IndraLab

Statements

BAP1 deubiquitinates H2AK119Ub. 6 / 6
| 6
reach
"cBioPortal functional prediction and our structural, biochemical, and cellular studies indicate all these mutations lead to a loss of function where BAP1/ASXL1 fails to effectively deubiquitinate H2AK119Ub, and thus causes aberrant accumulation of this chromatin modification."
36865140
reach
"Our data support a model where BAP1/ASXL1 deubiquitinates H2AK119Ub chromatin by anchoring to the nucleosomal acidic patch, DNA dyad, and the DNA exit regions using conserved arginine and lysine tracts."
36865140
reach
"These results further provide a molecular explanation for how >50 mutations in BAP1 and ASXL1 found in cancer can dysregulate H2AK119Ub deubiquitination, providing insight into understanding cancer etiology."
37556531
reach
"BAP1 deubiquitinates H2AK119Ub, regulating chromatin packing and gene expression (Scheuermann et al., 2010; Foglizzo et al., 2018)."
34818533
reach
"Our data support a model where BAP1/ASXL1 deubiquitinates H2AK119Ub chromatin by anchoring to the nucleosomal acidic patch, DNA dyad, and the DNA exit regions using conserved arginine and lysine tracts."
37556531
reach
"As is the case with the loss-of-function model, these data suggest that mutant ASXL1 inhibits PRC2 function, followed by upregulation of its target genes in a dominant-negative manner, which contribut[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
31945396