Monitor and Molecules

Drug Discovery Today

Volumn 6, Issue 20, 2001, Pages 1072-1073

  Gurwitz, David ^a   Eldar Finkelman, Hagit ^a  

^a TEL AVIV UNIVERSITY   (Israel)

Author keywords

[No Author keywords available]

Indexed keywords

2 (2,4 DICHLOROPHENYL) 3 (1 METHYL 3 INDOLYL)MALEIMIDE; 2 (3 CHLORO 4 HYDROXYANILINO) 3 (2 NITROPHENYL)MALEIMIDE; GLYCOGEN SYNTHASE KINASE 3; PROTEIN KINASE; PROTEIN KINASE INHIBITOR; UNCLASSIFIED DRUG;

DEGENERATIVE DISEASE; DRUG DEVELOPMENT; GENE OVEREXPRESSION; HUMAN; NERVE DEGENERATION; PROTEIN PHOSPHORYLATION; SHORT SURVEY; STROKE;

EID: 0035888331     PISSN: 13596446     EISSN: None     Source Type: Journal    
DOI: 10.1016/s1359-6446(01)02018-9     Document Type: Short Survey

References (12)

1. Signal transduction: signaling specificity - a complex affair
2. Phosphorylation of insulin receptor substrate 1 by glycogen synthase kinase 3 impairs insulin action
3. A molecular mechanism for the effect of lithium on development
4. Crystal structure of glycogen synthase kinase 3β: structural basis for phosphate-primed substrate specificity and autoinhibition
5. Structure of GSK3β reveals a primed phosphorylation mechanism
6. Anti-mitotic properties of indirubin-3′-monoxime, a CDK/GSK-3 inhibitor: induction of endoreplication following prophase arrest
7. Indirubin, the active constituent of a Chinese antileukaemia medicine, inhibits cyclin-dependent kinases
8. Selective small-molecule inhibitors of glycogen synthase kinase-3 activity protect primary neurones from death
9. Insulin rescues retinal neurons from apoptosis by a PI-3 kinase/Akt-mediated mechanism that reduces the activation of caspase-3
10. Glycogen synthase kinase-3β facilitates staurosporine- and heat-shock-induced apoptosis. Protection by lithium
11. Decreased nuclear β-catenin, tau hyperphosphorylation and neurodegeneration in GSK-3β conditional transgenic mice