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)

Intracellular transport mediated by kinesin superfamily proteins (KIFs) is a highly regulated process. The molecular mechanism of KIFs binding to their respective cargoes remains unclear. We report that KIF13A is a novel plus end-directed microtubule-dependent motor protein and associates with beta 1-adaptin, a subunit of the AP-1 adaptor complex. The cargo vesicles of KIF13A contained AP-1 and mannnose-6-phosphate receptor (M6PR). Overexpression of KIF13A resulted in mislocalization of the AP-1 and the M6PR. Functional blockade of KIF13A reduced cell surface expression of the M6PR. Thus, KIF13A transports M6PR-containing vesicles and targets the M6PR from TGN to the plasma membrane via direct interaction with the AP-1 adaptor complex.
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PMID:A novel motor, KIF13A, transports mannose-6-phosphate receptor to plasma membrane through direct interaction with AP-1 complex. 1110 27

Post-Golgi carriers of various newly synthesized axonal membrane proteins, which possess kinesin (KIF5)-driven highly processive motility, were transported from the TGN directly to axons. We found that KIF5 has a preference to the microtubules in the initial segment of axon. Low dose paclitaxel treatment caused missorting of KIF5, as well as axonal membrane proteins to the tips of dendrites. Microtubules in the initial segment of axons showed a remarkably high affinity to EB1-YFP, which was known to bind the tips of growing microtubules. These findings revealed unique features of the microtubule cytoskeletons in the initial segment, and suggested that they provide directional information for polarized axonal transport.
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PMID:Microtubules provide directional cues for polarized axonal transport through interaction with kinesin motor head. 1297 48

Different types of endosomal vesicles show distinct distribution patterns within cells. While early endosomes can be found throughout the cell, recycling endosomal vesicles and tubules tend to cluster near the microtubule organizing center in the perinuclear region in most cell types. The molecular mechanisms underlying the steady-state distribution and dynamics of various types of endosomal vesicles has long remained enigmatic. However, during the past decade it has become evident that microtubule-based motor proteins of the kinesin family play a pivotal role in the positioning of endosomes. Early endosomes were shown to cluster in the perinuclear area in the absence of KIF16B,1 KIF3A is required for the steady-state distribution of late endosomes/lysosomes,2 and KIF13A directs M6PR-containing vesicles from the TGN to the plasma membrane3 to name only a few examples. In the case of Tf-containing recycling endosomes antibody-injection experiments implicated kinesin-1, a heteromer comprised of KIF5 heavy and KLC light chains, as a motor for their transport towards the cell periphery.4 Indeed, KIF5B knockdown experiments confirmed that kinesin-1 is necessary to maintain the peripheral pool of recycling endosomes.5 But how is kinesin-1 linked to endosomal vesicles? Work from our own laboratory has identified the AP-1-binding protein Gadkin as a molecular link between AP-1-mediated traffic and kinesin-1-based transport along microtubules.5 This work as well as hypothetical models for kinesin-dependent endosomal membrane traffic will be discussed here.
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PMID:Gadkin: A novel link between endosomal vesicles and microtubule tracks. 2079 11