Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Schizophrenia (SZ) is characterized by a variety of complex positive, negative and cognitive symptoms that are differentially expressed in individual patients. Variability in symptom presentation indicates that multiple genes, many involved in neurodevelopment, contribute to the etiology of SZ. The myelin transcription factor 1-like (MYT1L) gene encodes the MYT1L protein that participates in several neurodevelopment pathways. The copy number variant of MYT1L gene is associated with SZ, and single-nucleotide polymorphisms (SNPs) of MYT1L contribute to major depressive disorder. To explore the association of MYT1L polymorphisms with SZ, we examined six SNPs of MYT1L in a Han Chinese population consisting of 528 paranoid schizophrenic patients and 528 healthy subjects. Our results showed that rs17039584 was significantly associated with SZ (A>G), even after Bonferroni correction. When subjects were divided by gender, the rs10190125 allele and genotype remained significantly associated with SZ in female patients. Moreover, we found that rs6742365 was associated with a family history of SZ in females. Other SNPs did not achieve statistical significance for SZ but were associated with individual phenotypes, as measured by the Positive and Negative Syndrome Scale (PANSS) inventory. Our findings suggest that MYT1L may represent a susceptibility gene for SZ in the Han Chinese population and show that a specific SNP may increase susceptibility in females.
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PMID:Association study of myelin transcription factor 1-like polymorphisms with schizophrenia in Han Chinese population. 2192 61

The differentiation and maturation of oligodendrocyte precursor cells (OPCs) is essential for myelination and remyelination in the CNS. The failure of OPCs to achieve terminal differentiation in demyelinating lesions often results in unsuccessful remyelination in a variety of human demyelinating diseases. However, the molecular mechanisms controlling OPC differentiation under pathological conditions remain largely unknown. Myt1L (myelin transcription factor 1-like), mainly expressed in neurons, has been associated with intellectual disability, schizophrenia, and depression. In the present study, we found that Myt1L was expressed in oligodendrocyte lineage cells during myelination and remyelination. The expression level of Myt1L in neuron/glia antigen 2-positive (NG2+) OPCs was significantly higher than that in mature CC1+ oligodendrocytes. In primary cultured OPCs, overexpression of Myt1L promoted, while knockdown inhibited OPC differentiation. Moreover, Myt1L was potently involved in promoting remyelination after lysolecithin-induced demyelination in vivo. ChIP assays showed that Myt1L bound to the promoter of Olig1 and transcriptionally regulated Olig1 expression. Taken together, our findings demonstrate that Myt1L is an essential regulator of OPC differentiation, thereby supporting Myt1L as a potential therapeutic target for demyelinating diseases.
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PMID:Myt1L Promotes Differentiation of Oligodendrocyte Precursor Cells and is Necessary for Remyelination After Lysolecithin-Induced Demyelination. 2939 65