CCNH antibodies are pivotal in studying Cyclin H’s role in:
CDK7 activation: Phosphorylates CDK2 and CDC2 to drive cell cycle progression .
Transcriptional regulation: Interacts with TFIIH and RNA polymerase II .
CCNH antibodies enable investigations into oncogenic pathways:
CtBP2 interaction: CCNH/CDK7 stabilizes CtBP2, enhancing tumor cell migration and invasion . Depleting CCNH reduces CtBP2 dimerization and repressive activity, impairing metastasis .
PD-L1 upregulation: Lnc-CCNH-8, a non-coding RNA, sponges miR-217 to increase PD-L1 expression, promoting immune evasion in hepatocellular carcinoma (HCC). CCNH antibodies may aid in studying this mechanism .
Cancer immunotherapy: CCNH antibodies may help stratify HCC patients for PD-1/PD-L1 inhibitors .
Targeted therapies: Inhibiting CCNH/CDK7 could disrupt CtBP2-mediated metastasis .
Biomarker development: Exosomal Lnc-CCNH-8 serves as a predictive marker for immunotherapy response .
The CAK complex regulates cell cycle progression by activating cdc2, CDK2, and CDK4 kinases through phosphorylation of a critical threonine residue in the T-loop of the CDK-cyclin complexes . The CAK complex can exist either in its free form or in association with transcription factor IIH (TFIIH), which can affect its substrate specificity . When bound to TFIIH, CAK preferentially phosphorylates the carboxy-terminal domain of RNA polymerase II, linking cell cycle control, transcriptional regulation, and DNA repair .
The Mouse Anti Human Cyclin-H Antibody is a polyclonal antibody produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy-terminus of cyclin H . These antibodies are purified by protein A and peptide affinity chromatography . The antibody detects endogenous levels of cyclin H and does not cross-react with other family members at physiological levels .