大量研究表明，癌症是由基因突变引起，基因突变可以由致癌剂引起，也可由DNA代谢过程中产生的碱基错配引起。为了确保遗传物质的完整和稳定，细胞有许多防止基因突变的系统，其中包括切除修复、直接修复、重组修复和错配修复。DNA损伤修复系统不仅通过矫正在DNA重组和复制过程中产生的碱基错配而保持基因组的稳定性，而且通过诱导DNA损伤细胞的凋亡而消除由突变细胞生长形成的癌变。

Novus提供大量与DNA损伤和修复研究相关的产品，方便广大科研用户。

产品引用文献：

1. [53BP1 Antibody NB100-904] Coleman KA, Greenberg RA. The BRCA1-RAP80 complex regulates DNA repair mechanism utilization by restricting end resection. J Biol Chem. 2011 Feb 18. [PMID 21335604]
2. [53BP1 Antibody NB100-904] Zhang Y-W, Regairaz M, Seiler JA, et al. Poly(ADP-ribose) polymerase and XPF- ERCC1 participate in distinct pathways for the repair of topoisomerase I-induced DNA damage in mammalian cells. Nucleic Acids Res. 2011.[PMID 21227924]
3. [53BP1 Antibody NB100-304] Zhang M, Atkinson RL, Rosen JM. Selective targeting of radiation-resistanttumor-initiating cells. Proc Natl Acad Sci U S A. 2010 Feb 23;107(8):3522-7. [PMID: 20133717]
4. [Blooms Syndrome Protein Blm Antibody (NBP1-46851] Rao VA, Fan AM, Meng L, Doe CF, North PS, Hickson ID, Pommier Y. Phosphorylation of BLM, dissociation from topoisomerase IIIalpha, and colocalization with gamma-H2AX after topoisomerase I-induced replication damage. Mol Cell Biol. 2005 Oct;25(20):8925-37.
5. [Blooms Syndrome Protein Blm Antibody NBP1-46851] Shimura T, Torres MJ, Martin MM, Rao VA, Pommier Y, Katsura M, Miyagawa K, Aladjem MI. Bloom’s syndrome helicase and Mus81 are required to induce transient double-strand DNA breaks in response to DNA replication stress. J Mol Biol. 2008 Jan 25;375(4):1152-64.
6. [FANCD2 Antibody NB100-182] Lyakhovich A, Surrallés J. Constitutive activation of caspase-3 and Poly ADP ribose polymerase cleavage in fanconi anemia cells. Mol Cancer Res. 2010 Jan;8(1):46-56. [PMID: 20068062]
7. [Ogg1 Antibody NB100-106] Karihtala P, Kauppila S, Puistola U, Jukkola-Vuorinen A. Absence of the DNA repair enzyme human 8-oxoguanine glycosylase is associated with an aggressive breast cancer phenotype. Br J Cancer. 2011 Nov 22. [PMID 22108520]

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