Inhibits DNA binding of TCF3/E47 homodimers and TCF3 (E47)/NEUROD1 heterodimers and acts as a strong repressor of Neurod1 and Myod-responsive genes, probably by heterodimerization with class a basic helix-loop-helix factors. Despite the presence of an intact basic domain, does not bind to DNA (By similarity). In the brain, may function as an area-specific transcription factor that regulates the postmitotic acquisition of area identities and elucidate the genetic hierarchy between progenitors and postmitotic neurons driving neocortical arealization. May be required for the survival of a specific population of inhibitory neurons in the superficial laminae of the spinal cord dorsal horn that may regulate pruritis. Seems to play a crucial role in the retinogenesis, in the specification of amacrine and bipolar subtypes. Forms with PRDM8 a transcriptional repressor complex controlling genes involved in neural development and neuronal differentiation (PubMed:22284184). Interacts with PRDM8. Brain-specific, with the highest expression in the cerebellum. Expressed at 11.5 dpc within the neuroblast layer (NBL) of the central retina. As retinogenesis progressed from central to peripheral retina from 12 dpc to 15.5 dpc, expression expanded to the entire retina with the majority of Bhlhb5+ cells being detected in the proliferating NBL. From 17.5 dpc to birth (P0), expression became restricted to the ganglion cell layer (GCL) and to the inner boundary of the NBL (INL; inner nuclear layer), presumably the newly formed ACL (amacrine cells). Predominantly expressed in post-mitotic cells in the developing retina. Expressed from 9.5 dpc in the neural tube, restricted to longitudinal ventral columns of neurons, extending from the hindbrain to the caudal spinal cord. In the developing cortex, at 12.5 dpc, expressed in the nascent cortical plate of the dorsal telencephalon (at protein level). During peak production of deep layer neurons between 12.5 and 13.5 dpc, restricted to postmigrational neurons, with no expression in the proliferative ventricular zone (VZ) or in migrating neurons. Between 15.5 and 17.5 dpc, when superficial layer neurons are generated, strongly expressed in the cortical plate and weakly in presumptive migrating neurons and in the subventricular zone (SVZ). Does not colocalize with proliferating progenitors in S or M phase in either the VZ or the SVZ; restricted to postmitotic glutamatergic projection neurons during neurogenesis. Not detected in cortical GABAergic interneurons or their extracortical sites of genesis, the medial and caudal ganglionic eminences (at protein level). Postnatally, down-regulation begins at the junction of the cingulate cortex and neocortex; by postnatal day 4 (P4), down-regulation well into the neocortex is observed anteriorly, with the exception of the most superficial layer. At P4, expressed in neocortical layers II, III, IV, and V. Within layer VI, expressed in only very rare scattered TBR1 negative neurons. Down-regulation continues from medial to lateral, exhibiting a markedly reduced expression by P14. Expression varies strikingly along the A-P axis with a precipitous decrease in the rostral cortical plate. At 12.5 dpc, highly expressed medially in the cingulate cortex with weak expression in the rest of the cortex. At 15.5 dpc, expressed in a high caudomedial to a low rostrolateral gradient. Between 15.5dpc and P0, expression increases laterally and the gradient gradually transforms into a sharp border between the presumptive rostral motor and sensory domains. During the first postnatal week, there is a further transformation from homogeneous expression across sensory cortex into discrete areas of high expression coincident with the primary sensory areas. At P4 and P7, expressed in primary visual cortex, primary auditory cortex and distinct primary somatosensory representations, including the vibrissal barrel field. In the spinal chord, transiently expressed in V1, V2, and dI6 interneurons at 10.5 dpc. Also observed in a subpopulation of late-born neurons that migrate to the superficial layers of the dorsal horn. Expression starts shortly after the neurons exit mitosis at 13.5 dpc and persisting for up to 2 weeks postnatally. At birth, about one-third of dorsal horn neurons expressing the protein are excitatory and two-thirds inhibitory. Also expressed in the developing eye and hair follicles, in the epithelial layer of the cochlea in the developing inner, and in the nasal epithelium. At 16.5 dpc, expressed outside the CNS, in particular in all sensory organs; in the nasal pits, transcripts can be detected in the olfactory epithelium. In the developing eye it can be found in the inner and outer retinal layer, and it is also detectable in the sensory layer of the cochlea in the developing inner ear. In addition, expression is found in the developing hair follicles, both in the epithelial component and in the dermal papilla, and in the skin. Null mice exhibits aberrant expression of brain area-specific genes and structural organization in the somatosensory and caudal motor cortices. In somatosensory cortex, vibrissal barrels display postsynaptic disorganization. In caudal motor cortex, anomalous differentiation of corticospinal motor neurons is observed, accompanied by failure of corticospinal tract formation. Mice also develop self-inflicted skin lesions and show significantly enhanced scratching responses to pruritic agents, due to the selective loss of a subset of spinal cord inhibitory interneurons.