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Эчтәлеккә күчү

CDKN1A

Wikipedia — ирекле энциклопедия проектыннан ([http://tt.wikipedia.org.ttcysuttlart1999.aylandirow.tmf.org.ru/wiki/CDKN1A latin yazuında])
CDKN1A
Нинди таксонда бар H. sapiens[d][1]
Кодлаучы ген CDKN1A[d][1]
Молекуляр функция связывание с ионом металла[d][2], связывание с белками плазмы[d][3][4][5][…], cyclin-dependent protein serine/threonine kinase inhibitor activity[d][2][6][7][…], ubiquitin protein ligase binding[d][8], cyclin binding[d][2], cyclin-dependent protein kinase activating kinase activity[d][9], cyclin-dependent protein serine/threonine kinase activity[d][10], protein kinase inhibitor activity[d][11][2], protein kinase binding[d][11] һәм protein-containing complex binding[d][11][2]
Күзәнәк компоненты цитоплазма[2][2], цитозоль[d][2][2], cyclin-dependent protein kinase holoenzyme complex[d][2][12], PCNA-p21 complex[d][4], perinuclear region of cytoplasm[d][2], төш[2][2][2][…], нуклеоплазма[d][2][13][2], ядрышко[d][13], ядерные тельца[d][2], protein-containing complex[d][13], cyclin-dependent protein kinase holoenzyme complex[d][12] һәм цитозоль[d][2]
Биологик процесс cellular response to extracellular stimulus[d][14], signal transduction by p53 class mediator[d][2], intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator[d][2], cellular response to heat[d][2], regulation of cyclin-dependent protein serine/threonine kinase activity[d][6][2], DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest[d][2][15], positive regulation of cell death[d][2], response to organic cyclic compound[d][2], negative regulation of cyclin-dependent protein serine/threonine kinase activity[d][2], stress-induced premature senescence[d][16], positive regulation of fibroblast proliferation[d][12], replicative senescence[d][2], response to hyperoxia[d][2], response to corticosterone[d][2], cellular response to amino acid starvation[d][17][2], positive regulation of programmed cell death[d][2], негативная регуляция апоптоза[d][2], response to glucocorticoid[d][2], response to arsenic-containing substance[d][2], regulation of DNA biosynthetic process[d][2], response to organic substance[d][2], negative regulation of gene expression[d][2], cellular response to DNA damage stimulus[d][16][2], negative regulation of G1/S transition of mitotic cell cycle[d][18], regulation of cell cycle[d][2], intrinsic apoptotic signaling pathway[d][19], клеточное старение[d][15], positive regulation of reactive oxygen species metabolic process[d][16][2], cellular response to UV-B[d][2][2], G2/M transition of mitotic cell cycle[d][14], positive regulation of B cell proliferation[d][2], negative regulation of cell growth[d][20], response to organonitrogen compound[d][2], регенерация органов[d][2], regulation of mitotic cell cycle[d][2], intestinal epithelial cell maturation[d][2], cellular response to ionizing radiation[d][16][2], клеточный цикл[d][2], Ras protein signal transduction[d][21], negative regulation of phosphorylation[d][20], response to toxic substance[d][2], response to UV[d][2], response to X-ray[d][2], негативная регуляция пролиферации клеток[d][22][14][2][…], protein stabilization[d][2], positive regulation of cyclin-dependent protein kinase activity[d][2], regulation of transcription by RNA polymerase II[d][2], DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediator[d][2], positive regulation of protein kinase activity[d][13], cellular response to gamma radiation[d][2], negative regulation of cyclin-dependent protein kinase activity[d][11], transcription initiation from RNA polymerase II promoter[d][2], G1/S transition of mitotic cell cycle[d][2][20], cytokine-mediated signaling pathway[d][2], negative regulation of vascular associated smooth muscle cell proliferation[d][23], regulation of cyclin-dependent protein serine/threonine kinase activity[d][6], негативная регуляция пролиферации клеток[d][22][14][20][…], cellular response to amino acid starvation[d][17] һәм cellular response to UV-B[d][2]

CDKN1A (ингл. ) — аксымы, шул ук исемдәге ген тарафыннан кодлана торган югары молекуляр органик матдә.[24][25]

