These results prompt us to propose RECQL5 as a gene that would be worth to analyze in larger studies to explore its possible implication in BC susceptibility.
increased RECQ5 levels stimulated 'alternative' HDR by single-stranded DNA donors which is normally suppressed by RAD51; this was accompanied by stimulation of mutagenic end-joining. These results suggest that in some tumors RECQ5 gene amplification may have profound consequences for genomic instability
It has been shown that conjugation of SUMO2 but not SUMO1 or SUMO3 to the essential replication factor PCNA is induced on transcribed chromatin by the RNAPII-bound helicase RECQ5.
the open and closed forms of RECQL5 were used together with a quantitative comparison of all current RecQ family structures to construct a mechanistic model for RECQL5 helicase activity
we have shown that increased expression of RECQL5 protein occurs and is likely to contribute to tumourigenesis in UCC and that the pharmacological targeting of the helicase activity of RECQL5 is a strong target for future small molecule inhibitor development.
interaction between RECQ5 and proliferating cell nuclear antigen (PCNA) promotes RAD18-dependent PCNA ubiquitination and the helicase activity of RECQ5 promotes the processing of replication intermediates.
Study characterized the G-quadruplex (GQ) unfolding activity of RECQ5 for different DNA constructs under different salt conditions showed that RECQ5 is overall a weak GQ destabilizer compared to Bloom and Werner
RECQL5 is a critical regulator of genome stability in myeloproliferative neoplasms and demonstrate that replication stress-associated cytotoxicity can be amplified specifically in JAK2V617F mutant cells through RECQL5-targeted synthetic lethality.
Expression of RECQL5 in breast cancer can drive proliferation supporting an oncogenic function for RECQL5 in breast cancer. RECQL5 is a promising biomarker in breast cancer.
PARylation is involved in the recruitment of RECQL5 and WRN to laser-induced DNA damage and RECQL5 and WRN have differential responses to PARylated PARP1 and Poly(ADP-ribose).
The data presented here provide evidence that RECQL5 plays a general role in the control of transcript elongation in human cells. In its absence transcript elongation rates increase the distribution profile of RNAPII is markedly altered across the genome and higher levels of RNAPII pausing or arrest (i.e. transcription stress) are detected.
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