Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.4.4 (kinesin)
 5,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mutations in the X-linked gene DCX result in lissencephaly in males, and abnormal neuronal positioning in females, suggesting a role for this gene product during neuronal migration. In spite of several known protein interactions, the involvement of DCX in a signaling pathway is still elusive. Here we demonstrate that DCX is a substrate of JNK and interacts with both c-Jun N-terminal kinase (JNK) and JNK interacting protein (JIP). The localization of this signaling module in the developing brain suggests its functionality in migrating neurons. The localization of DCX at neurite tips is determined by its interaction with JIP and by the interaction of the latter with kinesin. DCX is phosphorylated by JNK in growth cones. DCX mutated in sites phosphorylated by JNK affected neurite outgrowth, and the velocity and relative pause time of migrating neurons. We hypothesize that during neuronal migration, there is a need to regulate molecular motors that are working in the cell in opposite directions: kinesin (a plus-end directed molecular motor) versus dynein (a minus-end directed molecular motor).
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PMID:DCX, a new mediator of the JNK pathway. 1476 23

Molecular motors employ specific adaptor proteins to dock on transport cargos. Reporting in The Journal of Cell Biology, Fu and Holzbaur (2013) show that the adaptor JNK interacting protein 1 (JIP1) binds kinesin-1 and dynactin and controls bidirectional axonal amyloid precursor protein trafficking, suggesting a regulatory role for adaptors during cargo transport.
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PMID:Slide to the left and slide to the right: motor coordination in neurons. 2389 89