BID preferentially activates BAK while BIM preferentially activates BAX, affecting chemotherapy response - Wikidata - awgldk - TriplyDB

BID preferentially activates BAK while BIM preferentially activates BAX, affecting chemotherapy response

BID preferentially activates BAK while BIM preferentially activates BAX, affecting chemotherapy response

http://www.wikidata.org/entity/Q34182014

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Mitochondria, cholesterol and cancer cell metabolism Regulation of Bim in Health and Disease The BCL2 Family: Key Mediators of the Apoptotic Response to Targeted Anticancer Therapeutics Mito-priming as a method to engineer Bcl-2 addiction.Gli1 protein regulates the S-phase checkpoint in tumor cells via Bid protein, and its inhibition sensitizes to DNA topoisomerase 1 inhibitors Knockout Serum Replacement Promotes Cell Survival by Preventing BIM from Inducing Mitochondrial Cytochrome C Release RAS signaling promotes resistance to JAK inhibitors by suppressing BAD-mediated apoptosis.BIM is the primary mediator of MYC-induced apoptosis in multiple solid tissues.Drug-induced death signaling strategy rapidly predicts cancer response to chemotherapy.Rapamycin rescues ABT-737 efficacy in small cell lung cancer Small molecules reveal an alternative mechanism of Bax activation.A B-Cell Superantigen Induces the Apoptosis of Murine and Human Malignant B Cells.Motifs of VDAC2 required for mitochondrial Bak import and tBid-induced apoptosis.Constitutive BAK activation as a determinant of drug sensitivity in malignant lymphohematopoietic cells.Evidence for microRNA-31 dependent Bim-Bax interaction preceding mitochondrial Bax translocation during radiation-induced apoptosis.Synergistic anti-tumor activity and inhibition of angiogenesis by cotargeting of oncogenic and death receptor pathways in human melanoma Bid chimeras indicate that most BH3-only proteins can directly activate Bak and Bax, and show no preference for Bak versus Bax.Mitochondrial ATF2 translocation contributes to apoptosis induction and BRAF inhibitor resistance in melanoma through the interaction of Bim with VDAC1.Midazolam regulated caspase pathway, endoplasmic reticulum stress, autophagy, and cell cycle to induce apoptosis in MA-10 mouse Leydig tumor cells Identification of an activation site in Bak and mitochondrial Bax triggered by antibodies.Targeting MCL-1/BCL-XL Forestalls the Acquisition of Resistance to ABT-199 in Acute Myeloid Leukemia.Inhibition of BET bromodomain-dependent XIAP and FLIP expression sensitizes KRAS-mutated NSCLC to pro-apoptotic agents Enterovirus 71 2B Induces Cell Apoptosis by Directly Inducing the Conformational Activation of the Proapoptotic Protein Bax Bax/Bak activation in the absence of Bid, Bim, Puma, and p53.Analysis of transcription profile to reveal altered signaling pathways following the overexpression of human desumoylating isopeptidase 2 in pancreatic cancer cells.Programmed cell death during neuronal development: the sympathetic neuron model.Apoptosis induced by temozolomide and nimustine in glioblastoma cells is supported by JNK/c-Jun-mediated induction of the BH3-only protein BIM.The Bcl-2 family: structures, interactions and targets for drug discovery.Mitochondrial apoptosis: killing cancer using the enemy within.Emerging understanding of Bcl-2 biology: Implications for neoplastic progression and treatment.Mcl-1 is vital for neutrophil survival.Targeting mTOR for the treatment of B cell malignancies.Mutant BRAF Upregulates MCL-1 to Confer Apoptosis Resistance that Is Reversed by MCL-1 Antagonism and Cobimetinib in Colorectal Cancer.Mitochondria-Judges and Executioners of Cell Death Sentences.Directly targeting the mitochondrial pathway of apoptosis for cancer therapy using BH3 mimetics - recent successes, current challenges and future promise.Constitutive p53 heightens mitochondrial apoptotic priming and favors cell death induction by BH3 mimetic inhibitors of BCL-xL Harmine Hydrochloride Triggers G2 Phase Arrest and Apoptosis in MGC-803 Cells and SMMC-7721 Cells by Upregulating p21, Activating Caspase-8/Bid, and Downregulating ERK/Bad Pathway.Notch4 Signaling Confers Susceptibility to TRAIL-Induced Apoptosis in Breast Cancer Cells.Mouse cytotoxic T cell-derived granzyme B activates the mitochondrial cell death pathway in a Bim-dependent fashion.Physiological and Pharmacological Control of BAK, BAX, and Beyond.

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BID preferentially activates BAK while BIM preferentially activates BAX, affecting chemotherapy response

http://www.wikidata.org/entity/Q34182014

description

2013 nî lūn-bûn

@nan

2013 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2013 թվականի սեպտեմբերին հրատարակված գիտական հոդված

@hy

2013年の論文

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2013年論文

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2013年論文

@zh-hant

2013年論文

@zh-hk

2013年論文

@zh-mo

2013年論文

@zh-tw

2013年论文

@wuu

name

BID preferentially activates B ...... ffecting chemotherapy response

@ast

BID preferentially activates B ...... ffecting chemotherapy response

@en

BID preferentially activates B ...... ffecting chemotherapy response

@nl

type

label

BID preferentially activates B ...... ffecting chemotherapy response

@ast

BID preferentially activates B ...... ffecting chemotherapy response

@en

BID preferentially activates B ...... ffecting chemotherapy response

@nl

prefLabel

BID preferentially activates B ...... ffecting chemotherapy response

@ast

BID preferentially activates B ...... ffecting chemotherapy response

@en

BID preferentially activates B ...... ffecting chemotherapy response

@nl

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J.MOLCEL.2013.08.048

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P1476

BID preferentially activates B ...... ffecting chemotherapy response

@en

P2093

Annabelle Flanagan

http://www.w3.org/2001/XMLSchema#string

Anthony Letai

http://www.w3.org/2001/XMLSchema#string

Joshua J Sims

http://www.w3.org/2001/XMLSchema#string

Luv Patel

http://www.w3.org/2001/XMLSchema#string

Xiaoke Chi

http://www.w3.org/2001/XMLSchema#string

P2860

tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c

Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors

Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis

Bax crystal structures reveal how BH3 domains activate Bax and nucleate its oligomerization to induce apoptosis

Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family members

BH3 profiling identifies three distinct classes of apoptotic blocks to predict response to ABT-737 and conventional chemotherapeutic agents

Bim: a novel member of the Bcl-2 family that promotes apoptosis

BAX activation is initiated at a novel interaction site

Integrated genomic analyses of ovarian carcinoma

Proapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity

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751-765

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scholarly article

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10.1016/J.MOLCEL.2013.08.048

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6

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51

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David W Andrews

Peter K. Sorger

Kristopher A Sarosiek

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2013-09-01T00:00:00Z

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257202865

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24074954

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4164233

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