Product Name: CDK7/9Subtide
Product Number: PE-01BGR99
Size: 1 mg      Price:136.00
5 mg      $US297.00
20 mg      543.00
Peptide Name: CDK7/9Subtide

Product Use: For assaying the phosphotransferase activity of Cyclin-dependent protein-serine kinase 7 (UniProt ID P50613).

Peptide Production Method: Solid-phase peptide synthesis

Peptide Sequence: KKKYSPTSPSYSPTSPSYS

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: βAla-Cys

Peptide Molecular Mass Calculated: 2266.7 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid
Storage Conditions: -20°C

Peptide Recommended Enzyme: CDK7/9

Scientific Background: CDK7 (CAK1) is a protein-serine/threonine kinase of the CMGC group and CDK family. It is a protein kinase that functions in cell cycle control and in the regulation of RNA-polymerase II-mediated transcription as the catalytic subunit of the CDK-activating kinase (CAK) complex. Cyclin-dependent kinases (CDKs) are activated by the binding to a cyclin and mediate the progression through the cell cycle. Each different complex controls a specific transition between 2 subsequent phases in the cell cycle. CDK7 is required for both activation and complex formation of CDK1/cyclin-B during G2-M transition, and for activation of CDK2/cyclins during G1-S transition (but not complex formation). CDK7 phosphorylates many proteins including SPT5/SUPT5H, SF1/NR5A1, POLR2A, p53/TP53, CDK1, CDK2, CDK4, CDK6 and CDK11B/CDK11. CAK activates the cyclin-associated kinases CDK1, CDK2, CDK4 and CDK6 by direct threonine phosphorylation. CAK complexed to the core-TFIIH basal transcription factor activates RNA polymerase II by serine phosphorylation of the repetitive C-terminus domain (CTD) of its large subunit (POLR2A), allowing its escape from the promoter and elongation of the transcripts. Phosphorylation of POLR2A in complex with DNA promotes transcription initiation by triggering dissociation from DNA. Its expression and activity are constant throughout the cell cycle. Upon DNA damage, triggers p53/TP53 activation by phosphorylation, but is inactivated in turn by p53/TP53; this feedback loop may lead to an arrest of the cell cycle and of the transcription, helping in cell recovery, or to apoptosis. CDK7 is required for DNA-bound peptides-mediated transcription and cellular growth inhibition. In the presence of DNA-damage, CDK7 phosphorylates and activates p53/TP53, which then feeds back and inactives CDK7, leading to cell cycle arrest. Insertional mutagenesis studies in mice support a role for this protein kinase in mouse cancer oncogenesis.