Olig1, control peptide, 100 ul.
- Known as:
- Olig1, reference short protein sequence, 100 ul.
- Catalog number:
- P14141
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- Olig1 control peptide 100 .
Related genes to: Olig1, control peptide, 100 ul.
- Gene:
- OLIG1 NIH gene
- Name:
- oligodendrocyte transcription factor 1
- Previous symbol:
- -
- Synonyms:
- BHLHB6, bHLHe21
- Chromosome:
- 21q22.11
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-04
- Date modifiied:
- 2016-04-25
Related products to: Olig1, control peptide, 100 ul.
Related articles to: Olig1, control peptide, 100 ul.
- Myelin injury, a hallmark of several neurological diseases, is highly sensitive to glucose metabolism disruptions. Here, we reveal that oligodendrocytes (OLs) within demyelinating lesions exhibit reduced glycolytic efficiency and lactate production compared with mature OLs. Administration of lactate, the product of glycolysis, or specific overexpression of lactate dehydrogenase A (LDHA), the enzyme in lactate production, in Olig1 OLs significantly enhances remyelination. In contrast, conditional knockout of LDHA in the Olig1 lineage or CNPase premyelinating OLs leads to severe neuropathy with dysmyelination in a development-dependent and cell-specific manner. Mechanistic insights show that OLs within demyelinating lesions undergo lactylation silencing, a lactate-induced epigenetic modification that impedes myelin restoration. Furthermore, lactylation of LDHA and carbonic anhydrase II (CAII) couples glycolysis with OL maturation. Our findings elucidate the metabolic interplay among glycolysis, lactylation, and OL maturation and provide novel enzymatic therapeutic perspectives for demyelinating disorders, for which effective therapies are currently lacking. - Source: PubMed
Publication date: 2026/03/16
Bao Ming-YueLi Xiu-QingSun Qing-QingHe YanYin Yu-JingLi Si-HanDu Ruo-YanMa Gai-XinFeng Chen-YuHan BingJia RuiWang XuanWang Li-BinYan Ya-PingLi XingZhang Yuan - Yaks are important livestock in high-altitude regions, and their polled trait can effectively improve breeding and management efficiency. In this study, whole-genome resequencing combined with a GWAS was employed to identify a significantly associated region of approximately 273.6 kb on chromosome 1 (36,313,286-36,586,879 bp) in Xueduo yaks. This region contains 1001 significant single-nucleotide polymorphism (SNP) loci and is located within a long intergenic non-coding RNA (lincRNA) region. Candidate genes , and adjacent to this region were identified. Among these, the gene plays a crucial role in neural crest development, suggesting that it may be a core gene regulating horn development in yaks. Further analysis of Ashdan yaks (a polled breed developed from Datong yaks) indicated that the two breeds share the same candidate genes and a subset of associated genetic variants for the polled trait, suggesting a degree of genetic conservation underlying this trait across yak breeds. This study provides a theoretical basis for polled yak breeding. - Source: PubMed
Publication date: 2026/02/14
Zhong ChuangWang ZiyingLiu ShujieZhang ZhianCui Zhanhong - Motor Exit Point (MEP) glia are spinal cord-derived glial cells that myelinate peripheral motor axons, bridging the central and peripheral nervous systems. They have a hybrid profile, sharing features with oligodendrocytes and Schwann cells. Yet, significant gaps remain in our understanding of complex MEP glial lineage and identity. MEP glia express neural tube and canonical oligodendrocyte lineage markers and , as well as the neural crest marker . Here, we show that the oligodendrocyte markers and are not expressed in MEP glia. These findings refine the molecular signature of MEP glia, enhancing their peripheral identity. - Source: PubMed
Publication date: 2026/01/21
Dallo Tessa CFontenas Laura - Di-2-ethylhexyl phthalate (DEHP) is a widely used plasticizer with recognized sex-dependent neurotoxicity. However, research on adult neurotoxicity is scarce, especially in females. In this study, adult female rats were exposed to a high-dose experimental model of DEHP (500 mg/kg/day) for 28 days to systematically evaluate hippocampal neurotoxicity. We found that DEHP exposure significantly impaired spatial learning and memory. Transcriptomics revealed enrichment in oxidative stress, complement activation, and neurodegenerative pathways. Specifically, cellular and molecular analyses showed that DEHP induced mitochondrial structural defects and elevated markers of oxidative damage (8-OHdG and 3-NT). While the upregulation of mitochondrial and antioxidant proteins (COX4I1, SOD2, and NQO1) indicated an attempted compensatory response, it remained inadequate to restore redox homeostasis. Under this neurotoxic microenvironment, DEHP triggered early neurogenesis, marked by the upregulation of SOX2 and DCX; however, NeuN levels remained unchanged, suggesting that this compensatory effort failed to expand the mature neuronal population. Ultimately, these pathological processes culminated in neurodegeneration, as evidenced by reduced synaptic proteins, suppressed Olig1/2 expression, and increased tau phosphorylation. Collectively, this study provides a comprehensive neurotoxic profile of DEHP in adult female rats, filling a research gap in this field. - Source: PubMed
Publication date: 2026/01/14
Bai JingLi JiayuTang LeiSun WuxiangGao FujiaZhang XinBian RuiWang Ruimin - Multiple sclerosis (MS) is a long-lasting autoimmune condition characterized by myelin destruction and neurodegeneration. Research indicates that ferroptosis significantly influences MS pathogenesis, exacerbating neuronal tissue damage. Our study intended to explore the possible neuroprotective role of fisetin (FIS) in cuprizone (CPZ) model of MS and the associated molecular mechanisms. The 9-week experiment comprised a 5-week demyelination period in which C57BL/6 mice were provided with 0.2% w/w CPZ added to rodent chow, followed by a 4-week remyelination period in which mice were fed CPZ-free chow. FIS (80 mg/kg/day) was given by oral gavage to mice daily for 4 weeks starting in the 2nd week of demyelination. For remyelination, FIS was administered daily during the 4 weeks recovery. During demyelination, FIS significantly improved CPZ-induced behavioral and locomotor deficits, as demonstrated by tail suspension test and inverted screen grip strength test. LFB and H & E staining, MBP, GFAP and vimentin immunostaining revealed that FIS treatment significantly improved myelination, alleviated astrogliosis and neuronal injury in CPZ-fed mice throughout both phases. FIS attenuated ferroptosis and neuroinflammation during de- and remyelination as supported by reduced brain iron deposits, IL-1 β, MDA concentrations and restored GPX4. Moreover, FIS significantly downregulated NCOA4 and TfR1 gene expression and TfR1 protein level but upregulated FTH1 gene expression and ferritin protein level. Additionally, FIS upregulated Olig-1 during demyelination, but not remyelination. Fisetin has a potential neuroprotective effect in CPZ model of MS and can be studied as a promising adjuvant therapy to enhance remyelination and mitigate disability in MS patients possibly by modulating ferroptosis pathway. - Source: PubMed
Publication date: 2025/12/09
El-Ashmawy Nahla EKhedr Naglaa FHelmy Nada NIbrahim Amera O