IndraLab

Statements


USP1 activates BRCA1. 7 / 7
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"Knockdown or inhibition of USP1 resulted in replication fork destabilization and decreased viability of BRCA1 deficient cells, revealing a synthetic lethal relationship."

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"109 Inhibition of USP1 using the small molecules I-138 and ML323 reduced the viability of BRCA1-mutated breast and ovarian cancer cell lines."

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"The above bioinformatics analysis showed that the expression of USP1 could promote the expression of homologous recombination repair related genes (FANCD2 and BRCA1), which negatively correlates with clinical outcome in patients with hepatocellular carcinoma."

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"In contrast to the overexpression, the depletion of USP1 increased the number of BRCA1 foci but decreased the number of RIF1 foci in S/G2 cells (XREF_FIG, XREF_SUPPLEMENTARY)."

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"As expected, the number of BRCA1 foci reduced dramatically in Cdh1 depleted cells treated with HU, and the simultaneous depletion of USP1 with that of Cdh1 essentially restored BRCA1 focus number (XREF_FIG)."

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"As shown in XREF_FIG, the depletion of USP1 in control cells (no ectopic USP1 expression) expectedly caused an increase of BRCA1 IRIF but a decrease of RIF1 IRIF (as seen in XREF_FIG)."

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"USP1 inhibition or PARP inhibition promoted ssDNA gaps in the BRCA1-mutated organoids but not in the BRCA1-WT organoids (Fig. 2E)."