Involvement of Bcl-X(L) deamidation in E1A-mediated cisplatin sensitization of ovarian cancer cells (Q64378213)

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10 January 2020

title

Involvement of Bcl-X(L) deamidation in E1A-mediated cisplatin sensitization of ovarian cancer cells (English)

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10 January 2020

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Chang CY

1

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10 January 2020

Lin YM

2

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10 January 2020

Lee WP

3

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10 January 2020

Hsu HH

4

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10 January 2020

Chen EI

5

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10 January 2020

language of work or name

English

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publication date

1 April 2006

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10 January 2020

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10 January 2020

volume

25

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10 January 2020

page(s)

2656-2665

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10 January 2020

issue

18

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https://scigraph.springernature.com/pub.10.1038/sj.onc.1209294

10 January 2020

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cites work

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Adenovirus E1A, simian virus 40 tumor antigen, and human papillomavirus E7 protein share the capacity to disrupt the interaction between transcription factor E2F and the retinoblastoma gene product

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Bcl-xL deamidation is a critical switch in the regulation of the response to DNA damage

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Accurate transcription initiation by RNA polymerase II in a soluble extract from isolated mammalian nuclei

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Primary cells suppress oncogene-dependent apoptosis

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Akt is required for Axl-Gas6 signaling to protect cells from E1A-mediated apoptosis

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E2F: a link between the Rb tumor suppressor protein and viral oncoproteins

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Deamidation of human proteins

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Selective induction of p53 and chemosensitivity in RB-deficient cells by E1A mutants unable to bind the RB-related proteins

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Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences

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Regularization with a Pruning Prior

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Modulation of PI3K/Akt pathway by E1a mediates sensitivity to cisplatin.

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E1A induces phosphorylation of the retinoblastoma protein independently of direct physical association between the E1A and retinoblastoma products

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Association between an oncogene and an anti-oncogene: the adenovirus E1A proteins bind to the retinoblastoma gene product

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An oncogenic tyrosine kinase inhibits DNA repair and DNA-damage-induced Bcl-xL deamidation in T cell transformation

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