Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 280, Issue 45, Pages 37725-37731Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M507976200
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Funding
- NCI NIH HHS [CA73796, CA16038] Funding Source: Medline
- NIAMS NIH HHS [AR39190] Funding Source: Medline
- Telethon [TGM06S01, TGM03P14] Funding Source: Medline
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Glucocorticoid-induced tumor necrosis factor receptor ( GITR) is a member of the tumor necrosis factor receptor superfamily, is expressed in T lymphocytes, and exerts an anti-apoptotic function in these cells. We reported that GITR is also highly expressed in the skin, specifically in keratinocytes, and that it is under negative transcriptional control of p21(Cip1/WAF1), independently from the cell cycle. Although GITR expression is higher in p21-deficient keratinocytes and skin, it is down-modulated with differentiation and in response to UVB. The combined analysis of keratinocytes with increased GITR expression versus normal keratinocytes and skin of mice with a disruption of the GITR gene indicates that this protein protects keratinocytes from UVB-induced apoptosis both in vitro and in vivo.
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