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Anti-CtIP (Ser326) Antibody
Our Anti-CtIP (Ser326) rabbit polyclonal phosphospecific primary antibody from PhosphoSolutions is p
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q99708 |
|---|---|
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | 101942 Da |
| Gene ID | 5932 |
|---|---|
| Other Names | COM1 antibody, COM1_HUMAN antibody, CtBP interacting protein antibody, CtBP-interacting protein antibody, CtIP antibody, DNA endonuclease RBBP8 antibody, JWDS antibody, RB binding protein 8 endonuclease antibody, RBBP-8 antibody, RBBP8 antibody, Retinoblastoma-binding protein 8 antibody, Retinoblastoma-interacting protein and myosin-like antibody, Rim antibody, SAE2 antibody, SCKL2 antibody, Sporulation in the absence of SPO11 protein 2 homolog antibody |
| Target/Specificity | CtIP, C-terminal binding protein-interacting protein, is a DNA endonuclease activated by double stranded breaks (DSBs). DSB repairs can be performed by either one of two mechanisms; non-homologous end joining (NHEJ) or homologous recombination (HR). NHEJ is the predominant DSB repair pathway throughout the entire cell cycle, most importantly in the G1 phase (Rothkamm et al, 2003); while HR is important for repairing DSBs in S and G2 phases (Beucher et al, 2009). CtIP controls DSB resection; an event that only occurs in HR during G2-phase. Phosphorylation of Thr-847 dictates the resection efficiency (Huertas et al, 2008). Furthermore, it has been found that DSBs undergo resection and repair in G1-phase cells via a process requiring Plk3 phosphorylation of CtIP at Ser-327 and Thr-847 (Barton et al, 2014). Several additional phosphorylation sites within CtIP have been identified, but their significance in the repair of DNA have yet to be determined. |
| Format | Antigen Affinity Purified from Pooled Serum |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | Anti-CtIP (Ser326) Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Shipping | Blue Ice |
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Provided below are standard protocols that you may find useful for product applications.
Background
CtIP, C-terminal binding protein-interacting protein, is a DNA endonuclease activated by double stranded breaks (DSBs). DSB repairs can be performed by either one of two mechanisms; non-homologous end joining (NHEJ) or homologous recombination (HR). NHEJ is the predominant DSB repair pathway throughout the entire cell cycle, most importantly in the G1 phase (Rothkamm et al, 2003); while HR is important for repairing DSBs in S and G2 phases (Beucher et al, 2009). CtIP controls DSB resection; an event that only occurs in HR during G2-phase. Phosphorylation of Thr-847 dictates the resection efficiency (Huertas et al, 2008). Furthermore, it has been found that DSBs undergo resection and repair in G1-phase cells via a process requiring Plk3 phosphorylation of CtIP at Ser-327 and Thr-847 (Barton et al, 2014). Several additional phosphorylation sites within CtIP have been identified, but their significance in the repair of DNA have yet to be determined.
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