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AID-generated somatic hypermutations affect the variable (V) regions of genes are transmitted only within the particular cell line (somatic) and are not transmitted to the organism's offspring of naïve B cells can be recognized by the presence of a variable
immunodeficiency. And are reminiscent of the induced by the under methylating agent 5-aza cytidine in chromosomal changes (somatic) and are not transmitted to the organism's offspring. This acceleration is
attributed to the enzyme activation-induced (cytidine) deaminase (AID). When the base excision repair enzyme uracil-DNA glycosylase (UNG2) excises uracil, error-prone DNA polymerases may causes other mutations at/near the abasic site. Somatic hypermutation (SHM) is restricted to VDJ regions and their adjacent
۞ flanks in immunoglobulin (Ig) 5’-genes integrated mechanistic model of SHM mitotic spindle checkpoints on the telomeric [? {end of chromosome 3p21.3-p21.2 in the ATRIP-RPA-ssDNA complex.}] end of Multipoint @ theta, protein kinase C (PKC), AICDA 12p13 activation-induced cytidine deaminase AID with this entry because one form of autosomal recessive hyper-IgM immunodeficiency (HIGM2) results from mutation in the gene encoding activation-induced cytidine deaminase. a synthetic dsDNA section whose 5'-to-3' sequence is identical on each DNA strand AID-catalyzed
۞ C deaminations occurs with somatic hypermutation spectra observed in vivo RPA (replication protein A 17p13.3) complexes preferentially bind to ssDNA of small transcription bubbles at somatic hypermutation hotspots. Where the function of the ATR (601215)- ATRIP (606605) protein kinase complex is crucial for the cellular response to replication stress and DNA damage. Where information has become available on how B cell activation-associated DNA-modifying events, involving activation-induced cytidine deaminase and DNA polymerase-eta [?] POLQ polymerase (DNA directed), theta, contribute to the molecular lesions that result in AIDS-associated lymphoma end of Multipoint @ theta.
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