| Gene information | Literature | Expression | lncRNA | Mutation | Homolog |
Basic Information | |
|---|---|
Gene ID | 53335 |
Name | BCL11A |
Synonymous | B-cell CLL/lymphoma 11A (zinc finger protein);BCL11A;B-cell CLL/lymphoma 11A (zinc finger protein) |
Definition | B-cell CLL/lymphoma 11A (zinc finger protein) isoform 2|B-cell lymphoma/leukemia 11A|BCL-11A|BCL11A B-cell CLL/lymphoma 11A (zinc finger protein) isoform 1|C2H2-type zinc finger protein|COUP-TF-interacting protein 1|EVI-9|ecotropic viral integration site |
Position | 2p16.1 |
Gene type | protein-coding |
Title | Abstract |
| Gains of the proto-oncogene BCL11A and nuclear accumulation of BCL11A(XL) protein are frequent in primary mediastinal B-cell lymphoma. | Over the past decade, mouse models of cancer have come to resemble human disease much more closely than simple subcutaneous or orthotopic systems. Intervention strategies that work on these new model systems are more likely to have an impact clinically. We have shown recently that antiangiogenic stress imposed by loss of Id protein in endothelial progenitor cells results in dramatic central necrosis in breast tumors initiated in mice by overexpression of the her2/neu oncogene. tumor cells remain viable at the periphery, perhaps via the hypoxic response pathway which allows the lesions to expand. Inhibition of this pathway by the inactivation of the Hif-1alpha chaperone Hsp90 in combination with antiangiogenic stress leads to the first reported complete regression of these aggressive breast tumors. |
| The oncoprotein BCL11A binds to orphan nuclear receptor TLX and potentiates its transrepressive function. | Nuclear orphan receptor TLX (NR2E1) functions primarily as a transcriptional repressor and its pivotal role in brain development, glioblastoma, mental retardation and retinopathologies make it an attractive drug target. TLX is expressed in the neural stem cells (NSCs) of the subventricular zone and the hippocampus subgranular zone, regions with persistent neurogenesis in the adult brain, and functions as an essential regulator of NSCs maintenance and self-renewal. Little is known about the TLX social network of interactors and only few TLX coregulators are described. To identify and characterize novel TLX-binders and possible coregulators, we performed yeast-two-hybrid (Y2H) screens of a human adult brain cDNA library using different TLX constructs as baits. Our screens identified multiple clones of Atrophin-1 (ATN1), a previously described TLX interactor. In addition, we identified an interaction with the oncoprotein and zinc finger transcription factor BCL11A (CTIP1/Evi9), a key player in the hematopoietic system and in major blood-related malignancies. This interaction was validated by expression and coimmunoprecipitation in human cells. BCL11A potentiated the transrepressive function of TLX in an in vitro reporter gene assay. Our work suggests that BCL11A is a novel TLX coregulator that might be involved in TLX-dependent gene regulation in the brain. |