CDK8-CCNC-MED12 Protein, Human (Sf9, GST, FLAG, His)

The CDK8-CCNC-MED12 protein is an important component of the mediator complex, acting as a bridge for gene transcription regulation, transmitting information from gene-specific regulatory factors to RNA polymerase II. It is recruited to the promoter, assembles a preinitiation complex, and promotes transcription. CDK8-CCNC-MED12 Protein, Human (Sf9, GST, FLAG, His) is the recombinant human-derived CDK8-CCNC-MED12 protein, expressed by Sf9 insect cells , with N-6*His, N-Flag, N-GST labeled tag.

The CDK8-CCNC-MED12 protein is a crucial component of the Mediator complex, a coactivator integral to the regulation of gene transcription for nearly all RNA polymerase II-dependent genes. As part of the Mediator complex, it acts as a bridge, conveying information from gene-specific regulatory proteins to the basal RNA polymerase II transcription machinery. This complex is recruited to promoters through direct interactions with regulatory proteins, serving as a scaffold for the assembly of a functional pre-initiation complex with RNA polymerase II and general transcription factors. CDK8-CCNC-MED12 exerts its regulatory functions by phosphorylating the C-terminal domain (CTD) of the large subunit of RNA polymerase II, potentially inhibiting the formation of a transcription initiation complex. Furthermore, it phosphorylates CCNH, leading to the down-regulation of the TFIIH complex and subsequent transcriptional repression. Notably, CDK8-CCNC-MED12 is recruited through interaction with MAML1, contributing to the hyperphosphorylation of the intracellular domain of NOTCH and facilitating its degradation. These multifaceted roles underscore the significance of CDK8-CCNC-MED12 in orchestrating the intricate processes of gene transcription regulation.

Human

Sf9 insect cells

N-Flag;N-GST;N-His

P49336-1 (M1-Y464)&P24863-1 (M1-S283)&Q93074-1 (M1-D100)

1024&892&9968

79.8 kDa&36 kDa&12.2 kDa

Greater than 90% as determined by reducing SDS-PAGE.

<1 EU/μg, determined by LAL method.