Bad can act as a key regulator of T cell apoptosis and T cell development. - Wikidata - wikimedia - TriplyDB

Bad can act as a key regulator of T cell apoptosis and T cell development.

Bad can act as a key regulator of T cell apoptosis and T cell development.

http://www.wikidata.org/entity/Q36367710

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The growth-promoting activity of the Bad protein in chicken embryo fibroblasts requires binding to protein 14-3-3 Regulation of thymocyte homeostasis by Fliz1 Direct reversal of glucocorticoid resistance by AKT inhibition in acute lymphoblastic leukemia Expression of the Bcl-2 protein BAD promotes prostate cancer growth Deficiency of PTEN in Jurkat T cells causes constitutive localization of Itk to the plasma membrane and hyperresponsiveness to CD3 stimulation Akt phosphorylates and regulates the orphan nuclear receptor Nur77 Tcl1 enhances Akt kinase activity and mediates its nuclear translocation Complex formation and cooperation of protein kinase C theta and Akt1/protein kinase B alpha in the NF-kappa B transactivation cascade in Jurkat T cells Targeting of the transcription factor Max during apoptosis: phosphorylation-regulated cleavage by caspase-5 at an unusual glutamic acid residue in position P1 Deletion of Bid impedes cell proliferation and hepatic carcinogenesis Identification of a novel phosphorylation site, Ser-170, as a regulator of bad pro-apoptotic activity BAD detects coincidence of G2/M phase and growth factor deprivation to regulate apoptosis.Latent membrane protein 2A-mediated effects on the phosphatidylinositol 3-Kinase/Akt pathway.BH3-only proteins in apoptosis and beyond: an overview.Inhibition of apoptosis by gamma interferon in cells and mice infected with Chlamydia muridarum (the mouse pneumonitis strain of Chlamydia trachomatis).Individual and overlapping roles of BH3-only proteins Bim and Bad in apoptosis of lymphocytes and platelets and in suppression of thymic lymphoma development The kinase PDK1 is essential for B-cell receptor mediated survival signaling.Transgenic expression of CXCR3 on T cells enhances susceptibility to cutaneous Leishmania major infection by inhibiting monocyte maturation and promoting a Th2 response.Crosstalk pathway for inhibition of glucocorticoid-induced apoptosis by T cell receptor signaling.BIM and other BCL-2 family proteins exhibit cross-species conservation of function between zebrafish and mammals.PI3K/Akt and apoptosis: size matters.On the link between Bcl-2 family proteins and glucocorticoid-induced apoptosis.The proapoptotic BH3-only protein bim is expressed in hematopoietic, epithelial, neuronal, and germ cells.Interleukin-7 in T-cell acute lymphoblastic leukemia: an extrinsic factor supporting leukemogenesis?Glucocorticoids in T cell apoptosis and function.Protein kinase B regulates T lymphocyte survival, nuclear factor kappaB activation, and Bcl-X(L) levels in vivo CD28-dependent activation of protein kinase B/Akt blocks Fas-mediated apoptosis by preventing death-inducing signaling complex assembly.Transcription factor NFAT1 controls allergic contact hypersensitivity through regulation of activation induced cell death program.BAD overexpression inhibits cell growth and induces apoptosis via mitochondrial-dependent pathway in non-small cell lung cancer.Latent membrane protein 2A inhibits transforming growth factor-beta 1-induced apoptosis through the phosphatidylinositol 3-kinase/Akt pathway.Differences in Bcl-2 expression by T-cell subsets alter their balance after in vivo irradiation to favor CD4+Bcl-2hi NKT cells.BAD: undertaker by night, candyman by day.Phosphorylation of the transcription factor YY1 by CK2α prevents cleavage by caspase 7 during apoptosis.Bik subcellular localization in response to oxidative stress induced by chemotherapy, in Two different breast cancer cell lines and a Non-tumorigenic epithelial cell line.CaMKII-γ mediates phosphorylation of BAD at Ser170 to regulate cytokine-dependent survival and proliferation.Pro-apoptotic protein BIM in apoptosis of glucocorticoid-sensitive and -resistant acute lymphoblastic leukemia CEM cells.Bcl-2 activates a programme of premature senescence in human carcinoma cells.Dexamethasone inhibits maturation, cytokine production and Fc epsilon RI expression of human cord blood-derived mast cells.Selective glucocorticoid receptor translational isoforms reveal glucocorticoid-induced apoptotic transcriptomes.IL-7 determines the homeostatic fitness of T cells by distinct mechanisms at different signalling thresholds in vivo.

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Bad can act as a key regulator of T cell apoptosis and T cell development.

http://www.wikidata.org/entity/Q36367710

description

1999 nî lūn-bûn

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1999年の論文

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1999年学术文章

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1999年学术文章

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1999年学术文章

@zh-hans

1999年学术文章

@zh-my

1999年学术文章

@zh-sg

1999年學術文章

@yue

1999年學術文章

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1999年學術文章

@zh-hant

name

Bad can act as a key regulator of T cell apoptosis and T cell development.

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Bad can act as a key regulator of T cell apoptosis and T cell development.

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type

label

Bad can act as a key regulator of T cell apoptosis and T cell development.

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Bad can act as a key regulator of T cell apoptosis and T cell development.

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prefLabel

Bad can act as a key regulator of T cell apoptosis and T cell development.

@ast

Bad can act as a key regulator of T cell apoptosis and T cell development.

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Journal of Experimental Medicine

P1476

Bad can act as a key regulator of T cell apoptosis and T cell development

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P2093

C L Mok

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D Kioussis

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G Gil-Gómez

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M Coles

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M Tolaini

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O Williams

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S Taga

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T Norton

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P2860

Dimerization properties of human BAD. Identification of a BH-3 domain and analysis of its binding to mutant BCL-2 and BCL-XL proteins

Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death

Bcl-2 targets the protein kinase Raf-1 to mitochondria

The structure of the human CD2 gene and its expression in transgenic mice

Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery

BH3 domain of BAD is required for heterodimerization with BCL-XL and pro-apoptotic activity

Interference of BAD (Bcl-xL/Bcl-2-associated death promoter)-induced apoptosis in mammalian cells by 14-3-3 isoforms and P11

Interleukin-3-induced phosphorylation of BAD through the protein kinase Akt

Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cells

Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L)

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575-586

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3

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9927519

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apoptotic process

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2192908

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