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A novel ING2 isoform, ING2b, synergizes with ING2a to prevent cell cycle arrest and apoptosis
Author(s) -
Unoki Motoko,
Kumamoto Kensuke,
Robles Ana I.,
Shen Jiang Cheng,
Zheng Zhi-Ming,
Harris Curtis C.
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.10.024
Subject(s) - gene knockdown , gene isoform , apoptosis , cell cycle checkpoint , microbiology and biotechnology , cell growth , cell cycle , exon , biology , chemistry , cancer research , gene , genetics
We identified a novel inhibitor of growth family member 2 (ING2) isoform, ING2b, which shares exon 2 with ING2a, but lacks the N‐terminal p53 binding region. Contrary to ING2a, ING2b's promoter has no p53 binding sites. Consistently, activation of p53 led to suppression of ING2a, leaving ING2b unaffected. Through isoform‐specific targeting, we showed that ING2a knockdown suppressed cell growth only in the presence of p53, ING2b knockdown had no effect on cell growth, and knockdown of both induced cell cycle arrest and apoptosis independently of p53. ING2a and ING2b have compensatory roles that protect cells from cell cycle arrest and apoptosis and may be involved in development of chemotherapeutic resistance.