Tumor suppressor protein kinase Chk2 is a mediator of anoikis of intestinal epithelial cells (Q28582401)

31 January 2017

title

Tumor suppressor protein kinase Chk2 is a mediator of anoikis of intestinal epithelial cells (English)

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Byong Hoon Yoo

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Alexander Berezkin

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Yanfei Wang

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Anna Zagryazhskaya

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Kirill V. Rosen

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language of work or name

English

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publication date

15 July 2012

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International Journal of Cancer

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published in

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volume

131

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issue

2

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31 January 2017

page(s)

357–366

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Disruption of epithelial cell-matrix interactions induces apoptosis

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cites work

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The extracellular matrix as a cell survival factor

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Cell detachment triggers p38 mitogen-activated protein kinase-dependent overexpression of Fas ligand. A novel mechanism of Anoikis of intestinal epithelial cells

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Distribution of individual components of basement membrane in human colon polyps and adenocarcinomas as revealed by monoclonal antibodies

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Suppression of anoikis and induction of metastasis by the neurotrophic receptor TrkB

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Increased expression of apoptosis inhibitor protein XIAP contributes to anoikis resistance of circulating human prostate cancer metastasis precursor cells.

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Cellular tumorigenicity in nude mice: correlation with cell growth in semi-solid medium.

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Activation of RalA is critical for Ras-induced tumorigenesis of human cells.

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Activated Ras prevents downregulation of Bcl-X(L) triggered by detachment from the extracellular matrix. A mechanism of Ras-induced resistance to anoikis in intestinal epithelial cells

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Down-regulation of death-associated protein kinase-2 is required for beta-catenin-induced anoikis resistance of malignant epithelial cells

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Downregulation of the pro-apoptotic protein Bak is required for the ras-induced transformation of intestinal epithelial cells.

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EphA2: a determinant of malignant cellular behavior and a potential therapeutic target in pancreatic adenocarcinoma

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Acquisition of anoikis resistance promotes the emergence of oncogenic K-ras mutations in colorectal cancer cells and stimulates their tumorigenicity in vivo

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ras Oncogene triggers up-regulation of cIAP2 and XIAP in intestinal epithelial cells: epidermal growth factor receptor-dependent and -independent mechanisms of ras-induced transformation.

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Tumorigenic conversion of p53-deficient colon epithelial cells by an activated Ki-ras gene

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Oncogenic Ras inhibits anoikis of intestinal epithelial cells by preventing the release of a mitochondrial pro-apoptotic protein Omi/HtrA2 into the cytoplasm

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The hCds1 (Chk2)-FHA domain is essential for a chain of phosphorylation events on hCds1 that is induced by ionizing radiation

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Inhibition of eukaryotic translation elongation by cycloheximide and lactimidomycin

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Chk1 and Chk2 kinases in checkpoint control and cancer

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Chk2 is a tumor suppressor that regulates apoptosis in both an ataxia telangiectasia mutated (ATM)-dependent and an ATM-independent manner

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Chk2 activates E2F-1 in response to DNA damage

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The role of checkpoint kinase 1 in sensitivity to topoisomerase I poisons

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Chk1 signaling pathways that mediated G(2)M checkpoint in relation to the cellular resistance to the novel topoisomerase I poison BNP1350.

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Irinotecan: a new agent comes of age.

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A phase I clinical and pharmacokinetic study of the camptothecin glycoconjugate, BAY 38-3441, as a daily infusion in patients with advanced solid tumors

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The Chk2 protein kinase

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Apoptosis associated with deregulated E2F activity is dependent on E2F1 and Atm/Nbs1/Chk2.

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Identifiers

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31 January 2017

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