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Related Concept Videos

Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders01:27

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Schizophrenia is a neurodevelopmental disorder whose origins are rooted in complex genetic components. Despite our burgeoning understanding, the pathophysiology of this disorder remains incompletely deciphered.
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Schizophrenia, a severe psychiatric disorder, arises from a complex interplay of biological factors, including genetic predisposition, structural brain abnormalities, neurotransmitter dysregulation, and developmental irregularities. These factors collectively contribute to the onset and progression of the disorder, which typically manifests in late adolescence or early adulthood.
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Abnormal Proliferation02:23

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Phosphorylation01:02

Phosphorylation

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The addition or removal of phosphate groups from proteins is the most common chemical modification that regulates cellular processes. These modifications can affect the structure, activity, stability, and localization of proteins within cells as well as their interactions with other proteins.
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Microtubule Associated Proteins (MAPs)01:42

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Microtubule function and architecture are regulated by an array of specialized proteins called microtubule-associated proteins or MAPs. These proteins are widespread across different organisms and have conserved protein motifs, like the multi-TOG domain for tubulin binding found in the CLASP family of MAPs. Some MAPs are lineage-specific based on their conserved domains. Their functions depend upon the cytoskeletal architecture and cell type they are located within. In-plant cells, a specific...
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Updated: Nov 19, 2025

Standardized Data Acquisition for Neuromelanin-Sensitive Magnetic Resonance Imaging of the Substantia Nigra
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MAP2 is differentially phosphorylated in schizophrenia, altering its function.

M J Grubisha1, X Sun1,2, M L MacDonald1

  • 1Department of Psychiatry, Translational Neuroscience Program, School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.

Molecular Psychiatry
|February 2, 2021
PubMed
Summary
This summary is machine-generated.

Schizophrenia involves altered microtubule-associated protein 2 (MAP2) function due to phosphorylation, impacting neuronal structure and protein synthesis. This "MAP2opathy" offers a new therapeutic target for schizophrenia.

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Rab10 Phosphorylation Detection by LRRK2 Activity Using SDS-PAGE with a Phosphate-binding Tag
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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Schizophrenia (Sz) is a complex polygenic disorder with unclear underlying mechanisms.
  • Reduced microtubule-associated protein 2 (MAP2) immunoreactivity (MAP2-IR) is observed in Sz patients, independent of total MAP2 protein levels.

Purpose of the Study:

  • To investigate the role of MAP2 phosphorylation in schizophrenia pathogenesis.
  • To identify downstream molecular and cellular consequences of altered MAP2 function in Sz.

Main Methods:

  • Unbiased phosphoproteomics to quantify MAP2 phosphopeptides in Sz subjects.
  • Network analysis to link phosphopeptides to clinical and cellular phenotypes.
  • Computational modeling and experimental validation of MAP2 phosphorylation effects on microtubule binding.
  • Co-immunoprecipitation and mass spectrometry to identify the MAP2 interactome.
  • Generation and analysis of a phosphomimetic MAP2 transgenic mouse model (S1782E).

Main Results:

  • Nine out of 18 quantified MAP2 phosphopeptides were significantly altered in Sz subjects.
  • MAP2 phosphopeptides correlated with dendritic spine loss, synaptic protein levels, and clinical function.
  • Phosphorylation at serine 1782 (pS1782) was increased in Sz, impairing MAP2 binding to microtubules.
  • S1782E mice exhibited reduced dendritic complexity and spine density.
  • The MAP2 interactome is enriched for protein translation factors, and altered MAP2 function reduced protein synthesis.
  • Low MAP2-IR in Sz subjects correlated with reduced synaptic protein levels, a phenotype mirrored in S1782E mice.

Conclusions:

  • Altered MAP2 phosphorylation, termed "MAP2opathy," is a significant factor in schizophrenia.
  • This pathway impacts neuronal structure, synaptic protein synthesis, and overall brain function.
  • Targeting MAP2 phosphorylation presents a potential therapeutic strategy for schizophrenia.