Wikipedia

WAS

WAS (ингл. ) — аксымы, шул ук исемдәге ген тарафыннан кодлана торган югары молекуляр органик матдә.[20][21]

WAS
Нинди таксонда бар H. sapiens[d][1]
Кодлаучы ген белок синдрома Вискотта — Олдрича[d][1]
Молекуляр функция phospholipase binding[d][2], GTPase regulator activity[d][3], SH3 domain binding[d][4][2], связывание с белками плазмы[d][5][6][7][…], связывание похожих белков[d][8][7][9][…], actin binding[d][10], protein kinase binding[d][2], small GTPase binding[d][8][3] һәм actin filament binding[d][11]
Күзәнәк компоненты цитоплазма[10], cell-cell junction[d][10], vesicle membrane[d][10], actin cytoskeleton[d][3], экзосома[d][12], цитоскелет[d][10], цитозоль[d][10][3], микрофиламент[d][13], төш[10][14][15], микрофиламент[d][3][11], actin cortical patch[d][11], site of double-strand break[d][15], phagocytic vesicle[d][10] һәм экзосома[d][16]
Биологик процесс defense response[d][17], Fc-gamma receptor signaling pathway involved in phagocytosis[d][10], actin filament organization[d][10], negative regulation of cell motility[d][18], cвёртывание крови[d][17], positive regulation of Arp2/3 complex-mediated actin nucleation[d][10], actin filament-based movement[d][19], endosomal transport[d][10], actin filament polymerization[d][19], regulation of T cell antigen processing and presentation[d][18], иммун җавап[d][17], epidermis development[d][17], actin polymerization or depolymerization[d][3][10], T cell receptor signaling pathway[d][10], T cell activation[d][10], regulation of catalytic activity[d][10], Rho protein signal transduction[d][3], regulation of actin polymerization or depolymerization[d][3], regulation of lamellipodium assembly[d][3], Cdc42 protein signal transduction[d][3], regulation of stress fiber assembly[d][3], negative regulation of stress fiber assembly[d][3], actin cortical patch assembly[d][11], эндоцитоз[d][11], actin filament polymerization[d][10][15], actin filament-based movement[d][10][11], положительная регуляция транскрипции РНК полимеразой II промотор[d][14], positive regulation of actin nucleation[d][11], actin cortical patch localization[d][11], protein-containing complex assembly[d][3], cellular response to interferon-gamma[d][10], positive regulation of double-strand break repair via homologous recombination[d][15] һәм regulation of double-strand break repair via nonhomologous end joining[d][15]
Изображение Gene Atlas
 WAS Викиҗыентыкта

