Loss of S100A1 expression leads to Ca2+ release potentiation in mutant mice with disrupted CaM and S100A1 binding to CaMBD2 of RyR1-Reference-Cited by-同舟云学术

Loss of S100A1 expression leads to Ca2+ release potentiation in mutant mice with disrupted CaM and S100A1 binding to CaMBD2 of RyR1

Published:2018-08 Issue:15 Volume:6 Page:e13822
ISSN:2051-817X
Container-title:Physiological Reports
language:en
Short-container-title:Physiol Rep

Author:

Hernández-Ochoa Erick O.¹^ORCID,Melville Zephan¹,Vanegas Camilo¹,Varney Kristen M.¹²,Wilder Paul T.¹²,Melzer Werner³,Weber David J.¹²,Schneider Martin F.¹

Affiliation:

1. Department of Biochemistry and Molecular Biology; University of Maryland School of Medicine; Baltimore Maryland

2. Center for Biomolecular Therapeutics (CBT); University of Maryland School of Medicine; Maryland

3. Institute of Applied Physiology; Ulm University; Ulm Germany

Funder

National Institutes of Health

Deutsche Forschungsgemeinschaft

Interdisciplinary Training Program in Muscle Biology

Publisher

Wiley

Subject

Physiology (medical),Physiology

Link

http://onlinelibrary.wiley.com/wol1/doi/10.14814/phy2.13822/fullpdf

Reference84 articles.

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3. 1H, 13C and 15N NMR sequence-specific resonance assignments for rat apo-S100A1(alpha alpha);Baldisseri;J. Biomol. NMR,1999

4. Calmodulin binding and inhibition of cardiac muscle calcium release channel (ryanodine receptor);Balshaw;J. Biol. Chem.,2001

5. Modulation of intracellular calcium-release channels by calmodulin;Balshaw;J. Membr. Biol.,2002

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