Lymphocyte apoptosis: Mediation by increased type 3 inositol 1,4,5- trisphosphate receptor

Adil A. Khan, Mark J. Soloski, Alan H. Sharp, Gabriele Schilling, David M. Sabatini, Shi Hua Li, Christopher A. Ross, Solomon H. Snyder

Research output: Contribution to journalArticle

Abstract

B and T lymphocytes undergoing apoptosis in response to anti- immunoglobulin M antibodies and dexamethasone, respectively, were found to have increased amounts of messenger RNA for the inositol 1,4,5-trisphosphate receptor (IP3R) and increased amounts of IP3R protein. Immunohistochemical analysis revealed that the augmented receptor population was localized to the plasma membrane. Type 3 IP3R (IP3R3) was selectively increased during apoptosis, with no enhancement of type 1 IP3R (IP3R1). Expression of IP3R3 antisense constructs in S49 T cells blocked dexamethasone-induced apoptosis, whereas IP3R3 sense, IP3R1 sense, or IP3R1 antisense control constructs did not block cell death. Thus, the increases in IP3R3 may be causally related to apoptosis.

Original languageEnglish (US)
Pages (from-to)503-507
Number of pages5
JournalScience
Volume273
Issue number5274
DOIs
StatePublished - Jul 26 1996

    Fingerprint

ASJC Scopus subject areas

  • General

Cite this