Negative regulation of the mammalian UV response by Myc through association with Miz-1 (Q28212421)

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Michael Wanzel

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Vincent Beuger

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Carsten Frohme

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Dorothee Beul

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Tomi Hillukkala

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Juhani Syvaoja

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Hans-Peter Saluz

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Frank Haenel

The c-Myc protein induces cell cycle progression and apoptosis through dimerization with Max.

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language of work or name

English

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publication date

September 2002

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published in

Molecular Cell

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volume

10

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issue

3

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page(s)

509-21

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cites work

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Mad-Max transcriptional repression is mediated by ternary complex formation with mammalian homologs of yeast repressor Sin3

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The POZ domain: a conserved protein-protein interaction motif

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A Functional interaction between the human papillomavirus 16 transcription/replication factor E2 and the DNA damage response protein TopBP1

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A role for transcriptional repression of p21CIP1 by c-Myc in overcoming transforming growth factor beta -induced cell-cycle arrest

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Mice lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control

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Direct interaction of c-Myc with Smad2 and Smad3 to inhibit TGF-beta-mediated induction of the CDK inhibitor p15(Ink4B)

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Reciprocal regulation of adipogenesis by Myc and C/EBP alpha

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Myc represses the p21(WAF1/CIP1) promoter and interacts with Sp1/Sp3.

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Identification of c-MYC as a target of the APC pathway

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Disentangling the MYC web.

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c-Myc represses transcription in vivo by a novel mechanism dependent on the initiator element and Myc box II

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BRCT domain-containing protein TopBP1 functions in DNA replication and damage response

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An alternative pathway for gene regulation by Myc

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Keratinocytes exposed to ultraviolet radiation reveal three down-regulated genes with potential function in differentiation and cell cycle control

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TGFbeta influences Myc, Miz-1 and Smad to control the CDK inhibitor p15INK4b

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The mammalian UV response: c-Jun induction is required for exit from p53-imposed growth arrest

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Overexpression of c-Myc alters G(1)/S arrest following ionizing radiation

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Repression of p15INK4b expression by Myc through association with Miz-1

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c-Myc can induce DNA damage, increase reactive oxygen species, and mitigate p53 function: a mechanism for oncogene-induced genetic instability

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Reverse two-hybrid and one-hybrid systems to detect dissociation of protein-protein and DNA-protein interactions

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Myc-mediated apoptosis requires wild-type p53 in a manner independent of cell cycle arrest and the ability of p53 to induce p21waf1/cip1.

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Myc downregulation by transforming growth factor beta required for activation of the p15(Ink4b) G(1) arrest pathway.

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A DNA-topoisomerase-II-binding protein with eight repeating regions similar to DNA-repair enzymes and to a cell-cycle regulator

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A DNA damage-regulated BRCT-containing protein, TopBP1, is required for cell survival

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Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization

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10.1016/S1097-2765(02)00633-0

Identifiers

DOI

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Consolidated OpenCitations Corpus – April 2017

507630

507630

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Consolidated OpenCitations Corpus – April 2017

Consolidated OpenCitations Corpus – April 2017

1 reference