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)

p120 catenin (p120) is a component of adherens junctions and has been implicated in regulating cadherin-based cell adhesion as well as the activity of Rho small GTPases, but its exact roles in cell-cell adhesion are unclear. Using time-lapse imaging, we show that p120-GFP associates with vesicles and exhibits unidirectional movements along microtubules. Furthermore, p120 forms a complex with kinesin heavy chain through the p120 NH2-terminal head domain. Overexpression of p120, but not an NH2-terminal deletion mutant deficient in kinesin binding, recruits endogenous kinesin to N-cadherin. Disruption of the interaction between N-cadherin and p120, or the interaction between p120 and kinesin, leads to a delayed accumulation of N-cadherin at cell-cell contacts during calcium-initiated junction reassembly. Our analyses identify a novel role of p120 in promoting cell surface trafficking of cadherins via association and recruitment of kinesin.
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PMID:p120 catenin associates with kinesin and facilitates the transport of cadherin-catenin complexes to intercellular junctions. 1461 49

P0071 (plakophilin-4) is a member of the p120ctn subfamily of armadillo proteins that are essential for cell contact formation. Additionally, p0071 plays a role in cytokinesis, in which it regulates local activation of RhoA together with Ect2. Because spatiotemporal regulation is required for progression through cytokinesis, we analyzed when and how p0071 is targeted to the midbody to induce RhoA activation. We show that Ect2 precedes p0071 accumulation at the midbody and that targeting is mediated by different motor proteins. p0071 interacted with the kinesin-II family member KIF3b, and knockdown of KIF3b interfered with p0071 midbody recruitment whereas Ect2 or RhoA localization was not affected in these cells. Moreover, knockdown of KIF3b induced a similar phenotype as the p0071 knockdown, with reduced actin and phospho-myosin-light-chain accumulation at the midbody and decreased levels of active RhoA during cytokinesis. The lack of RhoA activation in KIF3b-deficient cells was not rescued by overexpression of wild-type p0071 but was substantially ameliorated by a p0071-MKLP1-motor-domain fusion protein that was targeted to the furrow independently of KIF3. These data indicate that p0071 and Ect2 are transported via distinct motors and identify a novel pathway implicating KIF3 in the regulation of actin organization during cytokinesis.
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PMID:Targeting of p0071 to the midbody depends on KIF3. 1933 49