Map4 Gene is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
{{Infobox gene
| symbol = MAP4
| name = Microtubule-Associated Protein 4
| chromosome = 3
| locus = 3p21.31
| geneID = 4134
| omim = 157138
| ensembl = ENSG00000011114
| uniprot | P27816
| uniprot_name = MAP4
| diseases = Alzheimer's Disease, Parkinson's Disease, Spinal Cord Injury
| diseases_ref = Baas et al., 2016, J Neurosci
}}
Microtubule-associated protein 4 (MAP4) is a neuronal protein that stabilizes microtubules and regulates microtubule dynamics in cells. The MAP4 gene is located on chromosome 3p21.31 and encodes a protein of 1862 amino acids. MAP4 is the predominant MAP expressed in non-neuronal cells but is also present in neurons where it interacts with tubulin to promote microtubule assembly and protect against depolymerization. Unlike tau (MAPT) which is neuron-specific, MAP4 is ubiquitously expressed and plays roles in cell division, intracellular transport, and cellular morphology. In neurodegeneration, MAP4 dysfunction may contribute to microtubule instability observed in Alzheimer's disease, Parkinson's disease, and spinal cord injury.
Microtubule-associated protein 4 (MAP4) is a cytoskeletal protein that binds to microtubules and regulates their stability, dynamics, and interaction with other cellular components. MAP4 is one of the MAP family proteins that modulate microtubule function in neurons and other cell types.
MAP4 binds to microtubules through:
MAP4 promotes microtubule stability by:
In neurons, MAP4 is crucial for:
MAP4 dysfunction contributes to AD pathogenesis:
In PD, MAP4 is affected through:
MAP4 expression changes after injury:
MAP4 is expressed in:
In neurons, MAP4 is localized to:
The study of Map4 Gene has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
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Yigit BN et al.. "Loss of Eml1 alters microtubule-associated protein networks in mouse brain heterotopia." Communications biology (2025) DOI:10.1038/s42003-025-08394-0
Shao W et al.. "Centrosome anchoring regulates progenitor properties and cortical formation." Nature (2020) DOI:10.1038/s41586-020-2139-6
Tokuraku K et al.. "Distinct neuronal localization of microtubule-associated protein 4 in the mammalian brain." Neuroscience letters (2010) DOI:10.1016/j.neulet.2010.08.038
Alfaro-Aco R, Thawani A, Petry S. "Biochemical reconstitution of branching microtubule nucleation." eLife (2020) DOI:10.7554/eLife.49797
López LA, Sheetz MP. "A microtubule-associated protein (MAP2) kinase restores microtubule motility in embryonic brain." The Journal of biological chemistry (1995)
Zaidi D et al.. "Forebrain Eml1 depletion reveals early centrosomal dysfunction causing subcortical heterotopia." The Journal of cell biology (2024) DOI:10.1083/jcb.202310157
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