research use only
Cat.No.: F7085
| Dilution |
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| Application |
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| WB, IP, IHC, IF |
| Reactivity |
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| Human, Mouse, Rat |
| Source |
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| Rabbit Monoclonal Antibody |
| Storage Buffer |
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| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
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| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW |
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| 35 kDa |
| Specificity |
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| Olig2 Antibody [C6H24] detects endogenous levels of total Olig2 protein. |
| Clone |
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| C6H24 |
| Synonym(s) |
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| Oligodendrocyte transcription factor 2; OLIG2 |
| Background |
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| Olig2 is a class II basic helix–loop–helix (bHLH) transcription factor that governs glial and neuronal fate decisions in the central nervous system, with essential roles in oligodendrocyte and motor neuron development. Olig2 contains a DNA‑binding bHLH domain and a distinct N‑terminal repression module that enables it to either activate or repress transcription depending on cofactor context, and its activity is further tuned by phosphorylation at specific serine residues that influence progenitor proliferation versus differentiation. Olig2 is expressed in neural progenitors of the ventricular zone, where it promotes oligodendrocyte lineage specification and maturation by directly upregulating Sox10 and reinforcing a positive feedback loop between Olig2 and Sox10 that maintains oligodendrocyte‑precursor and late‑differentiation programs, and it also acts as a fate‑restricting factor that suppresses neuronal differentiation in certain progenitor pools to preserve cycling progenitor states. In the cerebellum, Olig2 is transiently expressed in ventricular‑zone progenitors during early embryogenesis, where it controls the rate of neurogenesis and is required for the proper generation of Purkinje cells without affecting the production of some interneuron subtypes, indicating a stage‑specific role in cerebellar neuronal specification. Olig2 is universally expressed in diffuse gliomas regardless of grade and is required for the self‑renewal and proliferation of glioma‑initiating cells, and its phosphorylation‑dependent repression of CDK inhibitors such as CDKN1A sustains progenitor‑like growth and tumorigenic potential. |
| References |
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