NDLI: Minimal requirements for calcium oscillations driven by the IP3 receptor.

Content Provider	PubMed Central
Author	Hajnóczky, G. Thomas, A. P.
Abstract	Hormones and neurotransmitters that act through inositol 1,4,5-trisphosphate (IP3) can induce oscillations of cytosolic Ca2+ ([Ca2+]c), which render dynamic regulation of intracellular targets. Imaging of fluorescent Ca2+ indicators located within intracellular Ca2+ stores was used to monitor IP3 receptor channel (IP3R) function and to demonstrate that IP3-dependent oscillations of Ca2+ release and re-uptake can be reproduced in single permeabilized hepatocytes. This system was used to define the minimum essential components of the oscillation mechanism. With IP3 clamped at a submaximal concentration, coordinated cycles of IP3R activation and subsequent inactivation were observed in each cell. Cycling between these states was dependent on feedback effects of released Ca2+ and the ensuing [Ca2+]c increase, but did not require Ca2+ re-accumulation. [Ca2+]c can act at distinct stimulatory and inhibitory sites on the IP3R, but whereas the Ca2+ release phase was driven by a Ca2+-induced increase in IP3 sensitivity, Ca2+ release could be terminated by intrinsic inactivation after IP3 bound to the Ca2+-sensitized IP3R without occupation of the inhibitory Ca2+-binding site. These findings were confirmed using Sr2+, which only interacts with the stimulatory site. Moreover, vasopressin induced Sr2+ oscillations in intact cells in which intracellular Ca2+ was completely replaced with Sr2+. Thus, [Ca2+]c oscillations can be driven by a coupled process of Ca2+-induced activation and obligatory intrinsic inactivation of the Ca2+-sensitized state of the IP3R, without a requirement for occupation of the inhibitory Ca2+-binding site.
Related Links	http://dx.doi.org/10.1093/emboj/16.12.3533
Ending Page	3543
Page Count	11
Starting Page	3533
File Format	PDF
ISSN	14602075
e-ISSN	14602075
Journal	The EMBO Journal
Issue Number	12
Volume Number	16
Language	English
Publisher Date	1997-06-15
Access Restriction	Open
Subject Keyword	Biochemistry, Genetics and Molecular Biology(all) Immunology and Microbiology(all) Neuroscience(all) Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology and Microbiology Medicine Molecular Biology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

BANK regulates BCR-induced calcium mobilization by promoting tyrosine phosphorylation of IP3 receptor

Encoding of Ca2+ signals by differential expression of IP3 receptor subtypes.

NAADP induces Ca2+ oscillations via a two-pool mechanism by priming IP3- and cADPR-sensitive Ca2+ stores

Ca2+-sensor region of IP3 receptor controls intracellular Ca2+ signaling

Apoptosis driven by IP(3)-linked mitochondrial calcium signals.

Distinct requirements for chromatin assembly in transcriptional repression by thyroid hormone receptor and histone deacetylase.

Receptor-oriented intercellular calcium waves evoked by vasopressin in rat hepatocytes.

Identification of a Ras GTPase-activating protein regulated by receptor-mediated Ca2+ oscillations

Contrasting requirements for ubiquitylation during Fc receptor-mediated endocytosis and phagocytosis

Minimal requirements for calcium oscillations driven by the IP3 receptor.

Similar Documents

BANK regulates BCR-induced calcium mobilization by promoting tyrosine phosphorylation of IP3 receptor

Encoding of Ca2+ signals by differential expression of IP3 receptor subtypes.

NAADP induces Ca2+ oscillations via a two-pool mechanism by priming IP3- and cADPR-sensitive Ca2+ stores

Ca2+-sensor region of IP3 receptor controls intracellular Ca2+ signaling

Apoptosis driven by IP(3)-linked mitochondrial calcium signals.

Distinct requirements for chromatin assembly in transcriptional repression by thyroid hormone receptor and histone deacetylase.

Receptor-oriented intercellular calcium waves evoked by vasopressin in rat hepatocytes.

Identification of a Ras GTPase-activating protein regulated by receptor-mediated Ca2+ oscillations

Contrasting requirements for ubiquitylation during Fc receptor-mediated endocytosis and phagocytosis

Minimal requirements for calcium oscillations driven by the IP3 receptor.