NDLI: Morphogenesis of the telencephalic commissure requires scaffold protein JNK-interacting protein 3 (JIP3).

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Morphogenesis of the telencephalic commissure requires scaffold protein JNK-interacting protein 3 (JIP3).

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Barrett, Tamera Davis, Roger J. Delmotte, Marie-helene Flavell, Richard A. Weston, Claire R. Kelkar, Nyaya Sheppard, Barbara J.
Description	Author Affiliation: Kelkar N ( Howard Hughes Medical Institute and Program in Molecular Medicine, University of Massachusetts Medical School, 373 Plantation Street, Worcester, MA 01605, USA.);
Abstract	The murine JNK-interacting protein 3 (JIP3) protein (also known as JSAP1) is expressed exclusively in neurons and has been identified as a scaffold protein for the c-Jun NH2-terminal kinase (JNK) signaling pathway and as an adapter protein for cargo transport by the microtubule motor protein kinesin. To investigate the physiological function of JIP3, we examined the effect of Jip3 gene disruption in mice. The Jip3-/- mice were unable to breathe and died shortly after birth. Microscopic analysis demonstrated that Jip3 gene disruption causes severe defects in the morphogenesis of the telencephalon. Jip3-/- mice lack the telencephalic commissure, a major connection between the left and right hemispheres of the brain. The central nervous system abnormalities of Jip3-/- mice may be accounted for in part by a reduction in signal transduction by RhoA and its effector ROCK.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	17
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Adaptor Proteins, Signal Transducing Nerve Tissue Proteins Physiology Telencephalon Embryology Vesicular Transport Proteins Animals Gene Expression Regulation, Developmental Gene Targeting JNK Mitogen-Activated Protein Kinases Mice Mice, Inbred C57BL Mice, Knockout Mitogen-Activated Protein Kinases Metabolism Munc18 Proteins Deficiency Genetics Proteins Signal Transduction Abnormalities RhoA GTP-Binding Protein Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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