anti-Oligodendrocyte Lineage Transcription Factor 2 (OLIG2) Antibodies

Human Oligodendrocyte Lineage Transcription Factor 2 (OLIG2) interaction partners

1. Results show that Olig2(+) oligodendrocyte precursor-like glioma cells invade by single-cell vessel co-option and preserve the blood-brain barrier (BBB). Conversely, Olig2-negative glioma cells form dense perivascular collections and promote angiogenesis and BBB breakdown, leading to innate immune cell activation. Olig2 was found to regulate Wnt7b expression in a p53-dependent manner.

2. indicate Olig2 as an onco-requisite factor in diffuse intrinsic pontine glioma

3. OLIG2 immunoreactivity was observed in GABAergic cells of the proliferative zones of the MGE and septum, but not necessarily co-expressed with NKX2.1, and OLIG2 expression was also extensively seen in the LGE, CGE, and cortex

4. Data suggest positive feedback loops including oligodendrocyte transcription factor 2 (OLIG2): loops of epigenetic regulation.

5. Data show that oligodendrocyte transcription factor 2 (OLIG2) is epigenetically regulated via DNA methylation and expressed in a subset of AML patients.

6. Ectopic expression of phosphomimetic Olig2 is sufficient to block TGF-beta2-mediated invasion.

7. phosphorylation of the motif itself serves as a template to prime phosphorylation of additional serines and creates a highly charged "acid blob" in the amino terminus of Olig2.

8. Olig2 was expressed in cord blood eosinophils on d 24, when cord blood eosinophils are considered fully differentiated, but no earlier. It was also expressed in human peripheral-blood eosinophils but not neutrophils, monocytes, lymphocytes, or cord blood mast cells. Many genes, including eosinophil surface molecules, were up-regulated along with OLIG2. OLIG2 shRNA or siRNA downregulated SIGLEC-8 mRNA and protein.

9. Data indicate that transcription factors Sox10 and Olig2 play key roles in oligodendrocytes (OLs) specification.

10. Olig2 expressions were successfully detected in 12 (15.58%) of 77 SVZ type II Glioblastomas (GBs) and 16 (21.3%) of 75 SVZ type III GBs.

11. Olig2 was positive in 5 out of 44 ependymomas (11%) and 50 out of 54 (93%) non-ependymal tumors

12. The present study is the first to verify the associations of SNPs rs762178, rs1059004, and rs9653711 of the OLIG2 gene with OCD in a Chinese Han population. Thus, OLIG2 might serve as a potential target for OCD treatment

13. The results demonstrate that the expression of Olig2 in dental pulp stem cells reduces the expression of stem cell markers and induces the development of oligodendrocyte progenitors.

14. High Olig2 expression is associated with oligodendrogliomas.

15. OLIG2 is the most specific GSC marker.

16. Our study suggests that CGT expression is controlled by balanced expression of the negative modulator OLIG2 and positive regulator Nkx2.2, providing new insights into how expression of GalCer is tightly regulated in cell-type- and stage-specific manners.

17. Authors investigated the role of Pten in these two critical cellular compartments in adult and developing brains using methods for activation or suppression of PI3K signaling in glial and neuronal progenitors expressing Olig2.

18. LGR5 expression may be functionally correlated with the neurogenic competence, and be regulated by OLIG2 in stem-like cells in glioblastoma.

19. We found that the risk allele OLIG2 (A) was associated with reduced white matter integrity in the corona radiata bilaterally

20. Olig2-positive cells in glioneuronal tumors, and some of them also exhibited neuronal features

Zebrafish Oligodendrocyte Lineage Transcription Factor 2 (OLIG2) interaction partners

1. these data raise the possibility that cells expressing olig2 are intermediate targets that help guide facial motor neuron migration.

2. Study detected at least five different classes of olig2-positive cells in the telencephalon of the adult zebrafish.

3. By cooperating with Shh, FGF-receptor signalling controls the expression of olig2, a patterning gene essential for the specification of somatic motoneurons and oligodendrocytes.

