Recombinant Human TBR2 / Eomes protein (GST tag N-Terminus)

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

TBR2 also known as Eomes or Eomesodermin is a transcription factor with a molecular mass of approximately 72 kDa. It is a member of the T-box family and is expressed predominantly in the developing central nervous system especially in the intermediate progenitor cells in the subventricular zone of the cortex. TBR2 plays a significant role in neurogenesis by regulating the proliferation and differentiation of neuronal progenitor cells. This regulation ensures proper development of specific neural circuits critical for overall brain function.

Biological function summary

TBR2 is important in controlling the transition of neural progenitors during cortical development. It serves as an important marker for intermediate neuronal precursors highlighting its importance in the progression from radial glia to neurons. TBR2 does not function in a complex but works closely with the transcription factor Neurogenin 2 to control neuronal differentiation. Its activity determines the timing of neuronal differentiation making it indispensable for orderly cortical layer formation.

Pathways

TBR2 is involved in the Wnt signaling and Notch signaling pathways both key regulators of neurodevelopment. In the Wnt pathway TBR2 influences the balance between progenitor cell proliferation and differentiation by interacting with proteins such as Beta-catenin. In the Notch signaling pathway TBR2 modulates neural precursor cell fate decisions often in relation with proteins like DLL1. These pathways ensure proper brain structure and function by coordinating neural progenitor activity.

TBR2 mutations or misregulation can lead to neurodevelopmental disorders such as microcephaly and intellectual disabilities. The protein's association with these conditions reflects its critical role in cortical development and neuronal differentiation. TBR2's dysregulation is often observed alongside the malfunction of its pathway partners like Beta-catenin in the development of such disorders illustrating the intricate interplay of genetic and molecular factors underlying these diseases.