(Q24296818)

intrinsic apoptotic signaling pathway by p53 class mediator

GOA release 2020-03-11

1 reference

Journal of Biological Chemistry

GOA release 2020-03-11

author name string

Jörg Weiske

series ordinal

1

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Otmar Huber

series ordinal

2

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language of work or name

English

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publication date

15 September 2006

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published in

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volume

281

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issue

37

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page(s)

27356-66

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cites work

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The product of the ataxia-telangiectasia group D complementing gene, ATDC, interacts with a protein kinase C substrate and inhibitor

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The Histidine Triad Protein Hint Is Not Required for Murine Development or Cdk7 Function

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Deletion of histidine triad nucleotide-binding protein 1/PKC-interacting protein in mice enhances cell growth and carcinogenesis

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The histidine triad protein Hint1 interacts with Pontin and Reptin and inhibits TCF-beta-catenin-mediated transcription

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Pontin52, an interaction partner of beta-catenin, binds to the TATA box binding protein

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Pontin52 and reptin52 function as antagonistic regulators of beta-catenin signalling activity

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BAF53 forms distinct nuclear complexes and functions as a critical c-Myc-interacting nuclear cofactor for oncogenic transformation

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An ATPase/helicase complex is an essential cofactor for oncogenic transformation by c-Myc

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TIP49, but not TRRAP, modulates c-Myc and E2F1 dependent apoptosis

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The transcriptional targets of p53 in apoptosis control

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Mechanisms of cytochrome c release by proapoptotic BCL-2 family members

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Tip60 and p400 are both required for UV-induced apoptosis but play antagonistic roles in cell cycle progression

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Biochemical, crystallographic, and mutagenic characterization of hint, the AMP-lysine hydrolase, with novel substrates and inhibitors

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Coordinate expression of NADPH-dependent flavin reductase, Fre-1, and Hint-related 7meGMP-directed hydrolase, DCS-1

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Altered specificity of Hint-W123Q supports a role for Hint inhibition by ASW in avian sex determination

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Fhit modulation of the Akt-survivin pathway in lung cancer cells: Fhit-tyrosine 114 (Y114) is essential

21 January 2018

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Regulation of CAK kinase activity by p53

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Genetic, biochemical, and crystallographic characterization of Fhit-substrate complexes as the active signaling form of Fhit

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Replacement of Fhit in cancer cells suppresses tumorigenicity

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Designed FHIT alleles establish that Fhit-induced apoptosis in cancer cells is limited by substrate binding

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