Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.22 (cdc2)
 8,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of microtubule-associated proteins (MAPs) in growth cones has been analyzed by isolation of these structures and characterization of their proteins by immunofluorescence studies. Two major MAPs, MAP1B and tau, were present in growth cones of cerebellum neurons isolated from 5-day-old rats. Both MAPs could be modified by proline-dependent protein kinases (PDPK) with opposite effects. PDPK-modified MAP1B isoforms are present at the growth cones whereas PDPK-modified tau isoforms are absent. This result suggests a different role for each phosphoMAP. To look for a possible PDPK involved in the modification of MAP1B at the growth cone, the localization of MAP and cdc2 kinases was studied. Our results indicate that the distribution in neuronal cells of MAP kinase is compatible with a possible role of this protein in modifying MAP1B.
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PMID:Characterization of microtubule-associated protein phosphoisoforms present in isolated growth cones. 857 92

Cultures of cerebellar macroneurons were used to study the pattern of expression, subcellular localization, and function of the neuronal cdk5 activator p35 during laminin-enhanced axonal growth. The results obtained indicate that laminin, an extracellular matrix molecule capable of selectively stimulating axonal extension and promoting MAP1B phosphorylation at a proline-directed protein kinase epitope, selectively stimulates p35 expression, increases its association with the subcortical cytoskeleton, and accelerates its redistribution to the axonal growth cones. Besides, suppression of p35, but not of a highly related isoform designated as p39, by antisense oligonucleotide treatment selectively reduces cdk5 activity, laminin-enhanced axonal elongation, and MAP1b phosphorylation. Taken collectively, the present results suggest that cdk5/p35 may serve as an important regulatory linker between environmental signals (e.g., laminin) and constituents of the intracellular machinery (e.g., MAP1B) involved in axonal elongation.
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PMID:Evidence for the participation of the neuron-specific CDK5 activator P35 during laminin-enhanced axonal growth. 982 44

The signaling cascades governing neuronal migration are believed to link extracellular signals to cytoskeletal components. MAP1B is a neuron-specific microtubule-associated protein implicated in the control of the dynamic stability of microtubules and in the cross-talk between microtubules and actin filaments. Here we show that Reelin can induce mode I MAP1B phosphorylation, both in vivo and in vitro, through gsk3 and cdk5 activation. Additionally, mDab1 participates in the signaling cascade responsible for mode I MAP1B phosphorylation. Conversely, MAP1B-deficient mice display an abnormal structuring of the nervous system, especially in brain laminated areas, indicating a failure in neuronal migration. Therefore, we propose that Reelin can induce post-translational modifications on MAP1B that could correlate with its function in neuronal migration.
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PMID:A role of MAP1B in Reelin-dependent neuronal migration. 1559 Sep 13

Cyclin-dependent kinase 5 (Cdk5) functions in postmitotic neuronal cells and play roles in cell differentiation, cell migration, axonal guidance, and synaptic function. Here, we demonstrate that Drosophila cdk5 is dispensable for adult viability and fertility, a feature that allows us to study its physiological function in the whole animal model. For the adult, cdk5 is needed for proper locomotion and flight performance. Larvae lacking cdk5 in the presynaptic tissue display abnormal crawling motion, and their neuromuscular junctions (NMJ) are elongated and contain a higher number of boutons that are smaller. As a result of these two counteracting effects, the total synaptic area/NMJ is similar to wild type, leading to normal synaptic transmission, indicating that a compensatory mechanism is capable of correcting the problem caused by the lack of cdk5. futsch, the Drosophila MAP1B homolog, is also involved in NMJ morphogenesis, and analysis of the NMJ phenotype of the double mutant futsch(K68); cdk5(-) indicates that cdk5 is epistatic to futsch in this process.
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PMID:Drosophila cdk5 is needed for locomotive behavior and NMJ elaboration, but seems dispensable for synaptic transmission. 1926 80