期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 101, 期 8, 页码 2323-2327出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0308565100
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资金
- NHLBI NIH HHS [R01 HL055426, HL55426] Funding Source: Medline
- NIDA NIH HHS [K05 DA000074, P50 DA000266, DA-00074, DA-000266] Funding Source: Medline
- NIH HHS [NH65090] Funding Source: Medline
- NIMH NIH HHS [R37 MH018501, MH-18501, R01 MH018501] Funding Source: Medline
- NINDS NIH HHS [NS-043850, F32 NS043850] Funding Source: Medline
It has been considered that Ca2+ release is the causal trigger for Ca2+ entry after receptor activation. In DT40 B cells devoid of inositol 1,4,5-trisphosphate receptors (IP3R), the lack of Ca2+ entry in response to receptor activation is attributed to the absence of Ca2+ release. We reveal in this article that IP3R recognition of IP3 determines agonist-induced Ca2+ entry (ACE), independent of its Ca2+ release activity. In DT40 IP3R-/- cells, endogenous ACE can be rescued with type 1 IP3R mutants (both a DeltaC-terminal truncation mutant and a D2550A pore mutant), which are defective in Ca2+ release channel activity. Thus, in response to B cell receptor activation, ACE is restored in an IP3R-dependent manner without Ca2+ store release. Conversely, ACE cannot be rescued with mutant IP(3)Rs lacking IP3 binding (both the Delta90-110 and R265Q IP3-binding site mutants). We conclude that an IP3-dependent conformational change in the IP3R, not endoplasmic reticulum Ca2+ pool release, triggers ACE.
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