4. Loss of olig2 function prevents primary motor neuron and oligodendrocyte development, whereas olig2 overexpression promotes formation of excess primary motor neurons and oligodendrocytes.

5. Olig2 is required for repression of iro3 expression in the progenitor domain of ventral spinal cord

6. data indicate that Hedgehog & Wnt work in opposition across the dorsoventral axis of the cerebellum to regulate formation of olig2(+) neurons; we propose that Hedgehog limits the range of Wnt signaling, which is necessary for olig2(+) neuron development

7. commitment of basal diencephalic DA neurons is regulated by the combined action of the neural protein Olig2 and its downstream neuronal specific effector Sim1

Mouse (Murine) Oligodendrocyte Lineage Transcription Factor 2 (OLIG2) interaction partners

1. postnatal deletion of Olig2 caused NG2 cells in the neocortex but not in other gray matter regions to become protoplasmic astrocytes. However, NG2 cells in the neocortex became more resistant to astrocyte fate switch over the first 3 postnatal weeks.

2. findings reveal a tight coupling between the regulatory networks that control patterning and neuronal differentiation and demonstrate how Olig2 acts as the developmental pacemaker coordinating the spatial and temporal pattern of motor neuron generation

3. Cuprizone-induced schizophrenia-like symptoms involved olig2 upregulation. The silence of olig2 could prevent changes, likely through regulating MBP, CNPase, and GFAP expressions.

4. transient hypoxia at P7 altered the expression of Olig1 and Nkx2.2, resulting in delayed myelination in the external capsule.

5. Functionally, deletion of Olig2 alone results in a preferential reduction of Purkinje cells in the cerebellum, which is likely mediated by decreased neuronal generation from their cerebellar ventricular zone progenitors.

6. Olig2 is down-regulated in oligodendrocyte progenitor cells infected by Theiler's murine encephalomyelitis virus.

7. phosphorylation of the motif itself serves as a template to prime phosphorylation of additional serines and creates a highly charged "acid blob" in the amino terminus of Olig2.

8. OLIG2 modulates growth factor signaling in two distinct populations of glioma stem cells, characterized by expression of either the epidermal growth factor receptor (EGFR) or platelet-derived growth factor receptor alpha.

9. the dynamic interplay between HMGNs and H1 in chromatin epigenetically regulates the expression of OLIG1&2, thereby affecting oligodendrocyte development and myelination, and mouse behavior.

10. Olig2 was significantly upregulated and transcriptionally targeted the Gpr17 locus

11. Brg1 represses Olig2 expression and the specification of oligodendrocyte progenitors, but is required for OPC differentiation and oligodendrocyte maturation

12. Data show that oligodendrocyte transcription factor 2 (Olig2) deletion causes platelet-derived growth factor receptor (PDGFR) downregulation and reciprocal epidermal growth factor receptor (EGFR) upregulation.

13. This study suggests that Olig2 misexpression in neural stem cells elicits neurogenesis defects and neuronal cell death, which may contribute to developmental disorders including Down syndrome

14. OLIG2 is a multifunctional regulator of neural stem cell self-renewal

15. Olig2 expression is localized to the cochleovestibular ganglia from E12.5 through E14.5

16. Olig2 overexpression accelerates the differentiation of mouse embryonic stem cells into oligodendrocyte progenitor cells in vitro.

17. This study demonstrated that that OLIG2 overexpression in oligodendrocyte progenitor cells might be a possible therapeutic mechanism for enhancing myelin repair.

18. Results from expression pattern suggests that Olig2 may have an important role in the early stage of Purkinje cell development.

19. Prox1 controls binary fate decisions between motor neurons and V2 interneurons in progenitor cells via direct repression of Olig2 gene regulatory elements

20. Phosphorylated Olig2 is preferentially localized to a transcriptionally active compartment for regulation of gene expression.