Искәрмәләр

үзгәртү
  1. ↑ 1,0 1,1 UniProt
  2. ↑ 2,0 2,1 2,2 Lovering R. C., Levinsky R. J. Evidence that the Wiskott-Aldrich syndrome protein may be involved in lymphoid cell signaling pathways // J. Immunol. — Baltimore: 1996. — ISSN 0022-1767; 1550-6606 — PMID:8892607
  3. ↑ 3,00 3,01 3,02 3,03 3,04 3,05 3,06 3,07 3,08 3,09 3,10 3,11 3,12 M Symons, Derry J. M., B Karlak et al. Wiskott-Aldrich syndrome protein, a novel effector for the GTPase CDC42Hs, is implicated in actin polymerization // Cell — Cell Press, Elsevier BV, 1996. — ISSN 0092-8674; 1097-4172 — doi:10.1016/S0092-8674(00)81050-8 — PMID:8625410
  4. ↑ Zucconi A., Scita G., Disanza A. et al. Requirements for F-BAR proteins TOCA-1 and TOCA-2 in actin dynamics and membrane trafficking during Caenorhabditis elegans oocyte growth and embryonic epidermal morphogenesis // PLOS Genetics — PLoS, 2009. — ISSN 1553-7390; 1553-7404 — doi:10.1371/JOURNAL.PGEN.1000675 — PMID:19798448
  5. ↑ Bayer P. The Cdc42/Rac interactive binding region motif of the Wiskott Aldrich syndrome protein (WASP) is necessary but not sufficient for tight binding to Cdc42 and structure formation // J. Biol. Chem. / L. M. Gierasch — Baltimore [etc.]: American Society for Biochemistry and Molecular Biology, 1998. — ISSN 0021-9258; 1083-351X; 1067-8816 — doi:10.1074/JBC.273.29.18067 — PMID:9660763
  6. ↑ Quiles N. M., Geha R. S. Erk/Src phosphorylation of cortactin acts as a switch on-switch off mechanism that controls its ability to activate N-WASP // Mol. Cell. Biol. — ASM, 2004. — ISSN 0270-7306; 1098-5549; 1067-8824 — doi:10.1128/MCB.24.12.5269-5280.2004 — PMID:15169891
  7. ↑ 7,0 7,1 Cheng H., Skehan B. M., Campellone K. G. et al. Structural mechanism of WASP activation by the enterohaemorrhagic E. coli effector EspFU // Nature / M. Skipper — NPG, Springer Science+Business Media, 2008. — ISSN 1476-4687; 0028-0836 — doi:10.1038/NATURE07160 — PMID:18650809
  8. ↑ 8,0 8,1 Kim A. S., Kakalis L. T., N Abdul-Manan et al. Autoinhibition and activation mechanisms of the Wiskott-Aldrich syndrome protein // Nature / M. Skipper — NPG, Springer Science+Business Media, 2000. — ISSN 1476-4687; 0028-0836 — doi:10.1038/35004513 — PMID:10724160
  9. ↑ Cramer R., Ridley A. J., Blanchoin L. Phosphorylation of the WASP-VCA domain increases its affinity for the Arp2/3 complex and enhances actin polymerization by WASP // Mol. Cell — Cell Press, Elsevier BV, 2003. — ISSN 1097-2765; 1097-4164 — doi:10.1016/S1097-2765(03)00172-2 — PMID:12769847
  10. ↑ 10,00 10,01 10,02 10,03 10,04 10,05 10,06 10,07 10,08 10,09 10,10 10,11 10,12 10,13 10,14 10,15 10,16 10,17 10,18 GOA
  11. ↑ 11,0 11,1 11,2 11,3 11,4 11,5 11,6 11,7 Livstone M. S., Thomas P. D., Lewis S. E. et al. Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium // Brief. Bioinform. — OUP, 2011. — ISSN 1467-5463; 1477-4054 — doi:10.1093/BIB/BBR042 — PMID:21873635
  12. ↑ Buschow S. I., Stoorvogel W., Wauben M. MHC class II-associated proteins in B-cell exosomes and potential functional implications for exosome biogenesis // Immunology & Cell Biology — Wiley, 2010. — ISSN 0818-9641; 1440-1711 — doi:10.1038/ICB.2010.64 — PMID:20458337
  13. ↑ M Symons, Derry J. M., B Karlak et al. Wiskott-Aldrich syndrome protein, a novel effector for the GTPase CDC42Hs, is implicated in actin polymerization // Cell — Cell Press, Elsevier BV, 1996. — ISSN 0092-8674; 1097-4172 — doi:10.1016/S0092-8674(00)81050-8 — PMID:8625410
  14. ↑ 14,0 14,1 Candotti F. Nuclear role of WASp in the pathogenesis of dysregulated TH1 immunity in human Wiskott-Aldrich syndrome // Sci. Transl. Med. — AAAS, 2010. — ISSN 1946-6234; 1946-6242 — doi:10.1126/SCITRANSLMED.3000813 — PMID:20574068
  15. ↑ 15,0 15,1 15,2 15,3 15,4 Aparicio T. Nuclear ARP2/3 drives DNA break clustering for homology-directed repair // Nature / M. Skipper — NPG, Springer Science+Business Media, 2018. — 6 p. — ISSN 1476-4687; 0028-0836 — doi:10.1038/S41586-018-0237-5 — PMID:29925947
  16. ↑ Buschow S. I., Stoorvogel W., Wauben M. MHC class II-associated proteins in B-cell exosomes and potential functional implications for exosome biogenesis // Immunology & Cell Biology — Wiley, 2010. — ISSN 0818-9641; 1440-1711 — doi:10.1038/ICB.2010.64 — PMID:20458337
  17. ↑ 17,0 17,1 17,2 17,3 Derry J. M., Ochs H. D., U Francke Isolation of a novel gene mutated in Wiskott-Aldrich syndrome // Cell — Cell Press, Elsevier BV, 1994. — ISSN 0092-8674; 1097-4172 — doi:10.1016/0092-8674(94)90528-2 — PMID:8069912
  18. ↑ 18,0 18,1 Valitutti S. Wiskott-Aldrich syndrome protein controls antigen-presenting cell-driven CD4+ T-cell motility by regulating adhesion to intercellular adhesion molecule-1 // Immunology — Wiley-Blackwell, 2012. — ISSN 0019-2805; 1365-2567 — doi:10.1111/J.1365-2567.2012.03620.X — PMID:22804504
  19. ↑ 19,0 19,1 GOA
  20. ↑ HUGO Gene Nomenclature Commitee, HGNC:29223 (ингл.). әлеге чыганактан 2015-10-25 архивланды. 18 сентябрь, 2017 тикшерелгән.
  21. ↑ UniProt, Q9ULJ7 (ингл.). 18 сентябрь, 2017 тикшерелгән.

Чыганаклар

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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