Ask about this productRelated genes to: PRR18 antibody
- Gene:
- PRR18 NIH gene
- Name:
- proline rich 18
- Previous symbol:
- -
- Synonyms:
- MGC35308
- Chromosome:
- 6q27
- Locus Type:
- gene with protein product
- Date approved:
- 2007-06-14
- Date modifiied:
- 2016-10-25
Related products to: PRR18 antibody
Related articles to: PRR18 antibody
- The decreased ability of mature oligodendrocytes to produce myelin negatively affects remyelination in demyelinating diseases and aging, but the underlying mechanisms are incompletely understood. In the present study, we identify a mature oligodendrocyte-enriched transcriptional coregulator diabetes- and obesity-related gene (DOR)/tumor protein p53-inducible nuclear protein 2 (TP53INP2), downregulated in demyelinated lesions of donors with multiple sclerosis and in aged oligodendrocyte-lineage cells. Dor ablation in mice of both sexes results in defective myelinogenesis and remyelination. Genomic occupancy in oligodendrocytes and transcriptome profiling of the optic nerves of wild-type and Dor conditional knockout mice reveal that DOR and SOX10 co-occupy enhancers of critical myelinogenesis-associated genes including Prr18, encoding an oligodendrocyte-enriched, proline-rich factor. We show that DOR targets regulatory elements of genes responsible for α-ketoglutarate biosynthesis in mature oligodendrocytes and is essential for α-ketoglutarate production and lipid biosynthesis. Supplementation with α-ketoglutarate restores oligodendrocyte-maturation defects in Dor-deficient adult mice and improves remyelination after lysolecithin-induced demyelination and cognitive function in 17-month-old wild-type mice. Our data suggest that activation of α-ketoglutarate metabolism in mature oligodendrocytes can promote myelin production during demyelination and aging. - Source: PubMed
Publication date: 2024/09/12
Huang GuojiaoLi ZhidanLiu XuezhaoGuan MenglongZhou SonglinZhong XiaowenZheng TaoXin DazhuanGu XiaosongMu DezhiGuo YingkunZhang LinZhang LiguoLu Q RichardHe Xuelian - Tumors emerge by acquiring a number of mutations over time. The first mutation provides a selective growth advantage compared to adjacent epithelial cells, allowing the cell to create a clone that can outgrow the cells that surround it. Subsequent mutations determine the risk of the tumor progressing to metastatic cancer. Some secondary mutations may inhibit the aggressiveness of the tumor while still increasing the survival of the clone. Meaningful mutations in genes may provide a strong molecular foundation for developing novel therapeutic strategies for cancer. - Source: PubMed
Publication date: 2024/04/17
Liu QunZhang XiaohuaSong YanSi JunliLi ZhaoshuiDong Quanjiang - Identifying mutual neuroinflammatory axis in different experimental models of multiple sclerosis (MS) is essential to evaluate the de- and re-myelination processes and improve therapeutic interventions' reproducibility. - Source: PubMed
Publication date: 2023/06/01
Rahmat-Zaie RoyaAmini JavadHaddadi MohammadBeyer CordianSanadgol NimaZendedel Adib - Hereditary Parkinson's disease can be triggered by an autosomal dominant overdose of alpha-Synuclein (SNCA) or the autosomal recessive deficiency of PINK1. We recently showed that the combination of PINK1-knockout with overexpression of A53T-SNCA in double mutant (DM) mice potentiates phenotypes and reduces survival. Now we studied brain hemispheres of DM mice at age of 18 months in a hypothesis-free approach, employing a quantitative label-free global proteomic mass spectrometry scan of posttranslational modifications focusing on methyl-arginine. The strongest effects were documented for the adhesion modulator CMAS, the mRNA decapping/deadenylation factor PATL1, and the synaptic plasticity mediator CRTC1/TORC1. In addition, an intriguing effect was observed for the splicing factor PSF/SFPQ, known to interact with the dopaminergic differentiation factor NURR1 as well as with DJ-1, the protein responsible for the autosomal recessive PARK7 variant of PD. CRTC1, PSF, and DJ-1 are modulators of PGC1alpha and of mitochondrial biogenesis. This pathway was further stressed by dysregulations of oxygen sensor EGLN3 and of nuclear TMPO. PSF and TMPO cooperate with dopaminergic differentiation factors LMX1B and NURR1. Further dysregulations concerned PRR18, TRIO, HNRNPA1, DMWD, WAVE1, ILDR2, DBNDD1, and NFM. Thus, we report selective novel endogenous stress responses in brain, which highlight early dysregulations of mitochondrial homeostasis and midbrain vulnerability. - Source: PubMed
Publication date: 2016/03/01
Auburger GeorgGispert SuzanaBrehm Nadine