IndraLab

Statements

USP2 binds RECQL4. 11 / 11
2 | 2 7
sparser
"To support this notion, USP2 interacted with RECQL4 in coimmunoprecipitation experiments and NCS treatment significantly increased this interaction ( xref E )."
36436562
sparser
"The expression of helicase-defective RECQL4 mutant proteins (D605A and E606A in the Walker B motif) as well as WT RECQL4 proteins restored USP2 binding to laser-induced DSB sites in RECQL4-depleted cells."
36436562
sparser
"As shown in xref D , interaction between phospho-deficient USP2 (AA) and RECQL4 was not observed in the coimmunoprecipitation analysis."
36436562
sparser
"In contrast, phosphomimetic USP2 (EE) proteins stably interacted with RECQL4, both in the absence and presence of DNA damage ( xref D ), and inhibition of ATM kinase activity did not disrupt their interaction, although the interaction appeared to be slightly weak ( xref E )."
36436562
sparser
"Taken together, these results suggest that interaction of USP2 with RECQL4 through ATM-dependent phosphorylation of these two sites is not sufficient for the recruitment of USP2 to DSB sites."
36436562
sparser
"As shown in xref , xref , xref , USP2 stably interacted with RECQL4 in an ATM-dependent manner and recruitment of USP2 to DSB sites also requires RECQL4."
36436562
reach
"As shown in Figure 5D, interaction between phospho-deficient USP2 (AA) and RECQL4 was not observed in the coimmunoprecipitation analysis."
36436562
sparser
"Collectively, these data suggest that ATM is a key regulator for USP2 recruitment to DSB sites by phosphorylating USP2 at S2 and T137, which is essential for the interaction between USP2 and RECQL4."
36436562
reach
"Collectively, these data suggest that ATM is a key regulator for USP2 recruitment to DSB sites by phosphorylating USP2 at S2 and T137, which is essential for the interaction between USP2 and RECQL4."
36436562
biogrid
No evidence text available
36436562
biogrid
No evidence text available
36436562