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Monkey Exonuclease Activity

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

Application Methods: Western Blotting

Background: Flap endonuclease-1 (FEN-1) is a structure-specific nuclease with multiple functions in DNA processing pathways (1,2). The replication and DNA repair activities of FEN-1 are critical for genomic stability in the eukaryotic cell. Through interaction with proliferation cell nuclear antigen (PCNA), FEN-1 helps coordinate Okazaki fragment maturation by removing RNA-DNA primers (3). FEN-1 is also required for non-homologous end joining of double stranded DNA breaks in long patch base excision repair (4,5). The multi-functional activities of FEN-1 are regulated by various mechanisms, including protein partner interactions (6,7), post-translational modifications (8,9), and subcellular re-localization in response to cell cycle or DNA damage (10).

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

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, Monkey

Application Methods: Immunoprecipitation, Western Blotting

Background: 5’-3’ exoribonuclease 1 (XRN1) is a cytoplasmic exonuclease that degrades RNA containing a 5’-monophosphate to component mononucleotides. XRN1 is the primary exonuclease associated with ribosomes in the cytoplasm and is responsible for mRNA turnover (1,2). This turnover is facilitated in discrete structures in the cytoplasm called P-bodies that contain decapping and deadenylation proteins (3). XRN1 also plays a role in RISC-mediated mRNA degradation, as it associates with 3’ mRNA fragments generated by RISC cleavage. This process does not require uncapping or deadenylation (4). XRN1 plays a significant role in viral RNA degradation (5). As such, many viral genomes, including hepatitis C, Dengue, and West Nile, encode for XRN1-resistant long non-coding RNA that affect innate immunity and viral replication (6).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey

Application Methods: Immunoprecipitation, Western Blotting

Background: DNA polymerase γ (POLG, pol gamma) is a nuclear encoded protein that is responsible for mitochondrial genome replication in eukaryotic cells. The 140 kDa polymerase γ catalytic subunit forms a holoenzyme complex with a 55 kDa accessory protein (POLG2, pol γB) dimer, which confers processivity (1). In addition to polymerase activity, polymerase γ contains 3'-5' exonuclease activity for proofreading and 5′-deoxyribonucleic phosphate lyase activity that functions in DNA base excision repair (BER). The rate at which the catalytic subunit recognizes damaged DNA during DNA repair is enhanced by the pol γB accessory subunit (2). Mutations in the corresponding POLG gene are associated with several inherited neuropathies including progressive external ophthalmoplegia, myocerebrohepatopathy spectrum disorders and Alpers-Huttenlocher syndrome (3,4). Research studies indicate that mutations in the corresponding POLG gene may promote breast tumorigenesis (5).

$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).

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

Application Methods: Immunoprecipitation, Western Blotting

Background: 5'-3' exoribonuclease 2 (XRN2) is a nuclear exonuclease that degrades RNA containing a 5’-monophosphate to component mononucleotides. XRN2 also plays an important role in the termination of transcription at the 3’-end of genes by displacing RNA polymerase II (RNAPII) from the DNA strand (1,2). According to the ‘torpedo’ model of transcription termination, XRN2 gains access to the 5’ phosphate of the nascent RNA during co-transcriptional polyadenylation site cleavage. XRN2 degrades RNA at a faster rate than RNAPII-mediated RNA synthesis, resulting in the eviction of RNAPII from the template (3-5). In addition, XRN2 is essential for maturation of 5.8S and 28S ribosomal RNA and small nucleolar RNA molecules (2). Several research studies suggest that XRN2 plays a role in the quality control check of RNA molecules. XRN2 co-transcriptionally degrades aberrant nuclear mRNA transcripts that result from defective 5’mRNA capping, splicing, or 3’end formation (6). XRN2 exonuclease rapidly degrades hypomodified tRNA and excess miRNA molecules, indicating that XRN2 likely regulates tRNA and miRNA quality control as well (7-9).

$111
20 µl
$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey

Application Methods: Western Blotting

Background: The DNA repair protein Rad50 is a member of the structural maintenance of chromosomes family (SMC) and plays an important role in cell cycle checkpoint signaling and double-strand break repair in response to DNA damage (1-4). Rad50 forms a complex with Mre11 and Nbs1 that becomes activated in response to DNA damage (3). In normal human cells, the MRN complex acts to tether linear DNA molecules, providing a flexible link between DNA ends (1). Genomic instability and cancer have been shown to develop in cells with genetic mutations affecting the proteins in the MRN complex (2). ATM-dependent phosphorylation of Rad50 at Ser635 in response to DNA damage is important in regulating downstream signaling, DNA repair and checkpoint control (5).