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Tumor suppression by p53 is mediated in part by the antiangiogenic activity of endostatin and tumstatin.
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- Author(s): Folkman J;Folkman J
- Source:
Science's STKE : signal transduction knowledge environment [Sci STKE] 2006 Sep 26; Vol. 2006 (354), pp. pe35. Date of Electronic Publication: 2006 Sep 26.
- Publication Type:
Journal Article
- Language:
English
- Additional Information
- Source:
Publisher: American Association for the Advancement of Science Country of Publication: United States NLM ID: 100964423 Publication Model: Electronic Cited Medium: Internet ISSN: 1525-8882 (Electronic) Linking ISSN: 15258882 NLM ISO Abbreviation: Sci STKE Subsets: MEDLINE
- Publication Information:
Original Publication: Washington, D.C. : Stanford, CA : American Association for the Advancement of Science ; Stanford University Libraries, [1999-2007.
- Subject Terms:
- Abstract:
Recent research shows that p53 suppresses tumor angiogenesis by transcriptionally activating the alpha(II) collagen prolyl-4-hydroxylase gene. This results in the extracellular release of the potent endogenous angiogenesis inhibitors endostatin and tumstatin from collagens 18 and 4, respectively. The involvement of these inhibitors elucidates a molecular mechanism. By simultaneously repressing a multitude of proangiogenic pathways and by inducing antiangiogenic pathways, a tumor suppressor protein can prevent an incipient tumor from switching to the angiogenic phenotype. Thus, p53 guards the genome from cancer by controlling the three fundamental processes that are critical for growth of a primary tumor and its metastases-tumor cell proliferation, apoptosis, and tumor angiogenesis.
- Accession Number:
0 (Angiogenesis Inhibitors)
0 (Autoantigens)
0 (Collagen Type IV)
0 (Collagen Type XVIII)
0 (Endostatins)
0 (Tumor Suppressor Protein p53)
0 (type IV collagen alpha3 chain)
EC 1.14.11.2 (Procollagen-Proline Dioxygenase)
- Publication Date:
Date Created: 20060928 Date Completed: 20070510 Latest Revision: 20060927
- Publication Date:
20221213
- Accession Number:
10.1126/stke.3542006pe35
- Accession Number:
17003465
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