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Monoclonal Antibody Western Blotting 3'-5'-exodeoxyribonuclease Activity

$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Immunoprecipitation, Western Blotting

Background: TREX1 is a broadly expressed 3’ to 5’ exonuclease that acts on single-stranded DNA (ssDNA) to negatively regulate the interferon-stimulatory DNA (ISD) response (1-4). In humans, there are three TREX1 isoforms generated through alternative splicing with predicted molecular weights of 32, 33, and 39 kDa (2). The transcript for the 33 kDa isoform is the most abundant (2). Mice deficient in TREX1 accumulate intracellular ssDNA, which triggers the ISD response and eventually lethal autoimmunity (3,4). Mutations in TREX1 are associated with autoimmune diseases including Aicardi-Goutieres syndrome and systemic lupus erythematosus (5,6). In addition, TREX1 prevents the cell-intrinsic innate immune response to human immunodeficiency virus (HIV) by digesting excess HIV DNA that would normally trigger induction of type I interferon (7).

$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Western Blotting

Background: DNA damage resulting from genotoxic stress activates cellular checkpoints that prevent or delay cell division until either damaged DNA is repaired or the cell follows an apoptotic pathway. The Rad9 homolog A (Rad9A, Rad9) protein is part of a checkpoint protein complex that acts as an early sensor of DNA damage. Together with the Hus1 and Rad1 checkpoint proteins, Rad9 forms a heterotrimeric 9-1-1 complex with a ring structure similar to the processivity factor PCNA. The 9-1-1 complex induces multiple signaling pathways, including the ATM and ATR-activated DNA repair pathways (1,2). A functional 9-1-1 complex is required for ATR-dependent S phase checkpoint signaling (3).The 9-1-1 complex interacts with DNA topoisomerase 2-binding protein 1 (TopBP1) in response to DNA damage, activating ATR and causing signal amplification through further recruitment of TopBP1 (4). The 9-1-1 complex interacts with DNA mismatch repair proteins MSH2, MSH3, and MSH6 to play a role in mismatch repair (5). During an error-free DNA damage tolerance process, the 9-1-1 complex cooperates with polyubiquitinated PCNA and Exo1 nuclease to support switching of the replicative polymerase to the undamaged template (6).Research studies indicate that the two Rad9 paralogues (Rad9A and Rad9B) can both functionally complement one another and display distinct biological functions.Specifically, Rad9B senses nucleolar stress and causes a delay in the cell cycle at G1/S phase (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).