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Data show that loss of MAP1B function affects general cognitive ability through a profound, brain-wide WM deficit with likely disordered or compromised axons.
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MAP1B knockout neurons display a decrease in the density of presynaptic and postsynaptic terminals, which involves a reduction in the density of synaptic contacts, and an increased proportion of orphan presynaptic terminals. MAP1B knockout neurons present altered synaptic vesicle fusion events, and a decrease in the density of both synaptic vesicles and dense core vesicles at presynaptic terminals.
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MAP1B restricts the access of AMPARs to dendritic spines and the postsynaptic membrane, contributing to downregulating synaptic transmission
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MAP1B confers increased stability to tyrosinated and acetylated, but not detyrosinated microtubules.
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Both FMRP deficiency in Fmr1(I304N) mice and Fmr1 knockdown impeded the axonal delivery of miR-181d, Map1b, and Calm1 and reduced the protein levels of MAP1B and calmodulin in axons.
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MAP1B is a specific marker protein of the podocyte microtubular cytoskeleton.
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Although MAP1A and MAP1B protein levels are not affected in the tulp1-/- retina, they are no longer localized to the outer segment of photoreceptors.
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The morphology, phenotype, regional distribution, proliferative dynamics, and stage-specific marker expression of Map5 cells in the rabbit and mouse central nervous system, were characterized.
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The MAP1B-Tiam1-Rac1 relay is essential for spine structural plasticity and removal of AMPA receptors from synapses during long-term depression.
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MAP1B interacts directly with EB1 and EB3 (EBs), two core 'microtubule plus-end tracking proteins' ( TIPs), and sequesters them in the cytosol of developing neuronal cells.
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MKK7 is specifically phosphorylated in the neurite shaft which triggers Map1b phosphorylation to regulate microtubule bundling leading to neurite elongation.
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The interaction between the conserved COOH-terminal 125-amino acid domain (which is located in the light chains of MAP1A, MAP1B, and MAP1S) and alpha1-syntrophin is direct and occurs through the pleckstrin homology domain 2 (PH2).
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Mutation of the Map1b binding site of Na(v)1.6 prevented generation of sodium current in transfected cells. The data indicate that Map1b facilitates trafficking of Na(v)1.6 to the neuronal cell surface
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Microtubule associated protein 1B, a microtubule stabilizing protein, and clathrin heavy chain, the major component of the clathrin triskelion, were identified as interaction partners for dystonin-a
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important role for MAP1B in the formation and maturation of dendritic spines
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HuD simultaneously binds both RNA and MAP1B-light chain 1 (MAP1B-LC1) in vitro and that it tightly associates with microtubules in cells in an LC1-dependent manner
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MAP1S and MAP1B both are involved in regulating trafficking of NR3A-containing NMDAR.
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Participation of structural microtubule-associated proteins (MAPs) in the development of neuronal polarity.
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developmentally programmed FMRP expression represses the translation of microtubule associated protein 1B (MAP1B) and is required for the accelerated decline of MAP1B during active synaptogenesis in neonatal brain development
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Through MAP1B function, Reelin could modify the neuronal cytoskeleton of migration neurons
