Direct interaction of c-Myc with Smad2 and Smad3 to inhibit TGF-beta-mediated induction of the CDK inhibitor p15(Ink4B) (Q28216177)

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Min Liang

3

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Weiguo Zhai

4

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Xia Lin

A combination treatment of c-myc antisense DNA with all-trans-retinoic acid inhibits cell proliferation by downregulating c-myc expression in small cell lung cancer

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publication date

January 2002

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language of work or name

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9

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issue

1

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page(s)

133-43

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cites work

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Cooperation of E2F-p130 and Sp1-pRb complexes in repression of the Chinese hamster dhfr gene

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Defective repression of c-myc in breast cancer cells: A loss at the core of the transforming growth factor beta growth arrest program

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Myc-mediated transformation: the repression connection

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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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The Myc oncoprotein: a critical evaluation of transactivation and target gene regulation

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Inhibition of c-myc expression in cells by targeting an RNA-protein interaction using antisense oligonucleotides.

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c-Myc target genes involved in cell growth, apoptosis, and metabolism

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Transforming growth factor beta induces the cyclin-dependent kinase inhibitor p21 through a p53-independent mechanism

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Smads: transcriptional activators of TGF-beta responses

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Histone deacetylase 1 can repress transcription by binding to Sp1.

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MADR2 maps to 18q21 and encodes a TGFbeta-regulated MAD-related protein that is functionally mutated in colorectal carcinoma

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Transforming growth factor-beta (TGF-beta)-induced down-regulation of cyclin A expression requires a functional TGF-beta receptor complex. Characterization of chimeric and truncated type I and type II receptors

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The tumor suppressor Smad4/DPC4 and transcriptional adaptor CBP/p300 are coactivators for Smad3 in TGF-β-induced transcriptional activation

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Smad2, Smad3 and Smad4 cooperate with Sp1 to induce p15(Ink4B) transcription in response to TGF-beta

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

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Cdi1, a human G1 and S phase protein phosphatase that associates with Cdk2

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DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1

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p15INK4B is a potential effector of TGF-beta-induced cell cycle arrest

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Repression of the CDK activator Cdc25A and cell-cycle arrest by cytokine TGF-beta in cells lacking the CDK inhibitor p15

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Molecular mechanisms of inactivation of TGF-beta receptors during carcinogenesis

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Potential role of WAF1/Cip1/p21 as a mediator of TGF-beta cytoinhibitory effect

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Transforming Growth Factor β Activates the Promoter of Cyclin-dependent Kinase Inhibitor p15 through an Sp1 Consensus Site

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Transcriptional control by the TGF-beta/Smad signaling system

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TGFbeta signaling in growth control, cancer, and heritable disorders

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Regulation of the human p21/WAF1/Cip1 promoter in hepatic cells by functional interactions between Sp1 and Smad family members

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MYC oncogenes and human neoplastic disease

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Role of Smad proteins and transcription factor Sp1 in p21(Waf1/Cip1) regulation by transforming growth factor-beta.

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Specificity, diversity, and regulation in TGF-beta superfamily signaling.

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Kip/Cip and Ink4 Cdk inhibitors cooperate to induce cell cycle arrest in response to TGF-beta

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Transforming growth factor-beta-mediated p15(INK4B) induction and growth inhibition in astrocytes is SMAD3-dependent and a pathway prominently altered in human glioma cell lines

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New Myc-interacting proteins: a second Myc network emerges

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Transforming growth factor beta stabilizes p15INK4B protein, increases p15INK4B-cdk4 complexes, and inhibits cyclin D1-cdk4 association in human mammary epithelial cells

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

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

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Antitumor effects of antisense phosphorothioate c-myc oligodeoxynucleotides: a question of mechanism

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p53-independent role of MDM2 in TGF-beta1 resistance

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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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