Degenerative disorders caused by Bcl-2 deficiency prevented by loss of its BH3-only antagonist Bim
about
The Bcl-2 apoptotic switch in cancer development and therapyPuma cooperates with Bim, the rate-limiting BH3-only protein in cell death during lymphocyte development, in apoptosis inductionRegulation of Bim in Health and DiseaseA1/Bfl-1 in leukocyte development and cell deathDirect addition of BimL to mitochondria does not lead to cytochrome c releaseBIM regulates apoptosis during mammary ductal morphogenesis, and its absence reveals alternative cell death mechanismsConcomitant loss of proapoptotic BH3-only Bcl-2 antagonists Bik and Bim arrests spermatogenesisLoss of PKD1 and loss of Bcl-2 elicit polycystic kidney disease through distinct mechanismsCombined loss of proapoptotic genes Bak or Bax with Bim synergizes to cause defects in hematopoiesis and in thymocyte apoptosisPolycystic kidney disease prevented by transgenic RNA interferenceBim/Bcl-2 balance is critical for maintaining naive and memory T cell homeostasisInositol 1,3,4,5-tetrakisphosphate controls proapoptotic Bim gene expression and survival in B cells.Anti-apoptotic gene Bcl2 is required for stapes development and hearingCaspase-independent induction of apoptosis in human melanoma cells by the proapoptotic Bcl-2-related protein Nbk / Bik.BH3-only activator proteins Bid and Bim are dispensable for Bak/Bax-dependent thrombocyte apoptosis induced by Bcl-xL deficiency: molecular requisites for the mitochondrial pathway to apoptosis in platelets.ABT-199, a new Bcl-2-specific BH3 mimetic, has in vivo efficacy against aggressive Myc-driven mouse lymphomas without provoking thrombocytopenia.Shutdown of an acute T cell immune response to viral infection is mediated by the proapoptotic Bcl-2 homology 3-only protein Bim.Bim is responsible for the inherent sensitivity of the developing retinal vasculature to hyperoxia.Negative selection of semimature CD4(+)8(-)HSA+ thymocytes requires the BH3-only protein Bim but is independent of death receptor signaling.Bim regulation of lumen formation in cultured mammary epithelial acini is targeted by oncogenes.Mcl-1 promotes survival of thymocytes by inhibition of Bak in a pathway separate from Bcl-2.Contracting the 'mus cells'--does down-sizing suit us for diving into the memory pool?Regulation of microRNA expression and abundance during lymphopoiesis.Recent advances on skin-resident stem/progenitor cell functions in skin regeneration, aging and cancers and novel anti-aging and cancer therapies.T cell-specific inhibition of multiple apoptotic pathways blocks negative selection and causes autoimmunityExpression and transcriptional regulation of functionally distinct Bmf isoforms in B-chronic lymphocytic leukemia cells.Opposing effects of bim and bcl-2 on lung endothelial cell migrationEpigenetic silencing of Bim transcription by Spi-1/PU.1 promotes apoptosis resistance in leukaemiaElevated Mcl-1 perturbs lymphopoiesis, promotes transformation of hematopoietic stem/progenitor cells, and enhances drug resistance.Control of Bcl-2 expression by reactive oxygen speciesPro-apoptotic BIM is an essential initiator of physiological endothelial cell death independent of regulation by FOXO3.Bcl-2-regulated cell death signalling in the prevention of autoimmunity.The pro-apoptotic protein Bim is a microRNA target in kidney progenitors.The essential role of evasion from cell death in cancer.Viral versus cellular BCL-2 proteins.Destruction of tumor vasculature and abated tumor growth upon VEGF blockade is driven by proapoptotic protein Bim in endothelial cells.The Bcl-2 family: roles in cell survival and oncogenesis.Genome-wide meta-analysis in alopecia areata resolves HLA associations and reveals two new susceptibility lociPharmacological blockade of Bcl-2, Bcl-x(L) and Bcl-w by the BH3 mimetic ABT-737 has only minor impact on tumour development in p53-deficient mice.Bim and Bmf in tissue homeostasis and malignant disease.
P2860
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P2860
Degenerative disorders caused by Bcl-2 deficiency prevented by loss of its BH3-only antagonist Bim
description
2001 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
artículu científicu espublizáu en 2001
@ast
scientific journal article
@en
vedecký článok (publikovaný 2001/11/01)
@sk
vědecký článek publikovaný v roce 2001
@cs
wetenschappelijk artikel (gepubliceerd op 2001/11/01)
@nl
wissenschaftlicher Artikel
@de
наукова стаття, опублікована в листопаді 2001
@uk
مقالة علمية (نشرت في نوفمبر 2001)
@ar
name
Degenerative disorders caused ...... of its BH3-only antagonist Bim
@ast
Degenerative disorders caused ...... of its BH3-only antagonist Bim
@en
Degenerative disorders caused ...... of its BH3-only antagonist Bim
@nl
type
label
Degenerative disorders caused ...... of its BH3-only antagonist Bim
@ast
Degenerative disorders caused ...... of its BH3-only antagonist Bim
@en
Degenerative disorders caused ...... of its BH3-only antagonist Bim
@nl
prefLabel
Degenerative disorders caused ...... of its BH3-only antagonist Bim
@ast
Degenerative disorders caused ...... of its BH3-only antagonist Bim
@en
Degenerative disorders caused ...... of its BH3-only antagonist Bim
@nl
P50
P3181
P1433
P1476
Degenerative disorders caused ...... of its BH3-only antagonist Bim
@en
P2093
J. M. Adams
L. C. Zhang
P304
P3181
P356
10.1016/S1534-5807(01)00083-1
P407
P577
2001-11-01T00:00:00Z