TY - JOUR
T1 - Lymphocyte apoptosis
T2 - Mediation by increased type 3 inositol 1,4,5- trisphosphate receptor
AU - Khan, Adil A.
AU - Soloski, Mark J.
AU - Sharp, Alan H.
AU - Schilling, Gabriele
AU - Sabatini, David M.
AU - Li, Shi Hua
AU - Ross, Christopher A.
AU - Snyder, Solomon H.
PY - 1996/7/26
Y1 - 1996/7/26
N2 - 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.
AB - 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.
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U2 - 10.1126/science.273.5274.503
DO - 10.1126/science.273.5274.503
M3 - Article
C2 - 8662540
AN - SCOPUS:0029824312
SN - 0036-8075
VL - 273
SP - 503
EP - 507
JO - Science
JF - Science
IS - 5274
ER -