Chromosome 22 complements apoptosis in Fas- and TNF-resistant mutant UK110 cells

Kohji Noguchi, Mikihiko Naito, Hiroyuki Kugoh, Mitsuo Oshimura, Tetsuo Mashima, Naoya Fujita, Shin Yonehara, Takashi Tsuruo

Research output: Contribution to journalArticlepeer-review

20 Citations (Scopus)


Fas and p55 tumor necrosis factor receptor (TNFR) transfer an apoptosis signal when they are crosslinked with their ligands or agonistic antibodies. However, the signal transduction mechanism of apoptosis via Fas and p55 TNFR has not yet been elucidated. We previously described a recessive mutant UK110 from the human monocytic leukemia U937 cell line, that showed resistance against Fas- and p55 TNFR-mediated apoptosis. By cytogenetic analysis and microcell-fusion method, we demonstrate here that introduction of chromosome 22 can specifically restore the sensitivity to Fas- and TNF-mediated apoptosis in UK110 cells. Moreover, introduction of chromosome 22 into UK110 can complement the processing of interleukin-1 β converting enzyme (ICE)-like proteases, such as CPP32/Yama/Apopain and ICH-1L, after treatment with anti-Fas and anti-p55 TNFR antibodies. These results suggest that the product of a gene located on chromosome 22 participates in the Fas-and p55 TNFR-mediated apoptosis at a point upstream of ICE-like proteases.

Original languageEnglish
Pages (from-to)39-46
Number of pages8
Issue number1
Publication statusPublished - 1996 Aug 10


  • Apoptosis
  • Chromosome 22
  • Fas
  • Microcell-fusion
  • TNF

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research


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