|Application ||WB, E|
|Calculated MW||63397 Da|
|Antigen Region||10-40 aa|
|Other Names||Poly [ADP-ribose] polymerase 2, PARP-2, mPARP-2, ADP-ribosyltransferase diphtheria toxin-like 2, ARTD2, NAD(+) ADP-ribosyltransferase 2, ADPRT-2, Poly[ADP-ribose] synthase 2, pADPRT-2, Parp2, Adprt2, Adprtl2, Aspartl2|
|Target/Specificity||This PARP2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 10-40 amino acids from the N-terminal region of human PARP2.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||PARP2 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||Adprt2, Adprtl2, Aspartl2|
|Function||Involved in the base excision repair (BER) pathway, by catalyzing the poly(ADP-ribosyl)ation of a limited number of acceptor proteins involved in chromatin architecture and in DNA metabolism (PubMed:10364231). This modification follows DNA damages and appears as an obligatory step in a detection/signaling pathway leading to the reparation of DNA strand breaks (PubMed:10364231). Mediates serine ADP-ribosylation of target proteins following interaction with HPF1; HPF1 conferring serine specificity (By similarity).|
|Tissue Location||Widely expressed; the highest levels were in testis followed by ovary. Expression is correlated with proliferation, with higher levels occurring during early fetal development and organogenesis and in the highly proliferative cell compartments of adult|
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Provided below are standard protocols that you may find useful for product applications.
PARP2 is involved in the base excision repair (BER) pathway, by catalyzing the poly(ADP-ribosyl)ation of a limited number of acceptor proteins involved in chromatin architecture and in DNA metabolism. This modification follows DNA damages and appears as an obligatory step in a detection/signaling pathway leading to the reparation of DNA strand breaks.
Brunyanszki, A., et al. J. Invest. Dermatol. 130(11):2629-2637(2010)
Toller, I.M., et al. Cancer Res. 70(14):5912-5922(2010)
Nicolas, L., et al. Oncogene 29(19):2877-2883(2010)
Li, X., et al. J. Neurochem. 113(4):1012-1022(2010)
Quenet, D., et al. Exp. Cell Res. 315(16):2824-2834(2009)
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