한빛사논문
- 조회5,081
Abstract
Eun-Mi Hur1,2, Yong-Soo Park1,2, Yang Hoon Huh3,4, Seung Hyun Yoo3,4, Kyung-Chul Woo1,2, Bo-Hwa Choi1,2, and Kyong-Tai Kim1,2
1 National Research Laboratory of Molecular Neurophysiology, Pohang University of Science and Technology, Hyo-ja dong, San31, Pohang, 790-784, South Korea
2 Department of Life Science, Pohang University of Science and Technology, Hyo-ja dong, San31, Pohang, 790-784, South Korea
3 National Creative Research Initiative Center for Secretory Granule Research, Inha University College of Medicine, Jung Gu, Incheon 400-712, South Korea
4 Department of Biochemistry, Inha University College of Medicine, Jung Gu, Incheon 400-712, South Korea
Correspondence to Kyong-Tai Kim
Ca2+ is a highly versatile intracellular signal that regulates many different cellular processes, and cells have developed mechanisms to have exquisite control over Ca2+ signaling. Epidermal growth factor (EGF), which fails to mobilize intracellular Ca2+ when administrated alone, becomes capable of evoking [Ca2+]i increase and exocytosis after bradykinin (BK) stimulation in chromaffin cells. Here, we provide evidence that this sensitization process is coordinated by a macromolecular signaling complex comprised of inositol 1,4,5-trisphosphate receptor type I (IP3R1), cAMP-dependent protein kinase (PKA), EGF receptor (EGFR), and an A-kinase anchoring protein, yotiao. The IP3R complex functions as a focal point to promote Ca2+ release in two ways: (1) it facilitates PKA-dependent phosphorylation of IP3R1 in response to BK-induced elevation of cAMP, and (2) it couples the plasmalemmal EGFR with IP3R1 at the Ca2+ store located juxtaposed to the plasma membrane. Our study illustrates how the junctional membrane IP3R complex connects different signaling pathways to define the fidelity and specificity of Ca2+ signaling.
논문정보
- Research article
- 2005년 05월 (BRIC 등록일 )
- 국내 연구진
- 생명과학 > 세포생물학
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