Ca2+-induced inhibition of the cardiac Ca2+ channel depends on calmodulin

Proceedings of the National Academy of Sciences of the United States of America

Volumn 96, Issue 5, 1999, Pages 2435-2438

  Qin, Ning ^a   Olcese, Riccardo ^a   Bransby, Michael ^a   Lin, Tony ^a   Birnbaumer, Lutz ^a,b  

^a UNIVERSITY OF CALIFORNIA   (United States)

^b UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

EF hand; Heart; IQ motif

Indexed keywords

AGAROSE; BUFFER; CALCIUM CHANNEL; CALCIUM ION; CALMODULIN; EGTAZIC ACID; GLUTATHIONE TRANSFERASE; HYBRID PROTEIN; CALCIUM; RECOMBINANT PROTEIN;

ANIMAL CELL; ARTICLE; BINDING SITE; CALCIUM CELL LEVEL; CARBOXY TERMINAL SEQUENCE; CONTROLLED STUDY; HEART; NONHUMAN; OOCYTE; PRIORITY JOURNAL; PROTEIN PROTEIN INTERACTION; SITE DIRECTED MUTAGENESIS; XENOPUS; AMINO ACID SEQUENCE; ANIMAL; BIOSYNTHESIS; CELL MEMBRANE POTENTIAL; CHEMISTRY; FEMALE; GENETICS; METABOLISM; PHYSIOLOGY; PROTEIN CONFORMATION; XENOPUS LAEVIS;

ANIMALIA;

AMINO ACID SEQUENCE; ANIMALS; BINDING SITES; CALCIUM; CALCIUM CHANNELS; CALMODULIN; FEMALE; GLUTATHIONE TRANSFERASE; HEART; MEMBRANE POTENTIALS; MUTAGENESIS, SITE-DIRECTED; OOCYTES; PROTEIN CONFORMATION; RECOMBINANT FUSION PROTEINS; RECOMBINANT PROTEINS; XENOPUS LAEVIS;

EID: 0033514514     PISSN: 00278424     EISSN: None     Source Type: Journal    
DOI: 10.1073/pnas.96.5.2435     Document Type: Article

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