In base excision repair, an altered base is removed by a DNA glycosylase enzyme, followed by excision of the resulting sugar phosphate. The small gap left in the DNA helix is filled in by the sequential action of DNA polymerase and DNA ligase.

The repair of double-strand breaks in DNA via homologous and nonhomologous mechanisms to reform a continuous DNA helix.

Any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a stimulus indicating damage to its DNA from environmental insults or errors during metabolism.

The process of creating protein oligomers, compounds composed of a small number, usually between three and ten, of identical component monomers. Oligomers may be formed by the polymerization of a number of monomers or the depolymerization of a large protein polymer.

An instance of double-strand break repair via nonhomologous end joining that is independent of factors important for V(D)J recombination (as opposed to classical nonhomologous end joining). It often results in a deletion with microhomology (i.e. 5-25bp homology) at the repair junction. Among different subclasses of nonhomologous end joining (NHEJ), alternative NHEJ appears to play a significant role in the etiology of mutations that arise during cancer development and treatment.

Any process that stops, prevents, or reduces the frequency, rate or extent of double-strand break repair via homologous recombination.

The process of restoring DNA after damage. Genomes are subject to damage by chemical and physical agents in the environment (e.g. UV and ionizing radiations, chemical mutagens, fungal and bacterial toxins, etc.) and by free radicals or alkylating agents endogenously generated in metabolism. DNA is also damaged because of errors during its replication. A variety of different DNA repair pathways have been reported that include direct reversal, base excision repair, nucleotide excision repair, photoreactivation, bypass, double-strand break repair pathway, and mismatch repair pathway.

The process of restoring DNA after damage. Genomes are subject to damage by chemical and physical agents in the environment (e.g. UV and ionizing radiations, chemical mutagens, fungal and bacterial toxins, etc.) and by free radicals or alkylating agents endogenously generated in metabolism. DNA is also damaged because of errors during its replication. A variety of different DNA repair pathways have been reported that include direct reversal, base excision repair, nucleotide excision repair, photoreactivation, bypass, double-strand break repair pathway, and mismatch repair pathway.

The process of restoring DNA after damage. Genomes are subject to damage by chemical and physical agents in the environment (e.g. UV and ionizing radiations, chemical mutagens, fungal and bacterial toxins, etc.) and by free radicals or alkylating agents endogenously generated in metabolism. DNA is also damaged because of errors during its replication. A variety of different DNA repair pathways have been reported that include direct reversal, base excision repair, nucleotide excision repair, photoreactivation, bypass, double-strand break repair pathway, and mismatch repair pathway.

In base excision repair, an altered base is removed by a DNA glycosylase enzyme, followed by excision of the resulting sugar phosphate. The small gap left in the DNA helix is filled in by the sequential action of DNA polymerase and DNA ligase.

The repair of double-strand breaks in DNA via homologous and nonhomologous mechanisms to reform a continuous DNA helix.

Any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a stimulus indicating damage to its DNA from environmental insults or errors during metabolism.

Mutations occurring somatically that result in amino acid changes in the rearranged V regions of immunoglobulins.

Mutations occurring somatically that result in amino acid changes in the rearranged V regions of immunoglobulins.

The process of creating protein oligomers, compounds composed of a small number, usually between three and ten, of identical component monomers. Oligomers may be formed by the polymerization of a number of monomers or the depolymerization of a large protein polymer.

An instance of double-strand break repair via nonhomologous end joining that is independent of factors important for V(D)J recombination (as opposed to classical nonhomologous end joining). It often results in a deletion with microhomology (i.e. 5-25bp homology) at the repair junction. Among different subclasses of nonhomologous end joining (NHEJ), alternative NHEJ appears to play a significant role in the etiology of mutations that arise during cancer development and treatment.

Any process that stops, prevents, or reduces the frequency, rate or extent of double-strand break repair via homologous recombination.

The error-free repair of a double-strand break in DNA in which the broken DNA molecule is repaired using homologous sequences. A strand in the broken DNA searches for a homologous region in an intact chromosome to serve as the template for DNA synthesis. The restoration of two intact DNA molecules results in the exchange, reciprocal or nonreciprocal, of genetic material between the intact DNA molecule and the broken DNA molecule.

The process of restoring DNA after damage. Genomes are subject to damage by chemical and physical agents in the environment (e.g. UV and ionizing radiations, chemical mutagens, fungal and bacterial toxins, etc.) and by free radicals or alkylating agents endogenously generated in metabolism. DNA is also damaged because of errors during its replication. A variety of different DNA repair pathways have been reported that include direct reversal, base excision repair, nucleotide excision repair, photoreactivation, bypass, double-strand break repair pathway, and mismatch repair pathway.

In base excision repair, an altered base is removed by a DNA glycosylase enzyme, followed by excision of the resulting sugar phosphate. The small gap left in the DNA helix is filled in by the sequential action of DNA polymerase and DNA ligase.

A DNA repair process in which a small region of the strand surrounding the damage is removed from the DNA helix as an oligonucleotide. The small gap left in the DNA helix is filled in by the sequential action of DNA polymerase and DNA ligase. Nucleotide excision repair recognizes a wide range of substrates, including damage caused by UV irradiation (pyrimidine dimers and 6-4 photoproducts) and chemicals (intrastrand cross-links and bulky adducts).

The repair of double-strand breaks in DNA via homologous and nonhomologous mechanisms to reform a continuous DNA helix.

Any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a stimulus indicating damage to its DNA from environmental insults or errors during metabolism.

Removal of a DNA interstrand crosslink (a covalent attachment of DNA bases on opposite strands of the DNA) and restoration of the DNA. DNA interstrand crosslinks occur when both strands of duplex DNA are covalently tethered together (e.g. by an exogenous or endogenous agent), thus preventing the strand unwinding necessary for essential DNA functions such as transcription and replication.

The process of creating protein oligomers, compounds composed of a small number, usually between three and ten, of identical component monomers. Oligomers may be formed by the polymerization of a number of monomers or the depolymerization of a large protein polymer.

An instance of double-strand break repair via nonhomologous end joining that is independent of factors important for V(D)J recombination (as opposed to classical nonhomologous end joining). It often results in a deletion with microhomology (i.e. 5-25bp homology) at the repair junction. Among different subclasses of nonhomologous end joining (NHEJ), alternative NHEJ appears to play a significant role in the etiology of mutations that arise during cancer development and treatment.

An instance of double-strand break repair via nonhomologous end joining that is independent of factors important for V(D)J recombination (as opposed to classical nonhomologous end joining). It often results in a deletion with microhomology (i.e. 5-25bp homology) at the repair junction. Among different subclasses of nonhomologous end joining (NHEJ), alternative NHEJ appears to play a significant role in the etiology of mutations that arise during cancer development and treatment.

Any process that stops, prevents, or reduces the frequency, rate or extent of double-strand break repair via homologous recombination.

That part of the nuclear content other than the chromosomes or the nucleolus.