CLL cells are resistant to smac mimetics because of an inability to form a ripoptosome complex. - Wikidata - wikimedia - TriplyDB

CLL cells are resistant to smac mimetics because of an inability to form a ripoptosome complex.

CLL cells are resistant to smac mimetics because of an inability to form a ripoptosome complex.

http://www.wikidata.org/entity/Q42585598

about

Know the enemy as well as the weapons in hand: the aberrant death pathways and therapeutic agents in chronic lymphocytic leukemia Overcoming chemotherapy drug resistance by targeting inhibitors of apoptosis proteins (IAPs)USP11-dependent selective cIAP2 deubiquitylation and stabilization determine sensitivity to Smac mimetics.SMAC mimetic Debio 1143 synergizes with taxanes, topoisomerase inhibitors and bromodomain inhibitors to impede growth of lung adenocarcinoma cells.Reactivation of Smac-mediated apoptosis in chronic lymphocytic leukemia cells: mechanistic studies of Smac mimetic.Preclinical assesement of survivin and XIAP as prognostic biomarkers and therapeutic targets in gastroenteropancreatic neuroendocrine neoplasia.Inhibitor of Apoptosis (IAP) proteins in hematological malignancies: molecular mechanisms and therapeutic opportunities.Survivin and XIAP - two potential biological targets in follicular thyroid carcinoma.Selective IAP inhibition results in sensitization of unstimulated but not CD40-stimulated chronic lymphocytic leukaemia cells to TRAIL-induced apoptosis.Targeting inhibitor of apoptosis proteins by Smac mimetic elicits cell death in poor prognostic subgroups of chronic lymphocytic leukemia.Phenytoin-induced gingival overgrowth caused by death receptor pathway malfunction.Clinicopathological and functional implications of the inhibitor of apoptosis proteins survivin and XIAP in esophageal cancer.

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CLL cells are resistant to smac mimetics because of an inability to form a ripoptosome complex.

http://www.wikidata.org/entity/Q42585598

description

2013 nî lūn-bûn

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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name

CLL cells are resistant to sma ...... to form a ripoptosome complex.

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CLL cells are resistant to sma ...... to form a ripoptosome complex.

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type

label

CLL cells are resistant to sma ...... to form a ripoptosome complex.

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CLL cells are resistant to sma ...... to form a ripoptosome complex.

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prefLabel

CLL cells are resistant to sma ...... to form a ripoptosome complex.

@en

CLL cells are resistant to sma ...... to form a ripoptosome complex.

@nl

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CLL cells are resistant to sma ...... to form a ripoptosome complex

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A Krippner-Heidenreich

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A Malara

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C Maas

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E Eldering

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J A Elias

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J M Tromp

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P2860

IAP antagonists induce autoubiquitination of c-IAPs, NF-kappaB activation, and TNFalpha-dependent apoptosis

IAP antagonists target cIAP1 to induce TNFalpha-dependent apoptosis

cIAPs block Ripoptosome formation, a RIP1/caspase-8 containing intracellular cell death complex differentially regulated by cFLIP isoforms

TNF-alpha induces two distinct caspase-8 activation pathways

Suppression of apoptosis in mammalian cells by NAIP and a related family of IAP genes

TNF-dependent recruitment of the protein kinase RIP to the TNF receptor-1 signaling complex

A conserved family of cellular genes related to the baculovirus iap gene and encoding apoptosis inhibitors

Cloning and expression of apoptosis inhibitory protein homologs that function to inhibit apoptosis and/or bind tumor necrosis factor receptor-associated factors

c-IAP1 and c-IAP2 are critical mediators of tumor necrosis factor alpha (TNFalpha)-induced NF-kappaB activation

Autocrine TNFalpha signaling renders human cancer cells susceptible to Smac-mimetic-induced apoptosis

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e782

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scholarly article

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10.1038/CDDIS.2013.305

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4

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Rachel Thijssen

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2013-08-29T00:00:00Z

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