| Does Δ133p53 isoform trigger inflammation and autoimmunity? | |
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MedLine Citation:
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PMID: 22262184 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Autoimmune diseases are characterized by the immune system mounting a response against self. The exact etiology of autoimmune diseases and autoimmunity remain unclear. Here, we demonstrate that Δ133p53, an isoform of the tumor suppressor protein p53, is involved in the development of autoimmunity. We have previously generated a mouse model of Δ133p53 (Δ122p53). Δ122p53 mice develop an autoimmune/ inflammation-like phenotype that includes the production of autoantibodies, elevated levels of pro-inflammatory cytokines and lymphocyte aggregations in various organs. Microarray analysis reveals that expression of Δ122p53 induces a number of pro-inflammatory genes, including the STAT1 pathway and interferon-related transcription profile. Comparative genetic signatures have been observed in human SLE (systemic lupus erythematosus) patients, and we show that Δ133p53 regulates STAT1 in human cells. Our findings provide the first evidence of a role for p53 isoforms in the development of autoimmune disease. |
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Authors:
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Hamish Campbell; Tania Slatter; Aaron Jeffs; Reena Mehta; Carina Rubio; Margaret Baird; Antony Braithwaite |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-2-01 |
Journal Detail:
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Title: Cell cycle (Georgetown, Tex.) Volume: 11 ISSN: 1551-4005 ISO Abbreviation: - Publication Date: 2012 Feb |
Date Detail:
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Created Date: 2012-1-20 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101137841 Medline TA: Cell Cycle Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Children's Medical Research Institute; University of Sydney; Sydney, NSW Australia. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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