Искәрмәләр

[үзгәртү | вики-текстны үзгәртү]
  1. ↑ 1,0 1,1 UniProt
  2. ↑ 2,00 2,01 2,02 2,03 2,04 2,05 2,06 2,07 2,08 2,09 2,10 2,11 2,12 2,13 2,14 2,15 2,16 2,17 2,18 2,19 2,20 2,21 2,22 2,23 2,24 2,25 2,26 2,27 2,28 2,29 2,30 2,31 2,32 2,33 2,34 2,35 2,36 2,37 2,38 2,39 2,40 2,41 2,42 2,43 2,44 2,45 2,46 2,47 2,48 2,49 2,50 2,51 2,52 2,53 2,54 2,55 2,56 2,57 2,58 2,59 2,60 2,61 GOA
  3. ↑ Esteve-Puig R., Bech-Serra J. J., Hernandez-Losa J. et al. A mouse model uncovers LKB1 as an UVB-induced DNA damage sensor mediating CDKN1A (p21WAF1/CIP1) degradation // PLOS Genetics — PLoS, 2014. — ISSN 1553-7390; 1553-7404 — doi:10.1371/JOURNAL.PGEN.1004721 — PMID:25329316
  4. ↑ 4,0 4,1 Pagano M., Dutta A., Pagano M. et al. PCNA-dependent regulation of p21 ubiquitylation and degradation via the CRL4Cdt2 ubiquitin ligase complex // Genes Dev. — Cold Spring Harbor Laboratory Press, 2008. — ISSN 0890-9369; 1549-5477 — doi:10.1101/GAD.1676108 — PMID:18794347
  5. ↑ Hainsworth E., LaBaer J. Self-assembling protein microarrays // Science / H. Thorp — Northern America: AAAS, 2004. — ISSN 0036-8075; 1095-9203 — doi:10.1126/SCIENCE.1097639 — PMID:15232106
  6. ↑ 6,0 6,1 6,2 K Keyomarsi The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases // Cell — Cell Press, Elsevier BV, 1993. — ISSN 0092-8674; 1097-4172 — doi:10.1016/0092-8674(93)90499-G — PMID:8242751
  7. ↑ Leonardo A. D. DNA damage triggers a prolonged p53-dependent G1 arrest and long-term induction of Cip1 in normal human fibroblasts // Genes Dev. — Cold Spring Harbor Laboratory Press, 1994. — ISSN 0890-9369; 1549-5477 — doi:10.1101/GAD.8.21.2540 — PMID:7958916
  8. ↑ Zhi X., Zhao D., Wang Z. et al. E3 ubiquitin ligase RNF126 promotes cancer cell proliferation by targeting the tumor suppressor p21 for ubiquitin-mediated degradation // Cancer Res. / G. C. Prendergast — American Association for Cancer Research, 2013. — ISSN 0008-5472; 1538-7445 — doi:10.1158/0008-5472.CAN-12-0562 — PMID:23026136
  9. ↑ J LaBaer, Garrett M. D., Stevenson L. F. et al. New functional activities for the p21 family of CDK inhibitors // Genes Dev. — Cold Spring Harbor Laboratory Press, 1997. — ISSN 0890-9369; 1549-5477 — doi:10.1101/GAD.11.7.847 — PMID:9106657
  10. ↑ L. Connell-Crowley, Harper J. W., Goodrich D. W. Cyclin D1/Cdk4 regulates retinoblastoma protein-mediated cell cycle arrest by site-specific phosphorylation // Mol. Biol. Cell, — American Society for Cell Biology, 1997. — ISSN 1059-1524; 1939-4586; 1044-2030 — doi:10.1091/MBC.8.2.287 — PMID:9190208
  11. ↑ 11,0 11,1 11,2 11,3 Kriwacki R. W., L. Hengst, L. Tennant et al. Structural studies of p21Waf1/Cip1/Sdi1 in the free and Cdk2-bound state: conformational disorder mediates binding diversity // Proc. Natl. Acad. Sci. U.S.A. / M. R. Berenbaum — [Washington, etc.], USA: National Academy of Sciences [etc.], 1996. — ISSN 0027-8424; 1091-6490 — doi:10.1073/PNAS.93.21.11504 — PMID:8876165
  12. ↑ 12,0 12,1 12,2 Ruas M., Gregory F., Jones R. et al. CDK4 and CDK6 delay senescence by kinase-dependent and p16INK4a-independent mechanisms // Mol. Cell. Biol. — ASM, 2007. — ISSN 0270-7306; 1098-5549; 1067-8824 — doi:10.1128/MCB.02286-06 — PMID:17420273
  13. ↑ 13,0 13,1 13,2 13,3 Gyorffy B., Kiaris H. Cyclin-dependent kinase 8 mediates chemotherapy-induced tumor-promoting paracrine activities // Proc. Natl. Acad. Sci. U.S.A. / M. R. Berenbaum — [Washington, etc.], USA: National Academy of Sciences [etc.], 2012. — ISSN 0027-8424; 1091-6490 — doi:10.1073/PNAS.1206906109 — PMID:22869755
