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DNA Damage Response

DNA damage can occur for a variety of reasons. Mutations can be caused by environmental influences like chemicals, radiation, or even sunlight. Also, cells can make mistakes when replicating the DNA and making copies during cell cycle processes. DNA damage is involved in genetically inherited disorders, aging, and cancer. Maintaining an organism's genome is necessary in order to protect its integrity and assure proper functioning of the genetic material for the organism's survival. If repair mechanisms fail, the organism is at risk for many problems. In eukaryotes, there are numerous ways that DNA is protected from damage or repaired when damage is sensed. Cell cycle checkpoints govern the order and progression of cell cycle transitions in order to insure that the process is running free of errors. When errors are found, the cell cycle can be halted or discontinued in order to allow the DNA damage to be repaired. This insures that progeny cells do not inherent dangerous mutations. The G1 checkpoint is responsible for preventing damaged genetic material from being replicated. The S-phase checkpoint monitors cell-cycle progression and can decrease the rate at which DNA is synthesized if damage is sensed. G2 checkpoints can suspend the cell cycle before chromosome segregation. DNA repair takes place in a number of different processes by which a cell can correct the damage caused to DNA by many mutation sources. The ability of these repair mechanisms to function properly, however, is highly dependent on many factors like type of cell, age of cell, and environment. When DNA repair does not function properly and a cell is overrun by damage, the cell can be destroyed, become dormant, or replicate unregulated which can lead to a multitude of mutant cells causing tumors and cancers. DNA repair mechanisms include direct reversal of single strand damage or double strand breaks, and translesion synthesis. When a single strand of DNA has an error, its complimentary strand can be used to complete the correct sequence. When both strands have breaks, the ends can essentially be glued back together. This process is extremely complicated and errors and even genome arrangements can occur if it is not done correctly. Translesion synthesis involves the use of specialized polymerases that can repair lesions at locations of stalled DNA replication.

Anti-PNK antibody binds against the target polynucleotide kinase. PNK is localized in the nucleus and expressed in many tissues with the highest expression in spleen and testis. PNK catalyzes the phosphorylation of DNA at the 5 prime end and can dephosphorylate DNA at the 3 prime end. Polynucleotide kinase plays an important role in DNA repair. Defects in PNKP are the cause of microcephaly seizures and developmental delay. Microcephaly is a neurological condition that occurs when a child's brain does not develop properly. Symptoms include poor feeding, spasticity, and seizures. Anti-SNM1 antibody binds against the target SNM1. SMN1 is localized in the nucleus. SNM1 is a DNA-crosslink repair protein that responds to double-strand breaks formed by ionizing radiation and interstrand crosslinking.

Product Number Title Applications Host Clonality
AC21-0021-10 Anti-DDB1 Antibody (Cy5) ELISA, WB Goat Polyclonal
AC21-0021-11 Anti-DDB1 Antibody (Cy5.5) ELISA, WB Goat Polyclonal
AC21-0021-12 Anti-DDB1 Antibody (FITC) ELISA, WB Goat Polyclonal
AC21-0021-13 Anti-DDB1 Antibody (Glucose Oxidase) ELISA, WB Goat Polyclonal
AC21-0021-14 Anti-DDB1 Antibody (HRP) ELISA, WB Goat Polyclonal
AC21-0021-15 Anti-DDB1 Antibody (PE-Cy5) ELISA, WB Goat Polyclonal
AC21-0021-16 Anti-DDB1 Antibody (PE-Cy5.5) ELISA, WB Goat Polyclonal
AC21-0021-17 Anti-DDB1 Antibody (PE-Cy7) ELISA, WB Goat Polyclonal
AC21-0021-18 Anti-DDB1 Antibody (PerCP) ELISA, WB Goat Polyclonal
AC21-0021-19 Anti-DDB1 Antibody (PerCP-Cy5.5) ELISA, WB Goat Polyclonal
AC21-0021-20 Anti-DDB1 Antibody (Rhodamine) ELISA, WB Goat Polyclonal
AC21-0021-21 Anti-DDB1 Antibody (RPE) ELISA, WB Goat Polyclonal