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Monoclonal Antibody Endodeoxyribonuclease Activity

Also showing Monoclonal Antibody Western Blotting Endodeoxyribonuclease Activity

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey, Rat

Application Methods: Western Blotting

Background: DNA repair systems operate in all living cells to manage a variety of DNA lesions. Nucleotide excision repair (NER) is implemented in cases where bulky helix-distorting lesions occur, such as those brought about by UV and certain chemicals (1). Excision Repair Cross Complementing 4 (ERCC4, XPF) forms a complex with the ERCC1 excision repair protein to create an essential 5’ endonuclease responsible for lesion excision (2). ERCC1-XPF is also required for repair of DNA interstrand crosslinks (ICLs) (3) and involved in repair of double strand breaks (4). Mutations in the corresponding XPF gene cause specific forms of xeroderma pigmentosum, Cockayne syndrome, and Fanconi anemia, while altered XPF protein levels may be associated with disease progression and response to treatment in specific human cancers (5,6).

$111
20 µl
$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Immunohistochemistry (Frozen), Immunohistochemistry (Paraffin), Immunoprecipitation, Western Blotting

Background: Mre11, originally described in genetic screens from the yeast Saccharomyces cerevisiae in which mutants were defective in meiotic recombination (1), is a central part of a multisubunit nuclease composed of Mre11, Rad50 and Nbs1 (MRN) (2,3). The MRN complex plays a critical role in sensing, processing and repairing DNA double strand breaks. Defects lead to genomic instability, telomere shortening, aberrant meiosis and hypersensitivity to DNA damage (4). Hypomorphic mutations of Mre11 are found in ataxia-telangiectasia-like disease (ATLD), with phenotypes similar to mutations in ATM that cause ataxia-telangiectasia (A-T), including a predisposition to malignancy in humans (5). Cellular consequences of ATLD include chromosomal instability and defects in the intra-S phase and G2/M checkpoints in response to DNA damage. The MRN complex may directly activate the ATM checkpoint kinase at DNA breaks (6).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse, Rat

Application Methods: Immunofluorescence (Immunocytochemistry), Immunohistochemistry (Paraffin), Western Blotting

Background: Ape1 (Apurinic/Apyrimidic eEndonuclease 1), also known as Ref1 (Redox effector factor 1), is a multifunctional protein with several biological activities. These include roles in DNA repair and in the cellular response to oxidative stress. Ape1 initiates the repair of abasic sites and is essential for the base excision repair (BER) pathway (1). Repair activities of Ape1 are stimulated by interaction with XRCC1 (2), another essential protein in BER. Ape1 functions as a redox factor that maintains transcription factors in an active, reduced state but can also function in a redox-independent manner as a transcriptional cofactor to control different cellular fates such as apoptosis, proliferation and differentiation (3). Increased expression of Ape1 is associated with many types of cancers including cervical, ovarian, prostate, rhabdomyosarcomas and germ cell tumors (4). Ape1 has been shown to stimulate DNA binding of several transcription factors known to be involved in tumor progression such as Fos, Jun, NF-κB, PAX, HIF-1, HLF and p53 (4). Mutation of the Ape1 gene has also been associated with amyotrophic lateral sclerosis (ALS) (5,6).

$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Western Blotting

Background: DNA repair systems operate in all living cells to manage a variety of DNA lesions. Nucleotide excision repair (NER) is implemented in cases where bulky helix-distorting lesions occur, such as those brought about by UV and certain chemicals (1). Excision Repair Cross Complementing 1 (ERCC1) forms a complex with ERCC4/XPF, which acts as the 5’ endonuclease required to excise the lesion (2). ERCC1-XPF is also required for repair of DNA interstrand crosslinks (ICLs) (3) and involved in repair of double strand breaks (4). Research studies have shown that expression of ERCC1 is related to survival rate and response to chemotherapeutic drugs in several human cancers including non-small cell lung cancer (NSCLC) (5,6).

