Abstract
B cell leukemia 11b (Bcl11b) is a zinc finger protein transcription factor with a multiplicity of functions. It works as both a genetic suppressor and activator, acting directly, attaching to promoter regions, as well as indirectly, attaching to promoter-bound transcription factors. Bcl11b is a fundamental transcription factor in fetal development, with important roles for the differentiation and development of various neuronal subtypes in the central nervous system (CNS). It has been used as a specific marker of layer V subcerebral projection neurons as well as striatal interneurons. Bcl11b also has critical developmental functions in the immune, integumentary and cardiac systems, to the extent that Bcl11b knockout mice are incompatible with extra-uterine life. Bcl11b has been implicated in a number of disease states including Huntington's disease, Alzheimer's disease, HIV and T-Cell malignancy, amongst others. Bcl11b is a fascinating protein whose critical roles in the CNS and other parts of the body are yet to be fully explicated. This review summarizes the current literature on Bcl11b and its functions in development, health, and disease as well as future directions for research.
Highlights
B cell leukemia 11b (Bcl11b) is a zinc finger protein transcription factor with a multiplicity of functions
For example Bcl11b interacts with the orphan nuclear receptors known as chicken ovalbumin upstream promoter transcription factors COUP-TF (Avram et al, 2000) and nucleosome remodeling and histone deacetylation complex (NuRD; Cismasiu et al, 2005) to act as a powerful genetic repressor for a number of genes
From E18.5 to P21 Bcl11b expression was maintained in the cortex, hippocampus and basal ganglia and this pattern of expression remained through adulthood
Summary
Bcl11b directs pathfinding and development of axons in Corticospinal Motor Neurons (CSMNs), which are 1st order motor neurons that run in the pyramidal tracts providing descending control from the cortex to the spinal motor neurons (Chen et al, 2004). Arlotta et al (2005) found that on immunohistochemistry of wild type mice at E18, P3, P6, and P14 Bcl11b was co-expressed with Netrin-G1, csmn, Cadherin 13, and Cadherin 22, which are known to functionally direct axonal projections and delineate CSMNs from callosal projection neurons (Abbas et al, 2014). Bcl11b was identified as an interacting partner and regulator of the Notch signaling pathway in T cell lines (Yatim et al, 2012) but as yet this has not been confirmed in neurons
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