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TBR1 is a member of a conserved family of genes that share a common DNA-binding domain, the T-box. Additionally we are shipping TBR1 Antibodies (40) and many more products for this protein.
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T-Brain-1 (TBR1), a causative gene in autism spectrum disorders (ASDs), encodes a brain-specific (show CALY Proteins) T-box transcription factor.
trans-synaptic Zn mobilization by clioquinol, a Zn chelator and ionophore, rescues the social interaction deficits in Shank2 (show SHANK2 Proteins)-/- and Tbr1+/- mice
Transgenic overexpression of Wnt7b (show WNT7B Proteins) decreased expression of Tbr1 in both progenitor cells and post-mitotic neurons.
This study demonistrated that Tbr1 haploinsufficiency impairs amygdalar axonal projections and results in cognitive abnormality.
Results show that the expression of Tbr1 in neural stem and progenitor cells prevents them from following an astrocyte fate during olfactory bulb development.
TBR1 is a direct transcriptional repressor of Fezf2 (show FEZF2 Proteins) and a negative regulator of CS tract formation that restricts the laminar origin of CS axons specifically to L5.
TBR1 promotes the identity of corticothalamic neurons and represses subcerebral fates through reducing expression of Fezf2 and CTIP2.
Tbr1 coordinately regulates regional and laminar identity of postmitotic cortical neurons.
Af9/Mllt3 (show MLLT3 Proteins) interferes with Tbr1 expression through epigenetic modification of histone H3K79 during development of the cerebral cortex
While Tbr1 is expressed in postmitotic neurons, Tbr2 (show EOMES Proteins) (which is also expressed during gastrulation) is also expressed in neural progenitors.
TBR1 homodimerizes; it interacts with FOXP2 (show FOXP2 Proteins), a transcription factor implicated in speech/language disorders, and this interaction is disrupted by pathogenic mutations affecting either protein
This gene is a member of a conserved family of genes that share a common DNA-binding domain, the T-box. T-box genes encode transcription factors involved in the regulation of developmental processes. A similar protein has been disrupted in mice and shown to be critical for early cortical development, and causes loss of projection neurons in the olfactory bulbs and olfactory cortex. The C-terminal region this similar protein was found to be necessary and sufficient for association with the guanylate kinase domain of calcium/calmodulin-dependent serine protein kinase.
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