Ask about this productRelated genes to: OLIG2 antibody
- Gene:
- OLIG2 NIH gene
- Name:
- oligodendrocyte transcription factor 2
- Previous symbol:
- PRKCBP2, BHLHB1
- Synonyms:
- RACK17, OLIGO2, bHLHe19
- Chromosome:
- 21q22.11
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-19
- Date modifiied:
- 2017-01-11
Related products to: OLIG2 antibody
Related articles to: OLIG2 antibody
- Gliosarcoma of the central nervous system (CNS) is a rare and aggressive neoplasm exhibiting biphasic differentiation into glial and mesenchymal components. We report a primary gliosarcoma with mesenchymal differentiation resembling follicular dendritic cell sarcoma (FDCS). A 72-year-old man presented with a rim-enhancing lesion in the left frontotemporal parenchyma. Histologically, the tumor was biphasic, comprising a glioblastoma (GBM) component of diffusely infiltrative GFAP- and Olig2-positive oligodendroglial-like cells with microvascular proliferation, and an FDCS component composed of cohesive sheets, nests, and fascicles of CD21-, CD23-, and CD35-positive plump spindle cells. NGS analysis performed on the microdissected components revealed shared PTEN p.N48S mutations with high variant allele frequencies and MGMT promoter methylation, suggesting a monoclonal origin. Furthermore, the two components exhibited divergent genetic profiles: the glial component was characterized by an FGFR1 mutation, PDGFRA fusion, KIT/KDR amplification, and a whole-arm 1p/19q codeletion, whereas the sarcomatous component harbored an ERBB4 p.S853F mutation. These alterations predominantly converged on the RAS-MAPK and PI3K-AKT-mTOR signaling pathways. No IDH1/2 mutations, EGFR gene amplification, or TERT promoter mutations were detected in either component. This case represents the first documented instance of primary gliosarcoma with FDCS differentiation, thereby expanding its known differentiation spectrum. Furthermore, it demonstrates the necessity of separately analyzing each histological component in the diagnosis of challenging cases. - Source: PubMed
Zhou JingZhao ShaLi HaiYang ShudongPan Minhong - - Source: PubMed
Hu Y MZhang YWang Z MGan W J - A 19-year-old male sea otter (Enhydra lutris) exhibited systemic seizures, declining consciousness, temporary cardiopulmonary arrest, and right-side rotation. The sea otter died approximately one month after its initial seizure. Postmortem magnetic resonance imaging examination revealed a high-intensity region in the left frontal lobe. At necropsy, a gelatinous lesion in the left frontal lobe of the brain was revealed. Histopathologically, the lesion consisted of neoplastic proliferation of round to polyhedral monomorphic cells with a honeycomb growth pattern, small round nuclei, and cytoplasmic halos. The neoplastic cells were immunopositive for oligodendrocyte transcriptional factor-2 (OLIG2) and immunonegative for glial fibrillary acidic protein (GFAP). In this study, we describe the clinical signs and histopathological features of oligodendroglioma, which have rarely been reported in sea otters. - Source: PubMed
Publication date: 2026/05/07
Kezuka ChihoTokuno HisakiKuramochi MizukiMuramoto MomoyoFuruta KeisukeAkiyoshi HideoTanaka MiyuuIzawa TakeshiKuwamura Mitsuru - The cerebellum is involved in numerous motor functions, the adaptation and execution of smooth complex voluntary and fine movements. Glial cells are essential for maintaining healthy neurons. Studying the camel cerebellum was neglected even in recent research even in the Middle East and Asia where camels are reared. Therefore, we investigated the glia in camel cerebellum employing histochemical and immunohistochemical staining using GFAP, Olig2, S-100 and Iba1 for astrocytes, oligodendrocytes, Bergmann glia and fibrous astrocytes, and microglia, respectively. The camel cerebellum was collected from ten clinically healthy mature camel’s () heads. GFAP immunoreactivity was not detected in the molecular layer, suggesting that this astrocytic population does not express GFAP. The distribution of astrocytes is heterogeneous between different layers and within the same layer. Bergmann glia was arranged into 4–6 rows in the Purkinje cell layer. Their processes extend radially through the molecular layer and reach the pial surface. Its mean density was 5126 cells/1 mm. Oligodendrocytes were observed in the white matter and granular layer. The oligodendrocytes were either solitary or aligned in rows like beads along the nerve fascicles. Microglia were heterogeneous in both morphology and distribution in different layers and within the same layer. The white matter contains the highest mean density and they were elliptical and most processes run parallel to the nerve fibers. In the granular layer, elliptical- and oval bodies and their processes emerge from all over the cell bodies. The molecular layer contained oval microglia with short processes. Abundant Iba1 positive puncta distributed all over the molecular layer. The current study in camel is considered a step of comparative neuroglial biology across species. - Source: PubMed
Publication date: 2026/04/24
Attaai Abdelraheim HNoreldin Ahmed ENomir Ahmed GHussein Manal T - Pitt-Hopkins syndrome (PTHS) is a rare neurodevelopmental disorder that results from loss-of-function (LOF) mutations in the Transcription Factor 4 (TCF4) gene. PTHS closely resembles Rett syndrome (RTT), another neurodevelopmental disorder caused by mutations in the gene encoding Methyl CpG Binding Protein 2 (MECP2). We have recently shown that increasing MeCP2 levels, either genetically or via a viral vector approach, normalizes reciprocal behavioral phenotypes observed in Tcf4 and MECP2-overexpressing animals; in the current manuscript, we show that behavioral rescue also extends to a contextual fear learning task. Tcf4 heterozygous and knock-in mouse lines exhibit consistent myelination abnormalities, with an arrest of oligodendrocytes (OLs) at an immature stage. To address the hypothesis that correction of myelination defects is the potential mechanism underlying the behavioral rescue induced by MeCP2 increases in Tcf4 animals, we performed RNA-sequencing and protein expression studies. These experiments revealed that increasing MeCP2 does not dramatically affect the transcriptional profile induced by heterozygosity at Tcf4, as well as vice-versa, and subsequent molecular experiments suggest that OL gene expression and molecular phenotypes in Tcf4 animals are unchanged in the presence of an MECP2 transgene. However, we also find increased levels of Olig2 and Gfap co-expressing cells in Tcf4 mice in the presence of the MECP2 transgene, as well as the presence of cells with astrocytic morphology in the brains of these animals, suggesting a potential interplay of MeCP2 and TCF4 in astrocyte development. - Source: PubMed
Publication date: 2026/04/15
Vermudez Sheryl Anne DFreitas Geanne ABuch AditiMoxley YutaRajpal HemangiGogliotti Rocco GNiswender Colleen M