Recombinant Human DR1 protein (His tag N-Terminus)

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DR1 also known as negative cofactor 2 (NC2) is an important protein involved in the regulation of gene transcription. It has a molecular weight of approximately 19 kDa and is widely expressed in various tissues. DR1 functions mainly as a transcriptional repressor by interacting with the TATA-binding protein (TBP) therefore inhibiting TBP’s ability to initiate the transcription process. By forming a complex with NC2β also known as DRAP1 DR1 can bind to the TATA box during the transcription initiation step regulating the expression of a diverse range of genes.

Biological function summary

DR1 plays a critical role in chromatin remodeling and transcription regulation. It is a part of the DR1/DRAP1 complex which influences the basal transcription machinery. This complex modulates transcription from TATA-containing promoters by altering the TBP-induced DNA bending leading to changes in gene expression patterns that are necessary for cellular homeostasis and development. Its interaction with other transcriptional modifiers helps to finely tune the transcriptional responses of cells.

Pathways

DR1 is integral to the transcriptional regulation pathway specifically affecting the process of transcription initiation. The DR1/DRAP1 complex plays an essential role in maintaining the balance between activators and repressors at the promoter sites. It works closely with proteins like TBP-associated factors (TAFs) which are part of the transcription factor IID (TFIID) complex. This ensures that transcription is controlled precisely allowing cells to respond accurately to various signaling cues.

Dysregulation of DR1 has been linked to cancer and developmental disorders. For instance abnormalities in DR1 expression or function can contribute to the improper regulation of genes that control cell growth potentially leading to tumorigenesis. Additionally mutations or disruptions in DR1-associated pathways might be implicated in developmental disorders where gene transcription processes are adversely affected. Its interaction with other transcription factors involved in these pathways suggests a broader role in disease pathogenesis.