Signaling Differences from the A and B Isoforms of the Insulin Receptor (IR) in 32D Cells in the Presence or Absence of IR Substrate-1 | Zendy

Laura Sciacca | Zendy; Marco di Prisco | Zendy; Anguo Wu | Zendy; Antonino Belfiore | Zendy; Riccardo Vigneri | Zendy; Renato Baserga | Zendy

Open Access

Signaling Differences from the A and B Isoforms of the Insulin Receptor (IR) in 32D Cells in the Presence or Absence of IR Substrate-1

Author(s) -

Laura Sciacca,

Marco di Prisco,

Anguo Wu,

Antonino Belfiore,

Riccardo Vigneri,

Renato Baserga

Publication year - 2003

Publication title -

endocrinology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.674

H-Index - 257

eISSN - 1945-7170

pISSN - 0013-7227

DOI - 10.1210/en.2002-0136

Subject(s) - gene isoform , insulin receptor , receptor , haematopoiesis , biology , medicine , endocrinology , insulin , insulin receptor substrate , microbiology and biotechnology , signal transduction , cellular differentiation , cell culture , stem cell , biochemistry , gene , genetics , insulin resistance

The A isoform of the insulin receptor (IR) is frequently overexpressed in cancer cells and is activated by IGF-II as well as by insulin, whereas the B isoform is predominant in differentiated tissues and responds poorly to IGF-II. The IR substrate-1 (IRS-1), a docking protein for the IR, is known to send a mitogenic signal and to be a powerful inhibitor of cell differentiation. We have investigated the biological effects of the two IR isoforms in parental 32D hemopoietic cells, which do not express IRS-1, and in 32D-derived cells in which IRS-1 is ectopically expressed. The effects of the two isoforms on cell survival, differentiation markers and nuclear translocation of IRS-1 were compared. The results confirm that the A isoform responds to IGF-II and preferentially sends mitogenic, antiapoptotic signals, whereas the B form, poorly responsive to IGF-II, tends to send differentiation signals.

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