Overexpression of the Fanconi anemia group C gene (FAC) protects hematopoietic progenitors from death induced by Fas-mediated apoptosis

Jianxiang Wang, Tetsuya Otsuki, Hagop Youssoufian, Jerome Lo Ten Foe, Sonnie Kim, Marcel Devetten, Jianmei Yu, Youlin Li, Daniel Dunn, Johnson M. Liu

Research output: Contribution to journalArticle

43 Scopus citations

Abstract

Fanconi anemia is a rare, inherited disorder characterized by bone marrow failure, congenital malformations, and cancer susceptibility. The group C Fanconi anemia gene, FAC, identified by expression cloning methods, encodes a protein of unknown function that may be involved in the response to apoptotic stimuli. Hematopoietic progenitor cells from Fac knock-out mice are hypersensitive to IFN-γ, a molecule that can induce apoptosis through up- regulation of the Fas death receptor. In this study, we used FAC- overexpressing transgenic mice to examine the relationship between FAC and Fas-triggered cell death. Hematopoietic progenitors from FAC-transgenic mice were up to 10-fold less sensitive to the cytolytic effect of Fas-ligation. Our experiments implicate FAC in the regulation of apoptosis mediated by the Fas death receptor.

Original languageEnglish (US)
Pages (from-to)3538-3541
Number of pages4
JournalCancer Research
Volume58
Issue number16
StatePublished - Aug 15 1998

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Fingerprint Dive into the research topics of 'Overexpression of the Fanconi anemia group C gene (FAC) protects hematopoietic progenitors from death induced by Fas-mediated apoptosis'. Together they form a unique fingerprint.

  • Cite this

    Wang, J., Otsuki, T., Youssoufian, H., Lo Ten Foe, J., Kim, S., Devetten, M., Yu, J., Li, Y., Dunn, D., & Liu, J. M. (1998). Overexpression of the Fanconi anemia group C gene (FAC) protects hematopoietic progenitors from death induced by Fas-mediated apoptosis. Cancer Research, 58(16), 3538-3541.