  14. ↑ 14,0 14,1 14,2 14,3 Wall S. J., Zhong Z., DeClerck Y. A. The cyclin-dependent kinase inhibitors p15INK4B and p21CIP1 are critical regulators of fibrillar collagen-induced tumor cell cycle arrest // J. Biol. Chem. / L. M. Gierasch — Baltimore [etc.]: American Society for Biochemistry and Molecular Biology, 2007. — ISSN 0021-9258; 1083-351X; 1067-8816 — doi:10.1074/JBC.M702697200 — PMID:17553787
  15. ↑ 15,0 15,1 Sedivy J. M. Telomere shortening triggers senescence of human cells through a pathway involving ATM, p53, and p21(CIP1), but not p16(INK4a) // Mol. Cell — Cell Press, Elsevier BV, 2004. — ISSN 1097-2765; 1097-4164 — doi:10.1016/S1097-2765(04)00256-4 — PMID:15149599
  16. ↑ 16,0 16,1 16,2 16,3 Nelson G., Simillion C., Proctor C. J. et al. Feedback between p21 and reactive oxygen production is necessary for cell senescence // Mol. Syst. Biol. / R. Aebersold — EMBO, Wiley, 2010. — ISSN 1744-4292 — doi:10.1038/MSB.2010.5 — PMID:20160708
  17. ↑ 17,0 17,1 Ye J., Koumenis C. Translational Upregulation of an Individual p21Cip1 Transcript Variant by GCN2 Regulates Cell Proliferation and Survival under Nutrient Stress // PLOS Genetics — PLoS, 2015. — ISSN 1553-7390; 1553-7404 — doi:10.1371/JOURNAL.PGEN.1005212 — PMID:26102367
  18. ↑ Dutta A., Abbas T., Shibata E. et al. Selective ubiquitylation of p21 and Cdt1 by UBCH8 and UBE2G ubiquitin-conjugating enzymes via the CRL4Cdt2 ubiquitin ligase complex // Mol. Cell. Biol. — ASM, 2011. — ISSN 0270-7306; 1098-5549; 1067-8824 — doi:10.1128/MCB.05496-11 — PMID:21628527
  19. ↑ B Levkau, H Koyama, Raines E. W. et al. Cleavage of p21Cip1/Waf1 and p27Kip1 mediates apoptosis in endothelial cells through activation of Cdk2: role of a caspase cascade // Mol. Cell — Cell Press, Elsevier BV, 1998. — ISSN 1097-2765; 1097-4164 — doi:10.1016/S1097-2765(00)80055-6 — PMID:9660939
  20. ↑ 20,0 20,1 20,2 20,3 M Schreiber, Muller W. J., G Singh et al. Comparison of the effectiveness of adenovirus vectors expressing cyclin kinase inhibitors p16INK4A, p18INK4C, p19INK4D, p21(WAF1/CIP1) and p27KIP1 in inducing cell cycle arrest, apoptosis and inhibition of tumorigenicity // Oncogene — NPG, 1999. — ISSN 0950-9232; 1476-5594 — doi:10.1038/SJ.ONC.1202466 — PMID:10208428
  21. ↑ M Serrano Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a // Cell — Cell Press, Elsevier BV, 1997. — ISSN 0092-8674; 1097-4172 — doi:10.1016/S0092-8674(00)81902-9 — PMID:9054499
  22. ↑ 22,0 22,1 Verdin E. HDAC4 represses p21(WAF1/Cip1) expression in human cancer cells through a Sp1-dependent, p53-independent mechanism // Oncogene — NPG, 2008. — ISSN 0950-9232; 1476-5594 — doi:10.1038/ONC.2008.371 — PMID:18850004
  23. ↑ Brock M., Trenkmann M., Ulrich S. The hypoxia-induced microRNA-130a controls pulmonary smooth muscle cell proliferation by directly targeting CDKN1A // Int. J. Biochem. Cell Biol. — Elsevier BV, 2015. — ISSN 1357-2725; 0020-711X; 1878-5875 — doi:10.1016/J.BIOCEL.2015.02.002 — PMID:25681685
  24. ↑ HUGO Gene Nomenclature Commitee, HGNC:29223 (ингл.). әлеге чыганактан 2015-10-25 архивланды. 18 сентябрь, 2017 тикшерелгән.
  25. ↑ UniProt, Q9ULJ7 (ингл.). 18 сентябрь, 2017 тикшерелгән.

Чыганаклар

[үзгәртү | вики-текстны үзгәртү]
  • Степанов В.М. (2005). Молекулярная биология. Структура и функция белков. Москва: Наука. ISBN 5-211-04971-3.(рус.)
  • Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter (2002). Molecular Biology of the Cell (вид. 4th). Garland. ISBN 0815332181.(ингл.)


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