Regulation of insulin-like growth factor I receptor gene expression by the wilms’ tumor supressor WT1

No abstract is available for this paper.

• Publication year

  2007

• Venue

  Journal of Molecular Neuroscience

• Publication date

  Unknown publication date

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1007/BF02736791PMID 8873895
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Insulin-like growth factors in central nervous system tumors

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  1996cited by this paper
• Inhibition of cellular proliferation by the Wilms' tumor suppressor WT1 is associated with suppression of insulin-like growth factor I receptor gene expression

  1995cited by this paper
• Transcriptional repression of the insulin-like growth factor I receptor (IGF-I-R) gene by the tumor suppressor WT1 involves binding to sequences both upstream and downstream of the IGF-I-R gene transcription start site.

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• The role of the IGF‐I receptor in the growth and transformation of mammalian cells

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• The p53 tumor suppressor gene and pediatric brain tumors.

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  1994cited by this paper
• Molecular and cellular aspects of insulin-like growth factor action.

  1994cited by this paper
• The insulin-like growth factors.

  1993cited by this paper
• The WT1 Wilms tumor gene product: a developmentally regulated transcription factor in the kidney that functions as a tumor suppressor

  1993cited by this paper
• Insulin‐like Growth Factors in Central Nervous System Tumors

  1993cited by this paper
• WT1-mediated growth suppression of Wilms tumor cells expressing a WT1 splicing variant.

  1993cited by this paper
• Increased expression of the insulin-like growth factor I receptor gene, IGF1R, in Wilms tumor is correlated with modulation of IGF1R promoter activity by the WT1 Wilms tumor gene product.

  1993cited by this paper
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  1993cited by this paper
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• Wilms' tumour: reconciling genetics and biology.

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  1992cited by this paper
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  1990cited by this paper
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  1989cited by this paper
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  1989cited by this paper
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• Isolation of biologically active ribonucleic acid from sources enriched in ribonuclease.

  1979cited by this paper

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