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PMID:12372285
Citation |
Sasaki, Y, Cheng, C, Uchida, Y, Nakajima, O, Ohshima, T, Yagi, T, Taniguchi, M, Nakayama, T, Kishida, R, Kudo, Y, Ohno, S, Nakamura, F and Goshima, Y (2002) Fyn and Cdk5 mediate semaphorin-3A signaling, which is involved in regulation of dendrite orientation in cerebral cortex. Neuron 35:907-20 |
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Abstract |
Semaphorin-3A (Sema3A), a member of class 3 semaphorins, regulates axon and dendrite guidance in the nervous system. How Sema3A and its receptors plexin-As and neuropilins regulate neuronal guidance is unknown. We observed that in fyn- and cdk5-deficient mice, Sema3A-induced growth cone collapse responses were attenuated compared to their heterologous controls. Cdk5 is associated with plexin-A2 through the active state of Fyn. Sema3A promotes Cdk5 activity through phosphorylation of Tyr15, a phosphorylation site with Fyn. A Cdk5 mutant (Tyr15 to Ala) shows a dominant-negative effect on the Sema3A-induced collapse response. The sema3A gene shows strong interaction with fyn for apical dendrite guidance in the cerebral cortex. We propose a signal transduction pathway in which Fyn and Cdk5 mediate neuronal guidance regulated by Sema3A. |
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Keywords |
Animals; COS Cells; Cerebral Cortex/drug effects; Cerebral Cortex/physiology; Chick Embryo; Cyclin-Dependent Kinase 5; Cyclin-Dependent Kinases/deficiency; Cyclin-Dependent Kinases/genetics; Cyclin-Dependent Kinases/physiology; Dendrites/drug effects; Dendrites/physiology; Enzyme Inhibitors/pharmacology; Glycoproteins/physiology; Growth Cones/drug effects; Growth Cones/physiology; Humans; Mice; Mice, Mutant Strains; Proto-Oncogene Proteins/deficiency; Proto-Oncogene Proteins/genetics; Proto-Oncogene Proteins/physiology; Proto-Oncogene Proteins c-fyn; Semaphorin-3A; Signal Transduction/drug effects; Signal Transduction/physiology |
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Significance
Annotations
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