Ca2+/CaM controls Ca2+-dependent inactivation of NMDA receptors by dimerizing the NR1 C termini

Journal of Neuroscience

Volumn 28, Issue 8, 2008, Pages 1865-1870

  Wang, Chaojian ^a   Wang, Hong Gang ^a   Xie, Hui ^b   Pitt, Geoffrey S ^a,c  

^a DUKE UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b Och Spine at New York Presbyterian Hospitals   (United States)

^c DUKE UNIVERSITY   (United States)

Author keywords

Calcium; Calmodulin; Channel; Glutamate; Inactivation; NMDA receptors

Indexed keywords

ALPHA ACTININ; ALPHA ACTININ 2; CALMODULIN; EGTAZIC ACID; N METHYL DEXTRO ASPARTIC ACID RECEPTOR; N METHYL DEXTRO ASPARTIC ACID RECEPTOR 1; UNCLASSIFIED DRUG; CALCIUM; NR1 NMDA RECEPTOR;

ARTICLE; CALCIUM TRANSPORT; CARBOXY TERMINAL SEQUENCE; CONTROLLED STUDY; DIMERIZATION; EXCITOTOXICITY; GENE MUTATION; HUMAN; HUMAN CELL; IMMUNOBLOTTING; PRIORITY JOURNAL; PROTEIN DOMAIN; PROTEIN EXPRESSION; BINDING SITE; CELL LINE; CHEMISTRY; COMPARATIVE STUDY; DRUG ANTAGONISM; METABOLISM; PHYSIOLOGY;

BINDING SITES; CALCIUM; CALMODULIN; CELL LINE; DIMERIZATION; HUMANS; RECEPTORS, N-METHYL-D-ASPARTATE;

EID: 39749151626     PISSN: 02706474     EISSN: 02706474     Source Type: Journal    
DOI: 10.1523/JNEUROSCI.5417-07.2008     Document Type: Article

References (21)