$129
20 µl
$303
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey, Mouse, Rat

Application Methods: Immunohistochemistry (Paraffin), Western Blotting

Background: DNA repair systems operate in all living cells to manage a variety of DNA lesions. Nucleotide excision repair (NER) is implemented in cases where bulky helix-distorting lesions occur, such as those brought about by UV and certain chemicals (1). Excision Repair Cross Complementing 1 (ERCC1) forms a complex with ERCC4/XPF, which acts as the 5’ endonuclease required to excise the lesion (2). ERCC1-XPF is also required for repair of DNA interstrand crosslinks (ICLs) (3) and involved in repair of double strand breaks (4). Research studies have shown that expression of ERCC1 is related to survival rate and response to chemotherapeutic drugs in several human cancers including non-small cell lung cancer (NSCLC) (5,6).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey

Application Methods: Western Blotting

Background: DNA damage checkpoints are critical for regulated repair of damaged DNA and genome maintenance. CtIP/RBBP8 (CtBP-interacting protein), initially characterized as a binding partner for the trancription factor CtBP, has emerged as a regulator of both cell cycle progression and repair of DNA double strand breaks (DSB). Along with the DSB-sensing MRN complex (MRE11-RAD50-NBS1), CtIP functions in the generation of single stranded DNA at DSBs, a process required for signaling to DNA repair machinery (reviewed in 1). CtIP is thought to be critical in the transition between sensing of DSBs and repair by homologous recombination (HR) (2,3).In addition to HR, DSBs can also be repaired through nonhomologous end joining (NHEJ), and CtIP has been shown to have a role in signaling to the NHEJ pathway independently of its function in DSB end resection (4).CtIP is also involved in cellular tolerence of topoisomerase inhibitors camptothecin and etoposide, which are used to treat cancer through their ability to introduce DSBs in cycling cells (5).

$122
20 µl
$293
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey, Mouse, Rat

Application Methods: Immunofluorescence (Immunocytochemistry), Immunoprecipitation, Western Blotting

Background: Ribosomal protein S3 (rpS3) is a component of the 40S ribosomal subunit and is involved in translation. HSP90 interacts with both the amino-terminus and carboxy-terminus of rpS3, preventing its ubiquitination and degradation and thereby retaining the integrity of the ribosome (1). rpS3 has also been shown to function as an endonuclease during DNA damage repair (2,3). Furthermore, overexpression of rpS3 sensitizes lymphocytic cells to cytokine-induced apoptosis, indicating a third role for rpS3 during apoptosis (4). The functions of rpS3 during DNA damage repair and apoptosis have been mapped to two distinct domains (4).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey, Mouse, Rat

Application Methods: Immunoprecipitation, Western Blotting

Background: DNA double-strand breaks (DSBs) are potentially hazardous lesions that can be induced by ionizing radiation (IR), radiomimetic chemicals, or DNA replication inhibitors. Cells sense and repair DSBs via two distinct but partly overlapping signaling pathways, nonhomologous end joining (NHEJ) and homologous recombination (HR). Research studies have shown that defects in both pathways are associated with human disease, including cancer (reviewed in 1).DSBs that arise during S or G2 phase are repaired via homologous recombination (HR), using the replicated sister chromatid as a repair template. Rad51 recombinase, a eukaryotic homologue of E. coli RecA, polymerizes and forms a filament along single-stranded DNA, mediating HR with the help of auxiliary proteins, including Rad54 and BRCA2 (reviewed in 2,3). BRCA2 binds Rad51 and targets it to single-stranded DNA, allowing it to displace replication protein A (RPA) (4). Five Rad51 paralogs exist in vertebrates (XRCC2, XRCC3, Rad51B, Rad51C, and Rad51D) and they all appear to be required for efficient HR (5).Researchers have found that mutations in the Rad51 gene may be related to breast cancer risk (6). Some studies have implicated Rad51 as a potential marker for pancreatic cancer (7).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey

Application Methods: Immunoprecipitation, Western Blotting

Background: DNA double-strand breaks (DSBs) are potentially hazardous lesions that can be induced by ionizing radiation (IR), radiomimetic chemicals, or DNA replication inhibitors. Cells recognize and repair DSBs via two distinct but partly overlapping signaling pathways, nonhomologous end joining (NHEJ) and homologous recombination (HR). DNA repair via the HR pathway is restricted to S and G2 phases of the cell cycle, while NHEJ can occur during any phase. Defects in both pathways have been associated with human disease, including cancer (1).Artemis is a ubiquitously expressed NHEJ factor that exhibits endonuclease activity. Artemis functions in DNA repair by promoting nonhomologous end joining (2), as well as in cell cycle checkpoint control through ATM/ATR signaling (3).NHEJ machinery is also utilized in V(D)J recombination, a process that generates diversity in immunoglobulin and T cell receptor genes, and artemis is a key factor in this process (4,5). Mutations in the corresponding artemis gene (DCLRE1C) are associated with a radiosensitive type of severe combined immunodeficiency (SCID) in humans (6,7).