Fas ligand

A sensor for DNA damage critical in skin cancer etiology

Laurie L. Hill, Allal Ouhtit, Susan M. Loughlin, Margaret L. Kripke, Honnavara N. Ananthaswamy, Laurie B. Owen-Schaub

Research output: Contribution to journalArticle

213 Citations (Scopus)

Abstract

DNA-damaged cells can either repair the DNA or be eliminated through a homeostatic control mechanism termed 'cellular proofreading.' Elimination of DNA-damaged cells after ultraviolet radiation (UVR) through sunburn cell (apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found to be dependent on Fas ligand (FasL), a pro-apoptotic protein induced by DNA damage. Chronic exposure to UVR caused 14 of 20 (70 percent) FasL-deficient mice and 1 of 20 (5 percent) wild-type mice to accumulate p53 mutations in the epidermis. Thus, FasL-mediated apoptosis is important for skin homeostasis, suggesting that the dysregulation of Fas-FasL interactions may be central to the development of skin cancer.

Original languageEnglish
Pages (from-to)898-900
Number of pages3
JournalScience
Volume285
Issue number5429
DOIs
Publication statusPublished - Aug 6 1999

Fingerprint

Fas Ligand Protein
Skin Neoplasms
DNA Damage
Sunburn
Radiation
Skin
Apoptosis Regulatory Proteins
DNA
Keratinocytes
Epidermis
DNA Repair
Homeostasis
Apoptosis
Mutation

ASJC Scopus subject areas

  • General

Cite this

Hill, L. L., Ouhtit, A., Loughlin, S. M., Kripke, M. L., Ananthaswamy, H. N., & Owen-Schaub, L. B. (1999). Fas ligand: A sensor for DNA damage critical in skin cancer etiology. Science, 285(5429), 898-900. https://doi.org/10.1126/science.285.5429.898

Fas ligand : A sensor for DNA damage critical in skin cancer etiology. / Hill, Laurie L.; Ouhtit, Allal; Loughlin, Susan M.; Kripke, Margaret L.; Ananthaswamy, Honnavara N.; Owen-Schaub, Laurie B.

In: Science, Vol. 285, No. 5429, 06.08.1999, p. 898-900.

Research output: Contribution to journalArticle

Hill, LL, Ouhtit, A, Loughlin, SM, Kripke, ML, Ananthaswamy, HN & Owen-Schaub, LB 1999, 'Fas ligand: A sensor for DNA damage critical in skin cancer etiology', Science, vol. 285, no. 5429, pp. 898-900. https://doi.org/10.1126/science.285.5429.898
Hill LL, Ouhtit A, Loughlin SM, Kripke ML, Ananthaswamy HN, Owen-Schaub LB. Fas ligand: A sensor for DNA damage critical in skin cancer etiology. Science. 1999 Aug 6;285(5429):898-900. https://doi.org/10.1126/science.285.5429.898
Hill, Laurie L. ; Ouhtit, Allal ; Loughlin, Susan M. ; Kripke, Margaret L. ; Ananthaswamy, Honnavara N. ; Owen-Schaub, Laurie B. / Fas ligand : A sensor for DNA damage critical in skin cancer etiology. In: Science. 1999 ; Vol. 285, No. 5429. pp. 898-900.
@article{fd1fee823bef407e85b3ef57bab76097,
title = "Fas ligand: A sensor for DNA damage critical in skin cancer etiology",
abstract = "DNA-damaged cells can either repair the DNA or be eliminated through a homeostatic control mechanism termed 'cellular proofreading.' Elimination of DNA-damaged cells after ultraviolet radiation (UVR) through sunburn cell (apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found to be dependent on Fas ligand (FasL), a pro-apoptotic protein induced by DNA damage. Chronic exposure to UVR caused 14 of 20 (70 percent) FasL-deficient mice and 1 of 20 (5 percent) wild-type mice to accumulate p53 mutations in the epidermis. Thus, FasL-mediated apoptosis is important for skin homeostasis, suggesting that the dysregulation of Fas-FasL interactions may be central to the development of skin cancer.",
author = "Hill, {Laurie L.} and Allal Ouhtit and Loughlin, {Susan M.} and Kripke, {Margaret L.} and Ananthaswamy, {Honnavara N.} and Owen-Schaub, {Laurie B.}",
year = "1999",
month = "8",
day = "6",
doi = "10.1126/science.285.5429.898",
language = "English",
volume = "285",
pages = "898--900",
journal = "Science",
issn = "0036-8075",
publisher = "American Association for the Advancement of Science",
number = "5429",

}

TY - JOUR

T1 - Fas ligand

T2 - A sensor for DNA damage critical in skin cancer etiology

AU - Hill, Laurie L.

AU - Ouhtit, Allal

AU - Loughlin, Susan M.

AU - Kripke, Margaret L.

AU - Ananthaswamy, Honnavara N.

AU - Owen-Schaub, Laurie B.

PY - 1999/8/6

Y1 - 1999/8/6

N2 - DNA-damaged cells can either repair the DNA or be eliminated through a homeostatic control mechanism termed 'cellular proofreading.' Elimination of DNA-damaged cells after ultraviolet radiation (UVR) through sunburn cell (apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found to be dependent on Fas ligand (FasL), a pro-apoptotic protein induced by DNA damage. Chronic exposure to UVR caused 14 of 20 (70 percent) FasL-deficient mice and 1 of 20 (5 percent) wild-type mice to accumulate p53 mutations in the epidermis. Thus, FasL-mediated apoptosis is important for skin homeostasis, suggesting that the dysregulation of Fas-FasL interactions may be central to the development of skin cancer.

AB - DNA-damaged cells can either repair the DNA or be eliminated through a homeostatic control mechanism termed 'cellular proofreading.' Elimination of DNA-damaged cells after ultraviolet radiation (UVR) through sunburn cell (apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found to be dependent on Fas ligand (FasL), a pro-apoptotic protein induced by DNA damage. Chronic exposure to UVR caused 14 of 20 (70 percent) FasL-deficient mice and 1 of 20 (5 percent) wild-type mice to accumulate p53 mutations in the epidermis. Thus, FasL-mediated apoptosis is important for skin homeostasis, suggesting that the dysregulation of Fas-FasL interactions may be central to the development of skin cancer.

UR - http://www.scopus.com/inward/record.url?scp=0033529581&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033529581&partnerID=8YFLogxK

U2 - 10.1126/science.285.5429.898

DO - 10.1126/science.285.5429.898

M3 - Article

VL - 285

SP - 898

EP - 900

JO - Science

JF - Science

SN - 0036-8075

IS - 5429

ER -