disease:A chromosomal aberration involving OLIG2 may be a cause of a form of T-cell acute lymphoblastic leukemia (T-ALL). Translocation t(14;21)(q11.2;q22) with TCRA.,domain:The bHLH is essential for interaction with NKX2-2.,function:Required for oligodendrocyte and motor neuron specification in the spinal cord, as well as for the development of somatic motor neurons in the hindbrain. Cooperates with OLIG1 to establish the pMN domain of the embryonic neural tube. Antagonist of V2 interneuron and of NKX2-2-induced V3 interneuron development.,induction:By SHH. Also induced by NKX6-1 in the developing spinal cord, but not in the rostral hindbrain.,similarity:Contains 1 basic helix-loop-helix (bHLH) domain.,subcellular location:The NLS contained in the bHLH domain could be masked in the native form and translocation to the nucleus could be mediated by interaction either with class E bHLH partner protein or with NKX2-2.,subunit:Interacts with NKX2-2.,tissue specificity:Expressed in the brain, in oligodendrocytes. Strongly expressed in oligodendrogliomas, while expression is weak to moderate in astrocytomas. Expression in glioblastomas highly variable.,
Nucleus . Cytoplasm . The NLS contained in the bHLH domain could be masked in the native form and translocation to the nucleus could be mediated by interaction either with class E bHLH partner protein or with NKX2-2. .
Expressed in the brain, in oligodendrocytes. Strongly expressed in oligodendrogliomas, while expression is weak to moderate in astrocytomas. Expression in glioblastomas highly variable.
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