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

被引:235
作者
Khan, AA
Soloski, MJ
Sharp, AH
Schilling, G
Sabatini, DM
Li, SH
Ross, CA
Snyder, SH
机构
[1] JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205
[2] JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205
[3] JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT,BALTIMORE,MD 21205
[4] JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL & MOL SCI,BALTIMORE,MD 21205
关键词
D O I
10.1126/science.273.5274.503
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 (IP(3)R) and increased amounts of IP(3)R protein. Immunohistochemical analysis revealed that the augmented receptor population was localized to the plasma membrane. Type 3 IP(3)R (IP(3)R3) was selectively increased during apoptosis, with no enhancement of type 1 IP(3)R (IP(3)R1). Expression of IP(3)R3 antisense constructs in S49 T cells blocked dexamethasone-induced apoptosis, whereas IP(3)R3 sense, IP(3)R1 sense, or IP(3)R1 antisense control constructs did not block cell death. Thus, the increases in IP(3)R3 may be causally related to apoptosis.
引用
收藏
页码:503 / 507
页数:5
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