Sort   by:  
 Page size 
DNA double-strand breaks (DSBs) represent a threat to the genome because they can lead to loss of genetic information and chromosome rearrangements. The DNA repair protein p53 binding protein 1 (53BP1) protects the genome by limiting nucleolytic processing of DSBs by a mechanism that requires its ph...
ORGANISM(S): Mus musculus 
Activation induced cytidine deaminase (AID) initiates antibody gene diversification by creating U:G mismatches. However, AID is not specific for antibody genes. Off-target lesions can activate oncogenes or cause chromosome translocations. Despite its importance in these key transactions little is kn...
ORGANISM(S): Mus musculus 
Precisely how AID is recruited to these off-target sites is not entirely understood. To gain further insight into how AID selects its targets we compared AID-mediated translocations in two different cell types, B cells and mouse embryonic fibroblasts (MEFs). AID targets a distinct set of hotspots in...
ORGANISM(S): Mus musculus 
Programmed genetic rearrangements in lymphocytes require transcription at antigen receptor genes to promote accessibility for initiating double-strand break (DSB) formation critical for DNA recombination and repair. Here we show that activated B cells deficient in the PTIP component of the MLL3 (mix...
ORGANISM(S): Mus musculus 
Absence of 53BP1 influences the profile of DNA rearrangements in B lymphocytes.To determine whether the differences in translocation partner choice were due to differences in transcription, we compared the transcriptome of 53BP1 deficient and wild-type B cells by RNA-Seq and Polymerase II chromatin ...
ORGANISM(S): Mus musculus 
The antibody gene mutator AID promiscuously damages oncogenes and B cell identity genes leading to chromosomal translocations and tumorigenesis. Why non-immunoglobulin loci are susceptible to AID activity is unknown. Here we study AID-mediated lesions in the context of nuclear architecture and the B...
ORGANISM(S): Mus musculus 
Sort   by:  
 Page size