Crippling SWI-SNF makes tumors GLI-ful.

Nature medicine ·Vol. 16 ·No. 12 ·2010-12-00 ·Pages 1374-6

Reiter JF

Abstract

暂无摘要

MeSH Terms

Chromatin Assembly and Disassembly/genetics Chromosomal Proteins, Non-Histone/metabolism Cyclin D1/metabolism DNA-Binding Proteins/metabolism Gene Expression Regulation, Neoplastic/genetics Humans Models, Biological Receptors, G-Protein-Coupled/genetics Rhabdoid Tumor/genetics SMARCB1 Protein Signal Transduction/genetics Smoothened Receptor Transcription Factors/metabolism Zinc Finger Protein GLI1

Chemicals

Chromosomal Proteins, Non-Histone DNA-Binding Proteins GLI1 protein, human Receptors, G-Protein-Coupled SMARCB1 Protein SMARCB1 protein, human SMO protein, human Smoothened Receptor Transcription Factors Zinc Finger Protein GLI1 Cyclin D1

Authors & Affiliations

1 authors, click to expand affiliations / ORCID

Reiter Jeremy F

References (13)

13 references, click to expand

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The SWI/SNF chromatin-remodeling complex subunit SNF5 is essential for hepatocyte differentiation.
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Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation.
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c-MYC interacts with INI1/hSNF5 and requires the SWI/SNF complex for transactivation function.
Nat Genet. 1999 May;22(1):102-5 PMID: 10319872
Induction of basal cell carcinomas and trichoepitheliomas in mice overexpressing GLI-1.
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Fetal and neonatal rhabdoid tumor.
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Article Info

Journal

Nature medicine

Abbr.

Nat Med

ISSN

1546-170X

DOI

10.1038/nm1210-1374

Published

2010-12-00

Pages

1374-6

Language

English

Region

United States

NLM ID

9502015

Subset

Corrections

CommentOn

PMID: 21076395

External Links

PubMed source DOI: 10.1038/nm1210-1374 View journal details

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