CDK12 Antibody [N24C20] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat

Usage Information

Dilution
WB1:1000 IP1:30 IHC1:500

Application
WB, IP, IHC

Reactivity
Human, Mouse, Rat

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
164 kDa 205 kDa,124 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
CDK12 Antibody [N24C20] detects endogenous levels of total CDK12 protein.

Clone
N24C20

Synonym(s)
CRK7, CRKRS, KIAA0904, CDK12, Cyclin-dependent kinase 12, Cell division cycle 2-related protein kinase 7, Cell division protein kinase 12, CrkRS, CDC2-related protein kinase 7, Hcdk12

Background
CDK12 is a transcription‑associated cyclin‑dependent kinase that forms an active complex with cyclin K and functions as a carboxyl‑terminal domain (CTD) kinase for RNA polymerase II, thereby acting as a global regulator of transcription elongation and RNA processing with particular impact on long genes involved in DNA damage responses and genome maintenance. The kinase contains a canonical CDK catalytic core with an activation loop and a large C‑terminal extension that contributes to CTD binding and substrate selectivity, and the CDK12–cyclin K complex phosphorylates Ser2 and Ser5 residues within heptad repeats of the RNAPII CTD, enhancing processive elongation and productive transcription across gene bodies. CDK12 activity stimulates RNAPII elongation on a broad set of protein‑coding genes and also influences transcription termination, co‑transcriptional splicing, and RNA turnover, in part through direct phosphorylation of RNA‑processing factors that associate with the elongating polymerase. CDK12 has a strong functional bias toward long, complex genes encoding key DNA damage response and homologous recombination proteins such as BRCA1, ATR, FANCI, and other HR factors; inhibition or loss of CDK12 causes gene length‑dependent elongation defects, premature cleavage and polyadenylation within introns, and marked down‑regulation of these DDR transcripts, leading to reduced DNA repair capacity and genomic instability. This selectivity arises from the combination of CTD phosphorylation defects and altered regulation of pre‑mRNA processing at intronic polyadenylation sites, making long DDR genes particularly sensitive to reduced CDK12‑dependent elongation and processing. CDK12 also regulates expression of core DNA replication genes and other cell‑cycle regulators by controlling RNAPII processivity over these loci, thereby contributing to proper G1/S progression and coordination between replication and repair. In cancer, recurrent CDK12 loss‑of‑function mutations occur in high‑grade serous ovarian carcinoma, prostate cancer, and other tumor types and associate with tandem duplications, focal genomic rearrangements, and a distinct genomic instability signature that reflects defective transcription of homologous recombination genes rather than direct catalytic lesions in replication or repair enzymes.

Background

CDK12 is a transcription‑associated cyclin‑dependent kinase that forms an active complex with cyclin K and functions as a carboxyl‑terminal domain (CTD) kinase for RNA polymerase II, thereby acting as a global regulator of transcription elongation and RNA processing with particular impact on long genes involved in DNA damage responses and genome maintenance. The kinase contains a canonical CDK catalytic core with an activation loop and a large C‑terminal extension that contributes to CTD binding and substrate selectivity, and the CDK12–cyclin K complex phosphorylates Ser2 and Ser5 residues within heptad repeats of the RNAPII CTD, enhancing processive elongation and productive transcription across gene bodies. CDK12 activity stimulates RNAPII elongation on a broad set of protein‑coding genes and also influences transcription termination, co‑transcriptional splicing, and RNA turnover, in part through direct phosphorylation of RNA‑processing factors that associate with the elongating polymerase. CDK12 has a strong functional bias toward long, complex genes encoding key DNA damage response and homologous recombination proteins such as BRCA1, ATR, FANCI, and other HR factors; inhibition or loss of CDK12 causes gene length‑dependent elongation defects, premature cleavage and polyadenylation within introns, and marked down‑regulation of these DDR transcripts, leading to reduced DNA repair capacity and genomic instability. This selectivity arises from the combination of CTD phosphorylation defects and altered regulation of pre‑mRNA processing at intronic polyadenylation sites, making long DDR genes particularly sensitive to reduced CDK12‑dependent elongation and processing. CDK12 also regulates expression of core DNA replication genes and other cell‑cycle regulators by controlling RNAPII processivity over these loci, thereby contributing to proper G1/S progression and coordination between replication and repair. In cancer, recurrent CDK12 loss‑of‑function mutations occur in high‑grade serous ovarian carcinoma, prostate cancer, and other tumor types and associate with tandem duplications, focal genomic rearrangements, and a distinct genomic instability signature that reflects defective transcription of homologous recombination genes rather than direct catalytic lesions in replication or repair enzymes.

References
https://pubmed.ncbi.nlm.nih.gov/30988284/ https://pubmed.ncbi.nlm.nih.gov/32805052/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%