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

Volumn 99, Issue 12, 2002, Pages 8430-8435

A glutamate residue at the C terminus regulates activity of inward rectifier K+ channels: Implication for Andersen's syndrome

(8) Chen, Lei a,c Kawano, Takeharu a,b Bajic, Sibinka a Kaziro, Yoshito b Itoh, Hiroshi b,d Art, Jonathan J a Nakajima, Yasuko a Nakajima, Shigehiro a,e

a UNIVERSITY OF ILLINOIS AT CHICAGO (United States)

b TOKYO INSTITUTE OF TECHNOLOGY (Japan)

c College of Physicians and Surgeons ^* (United States)

d NARA INSTITUTE OF SCIENCE AND TECHNOLOGY (Japan)

e UNIVERSITY OF ILLINOIS (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ALANINE; ASPARTIC ACID; COMPLEMENTARY DNA; GLUTAMIC ACID; ION CHANNEL; POTASSIUM CHANNEL; POTASSIUM ION;

AMINO ACID SUBSTITUTION; ANDERSEN SYNDROME; ARTICLE; CELL CULTURE; EMBRYO; GENE MUTATION; HEART ARRHYTHMIA; HUMAN; HUMAN CELL; IMMUNOCYTOCHEMISTRY; KIDNEY CELL; MEMBRANE ELECTROPHYSIOLOGY; PERIODIC PARALYSIS; PRIORITY JOURNAL; SYNDROME DELINEATION;

AMINO ACID SEQUENCE; AMINO ACID SUBSTITUTION; CELL LINE; G PROTEIN-COUPLED INWARDLY-RECTIFYING POTASSIUM CHANNELS; GLUTAMIC ACID; HUMANS; ION CHANNEL GATING; LONG QT SYNDROME; MOLECULAR SEQUENCE DATA; MUTAGENESIS, SITE-DIRECTED; PARALYSES, FAMILIAL PERIODIC; POTASSIUM CHANNELS; POTASSIUM CHANNELS, INWARDLY RECTIFYING; RECOMBINANT PROTEINS; TRANSFECTION;

EID: 0037062467 PISSN: 00278424 EISSN: None Source Type: Journal
DOI: 10.1073/pnas.122682899 Document Type: Article

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