Disease relevance of Map1b

• These results suggest that Abeta does not induce deleterious full-length MAP1B directly, but overexpression of full-length MAP1B might act as an effector of cell death in neurodegenerative disorders related to cytoskeletal abnormalities [1].
• In pheochromocytoma 12 (PC12) cells and sympathetic neurons, nerve growth factor (NGF) engagement with the tropomyosin-related tyrosine kinase (TrkA) receptor activates the serine/threonine kinase glycogen synthase kinase 3beta (GSK3beta), enabling it to phosphorylate the microtubule-associated protein 1B (MAP1B) [2].
• In adults, microtubule-associated protein-1a and microtubule-associated protein-1b are present in all sciatic nerve axons and in motor and dorsal root ganglion neurons [3].
• Our studies show that (i) MAP1B is a temporal and regional marker for rapid and acute epileptic seizures and (ii) long-term increases in MAP1B in the perforant path might play a role in PTZ-induced seizures [4].

High impact information on Map1b

• Since MAP5, in particular, a phosphorylated species, is known to be involved in neurite outgrowth, this result supports the sprouting hypothesis [5].
• These results, together with in vivo data from immunogold methods, demonstrate that MAP1B is a component of cross-bridges between microtubules in neurons [6].
• Two monoclonal antibodies, 5E6 and 1B6, were raised against microtubule-associated protein 1B (MAP1B), a major component of the neuronal cytoskeleton [6].
• Microtubule-associated protein 1B: molecular structure, localization, and phosphorylation-dependent expression in developing neurons [6].
• In spinal cord, neuraxin transcripts were abundant in motoneurons which also expressed glycine receptor subunit mRNA [7].

Biological context of Map1b

• The gene encoding neuraxin appears to be unique in the haploid rat genome and conserved in higher vertebrates [7].
• In contrast, overexpression of MAP1B fragments containing the N-terminal 126 amino acids promoted neurite outgrowth and neuronal apoptosis [1].
• GSK3beta phosphorylation of MAP1B acts as a molecular switch to regulate microtubule dynamics in growing axons, and hence the rate of axon growth [2].
• During embryogenesis microtubule-associated protein-1b and tau are present in all neurons and axons, microtubule-associated protein-2 is present in neurons but not in axons, and there is no microtubule-associated protein-1a [3].
• Microtubule-associated protein 1B (MAP1B) is a major constituent of the neuronal cytoskeleton that is expressed at high levels during early brain development and plays a role in axonal growth and neuronal plasticity [8].

Anatomical context of Map1b

• In view of earlier work indicating that rapid transport is associated with the microtubule domain in the IDPN-treated axon, it now appears that MAP 1A and MAP 1B may play a role in this process [9].
• Northern blot and in situ hybridization revealed neuraxin mRNA to be expressed throughout the rodent central nervous system (CNS) [7].
• Phosphorylated MAP1B was expressed in high levels during the early stages of development in brain, spinal cord, and sciatic nerve and decreased rapidly to undetectable levels postnatally except for sciatic nerve where it remained detectable [10].
• Immunostaining also confirmed Western blot analysis indicating that MAP1B was initially abundant within the spinal cord but was at later stages present only in motor neurons and the central processes of DRG neurons [10].
• MAP1B and GSK3beta are expressed throughout the PC12 cell but MAP1B-P expression is restricted to the growth cones and neurites [11].

Associations of Map1b with chemical compounds

• In the present work we tested the hypothesis that the attenuation of neural plasticity in old age could be the result of an altered temporal relationship between factors promoting brain plasticity [microtubule-associated protein 1B (MAP1B)] and neurotoxic factors such as C-terminal betaAPP [12].
• Microtubule-associated protein 1B-light chain 1 enhances activation of Rap1 by exchange protein activated by cyclic AMP but not intracellular targeting [13].
• Pentylenetetrazole-induced seizure up-regulates levels of microtubule-associated protein 1B mRNA and protein in the hippocampus of the rat [14].
• By 5-10 days the levels of MAP1B in the pyramidal cells in the CA3 region decreased to very low levels; rather, heavy staining of interneuron-like cells and "strings-of-bead" structures all over the hippocampus and at the stratum oriens/alveus border were seen [4].
• Activation of a serine/threonine kinase that phosphorylates microtubule-associated protein 1B in vitro by growth factors and phorbol esters in quiescent rat fibroblastic cells [15].

Regulatory relationships of Map1b

• Microtubule-associated protein 1B (MAP1B) is expressed mainly in the brain during early development and plays important roles in the regulation of microtubule dynamics which is essential to neurite outgrowth and elongation [16].

Other interactions of Map1b

• Accelerated accumulation of N- and C-terminal beta APP fragments and delayed recovery of microtubule-associated protein 1B expression following stroke in aged rats [12].
• Neuraxin, a novel putative structural protein of the rat central nervous system that is immunologically related to microtubule-associated protein 5 [7].
• We have previously shown that the phosphorylated form of microtubule-associated protein 1B (MAP1B-P), which is located in growing axons during development and regeneration, remains detectable in the adult central nervous system only in areas that undergo morphologic plasticity (Nothias et al. [1996] J. Comp. Neurol. 368:317-334) [17].
• The RNA blots were also probed with beta-actin and beta-tubulin to compare the levels of MAP1B mRNA with other cytoskeletal elements and as controls for the quality of the RNA [18].
• The regulation of MAP1B mRNA during development was studied in whole brain, cerebral cortex, hypothalamus, brainstem, and olfactory bulbs [18].

Analytical, diagnostic and therapeutic context of Map1b

• To learn which of the MAPs were present in the microtubule bundles in the axon, sections of axons from IDPN-treated rats were examined by immunofluorescence microscopy using antibodies to MAP 1A, MAP 1B, MAP 2, and tubulin [9].
• Sequence analysis identified a novel type of neuron-specific protein (named neuraxin) which is characterized by an unusual amino acid composition, 12 central heptadecarepeats and putative protein and/or membrane interaction sites [7].
• Phosphorylated MAP1B is induced in central sprouting of primary afferents in response to peripheral injury but not in response to rhizotomy [19].
• Using Northern blot analysis, it was shown that the level of MAP 1B mRNA increased dramatically upon nerve growth factor-induced PC12 cell differentiation [20].
• A substrate of ecto-protein kinase is microtubule-associated protein 1B in cortical cell cultures undergoing synaptogenesis [21].

References