.
↑ Sassone J, Colciago C, Marchi P, Ascardi C, Alberti L, Di Pardo A, et al. (January 2010). "Mutant Huntingtin induces activation of the Bcl-2/adenovirus E1B 19-kDa interacting protein (BNip3)". Cell Death & Disease. 1 (1): e7. doi:10.1038/cddis.2009.6. PMC 3032515. PMID 21364626.
↑ Liu KE, Frazier WA (2015-06-23). "Phosphorylation of the BNIP3 C-Terminus Inhibits Mitochondrial Damage and Cell Death without Blocking Autophagy". PLOS ONE. 10 (6): e0129667. Bibcode:2015PLoSO..1029667L. doi:10.1371/journal.pone.0129667. PMC 4477977. PMID 26102349.

مشارکت‌کنندگان ویکی‌پدیا. «BNIP3». در دانشنامهٔ ویکی‌پدیای انگلیسی، بازبینی‌شده در ۲۸ اکتبر ۲۰۲۰.

برای مطالعهٔ بیشتر

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Yasuda M, Han JW, Dionne CA, Boyd JM, Chinnadurai G (February 1999). "BNIP3alpha: a human homolog of mitochondrial proapoptotic protein BNIP3". Cancer Research. 59 (3): 533–7. PMID 9973195.
Ohi N, Tokunaga A, Tsunoda H, Nakano K, Haraguchi K, Oda K, et al. (April 1999). "A novel adenovirus E1B19K-binding protein B5 inhibits apoptosis induced by Nip3 by forming a heterodimer through the C-terminal hydrophobic region". Cell Death and Differentiation. 6 (4): 314–25. doi:10.1038/sj.cdd.4400493. PMID 10381623.
Ray R, Chen G, Vande Velde C, Cizeau J, Park JH, Reed JC, et al. (January 2000). "BNIP3 heterodimerizes with Bcl-2/Bcl-X(L) and induces cell death independent of a Bcl-2 homology 3 (BH3) domain at both mitochondrial and nonmitochondrial sites". The Journal of Biological Chemistry. 275 (2): 1439–48. doi:10.1074/jbc.275.2.1439. PMID 10625696.
Vande Velde C, Cizeau J, Dubik D, Alimonti J, Brown T, Israels S, et al. (August 2000). "BNIP3 and genetic control of necrosis-like cell death through the mitochondrial permeability transition pore". Molecular and Cellular Biology. 20 (15): 5454–68. doi:10.1128/MCB.20.15.5454-5468.2000. PMC 85997. PMID 10891486.
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Lamy L, Ticchioni M, Rouquette-Jazdanian AK, Samson M, Deckert M, Greenberg AH, Bernard A (June 2003). "CD47 and the 19 kDa interacting protein-3 (BNIP3) in T cell apoptosis". The Journal of Biological Chemistry. 278 (26): 23915–21. doi:10.1074/jbc.M301869200. PMID 12690108.
Kothari S, Cizeau J, McMillan-Ward E, Israels SJ, Bailes M, Ens K, et al. (July 2003). "BNIP3 plays a role in hypoxic cell death in human epithelial cells that is inhibited by growth factors EGF and IGF". Oncogene. 22 (30): 4734–44. doi:10.1038/sj.onc.1206666. PMID 12879018.
Okami J, Simeone DM, Logsdon CD (August 2004). "Silencing of the hypoxia-inducible cell death protein BNIP3 in pancreatic cancer". Cancer Research. 64 (15): 5338–46. CiteSeerX 10.1.1.326.628. doi:10.1158/0008-5472.CAN-04-0089. PMID 15289340. S2CID 16163067.
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پیوند به بیرون

مکان ژنوم BNIP3 انسانی و صفحهٔ جزئیات ژنی BNIP3 در سامانه جستجوی بانک ژنی دانشگاه کالیفرنیا، سانتا کروز.

[refGRCm38Ensembl-1] 1 2 3 GRCm38: Ensembl release 89: ENSMUSG00000078566 - Ensembl, May 2017

[2] "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[3] "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[pmid7954800-4] Boyd JM, Malstrom S, Subramanian T, Venkatesh LK, Schaeper U, Elangovan B, et al. (October 1994). "Adenovirus E1B 19 kDa and Bcl-2 proteins interact with a common set of cellular proteins". Cell. 79 (2): 341–51. doi:10.1016/0092-8674(94)90202-X. PMID 7954800. S2CID 38609845.

[5] Sassone J, Colciago C, Marchi P, Ascardi C, Alberti L, Di Pardo A, et al. (January 2010). "Mutant Huntingtin induces activation of the Bcl-2/adenovirus E1B 19-kDa interacting protein (BNip3)". Cell Death & Disease. 1 (1): e7. doi:10.1038/cddis.2009.6. PMC 3032515. PMID 21364626.

[:1-6] Liu KE, Frazier WA (2015-06-23). "Phosphorylation of the BNIP3 C-Terminus Inhibits Mitochondrial Damage and Cell Death without Blocking Autophagy". PLOS ONE. 10 (6): e0129667. Bibcode:2015PLoSO..1029667L. doi:10.1371/journal.pone.0129667. PMC 4477977. PMID 26102349.

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