FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4387142675> ?p ?o ?g. }

• W4387142675 endingPage "168294" @default.
• W4387142675 startingPage "168294" @default.
• W4387142675 abstract "Faithful genome duplication is a challenging task for dividing mammalian cells, particularly under replication stress where timely resolution of late replication intermediates (LRIs) becomes crucial prior to cell division. In human cancer cells, mitotic DNA repair synthesis (MiDAS) is described as a final mechanism for the resolution of LRIs to avoid lethal chromosome mis-segregation. RAD52-driven MiDAS achieves this mission in part by generating gaps/breaks on metaphase chromosomes, which preferentially occur at common fragile sites (CFS). We previously demonstrated that a MiDAS mechanism also exists in untransformed and primary human cells, which is RAD52 independent but requires FANCD2. However, the properties of this form of MiDAS are not well understood. Here, we report that FANCD2-driven MiDAS in untransformed human cells: 1) requires a prerequisite step of FANCD2 mono-ubiquitination by a subset of Fanconi anemia (FA) proteins, 2) primarily acts to preserve CFS stability but not to prevent chromosome mis-segregation, and 3) depends on HELQ, which potentially functions at an early step. Hence, FANCD2-driven MiDAS in untransformed cells is built to protect CFS stability, whereas RAD52-driven MiDAS in cancer cells is likely adapted to prevent chromosome mis-segregation at the cost of CFS expression. Notably, we also identified a novel form of MiDAS, which surfaces to function when FANCD2 is absent in untransformed cells. Our findings substantiate the complex nature of MiDAS and a link between its deficiencies and the pathogenesis of FA, a human genetic disease." @default.
• W4387142675 created "2023-09-29" @default.
• W4387142675 creator A5002907157 @default.
• W4387142675 creator A5056199605 @default.
• W4387142675 creator A5061007251 @default.
• W4387142675 creator A5084692613 @default.
• W4387142675 creator A5089175580 @default.
• W4387142675 creator A5092962366 @default.
• W4387142675 creator A5092962367 @default.
• W4387142675 creator A5092962368 @default.
• W4387142675 date "2023-11-01" @default.
• W4387142675 modified "2023-10-15" @default.
• W4387142675 title "Mitotic DNA synthesis in untransformed human cells preserves common fragile site stability via a FANCD2-driven mechanism that requires HELQ" @default.
• W4387142675 cites W1965749659 @default.
• W4387142675 cites W1966302019 @default.
• W4387142675 cites W1968245004 @default.
• W4387142675 cites W1974993967 @default.
• W4387142675 cites W1978947118 @default.
• W4387142675 cites W1987316571 @default.
• W4387142675 cites W1991841649 @default.
• W4387142675 cites W2002060477 @default.
• W4387142675 cites W2003058744 @default.
• W4387142675 cites W2006303534 @default.
• W4387142675 cites W2010787386 @default.
• W4387142675 cites W2015969693 @default.
• W4387142675 cites W2016294195 @default.
• W4387142675 cites W2024073282 @default.
• W4387142675 cites W2025555587 @default.
• W4387142675 cites W2026877007 @default.
• W4387142675 cites W2028637581 @default.
• W4387142675 cites W2043051674 @default.
• W4387142675 cites W2043828851 @default.
• W4387142675 cites W2049576185 @default.
• W4387142675 cites W2052483270 @default.
• W4387142675 cites W2063693599 @default.
• W4387142675 cites W2067207497 @default.
• W4387142675 cites W2067573570 @default.
• W4387142675 cites W2070879510 @default.
• W4387142675 cites W2073031672 @default.
• W4387142675 cites W2078852555 @default.
• W4387142675 cites W2079987545 @default.
• W4387142675 cites W2082978061 @default.
• W4387142675 cites W2083158919 @default.
• W4387142675 cites W2084310601 @default.
• W4387142675 cites W2085909080 @default.
• W4387142675 cites W2087634145 @default.
• W4387142675 cites W2101185225 @default.
• W4387142675 cites W2107632586 @default.
• W4387142675 cites W2114907977 @default.
• W4387142675 cites W2115626825 @default.
• W4387142675 cites W2125047184 @default.
• W4387142675 cites W2138204634 @default.
• W4387142675 cites W2147937291 @default.
• W4387142675 cites W2153314251 @default.
• W4387142675 cites W2161854614 @default.
• W4387142675 cites W2161897911 @default.
• W4387142675 cites W2162561014 @default.
• W4387142675 cites W2166834621 @default.
• W4387142675 cites W2187574279 @default.
• W4387142675 cites W2260252265 @default.
• W4387142675 cites W2353728735 @default.
• W4387142675 cites W2561547057 @default.
• W4387142675 cites W2563646853 @default.
• W4387142675 cites W2564798923 @default.
• W4387142675 cites W2566709727 @default.
• W4387142675 cites W2613072143 @default.
• W4387142675 cites W2620853354 @default.
• W4387142675 cites W2735425869 @default.
• W4387142675 cites W2766485883 @default.
• W4387142675 cites W2783847765 @default.
• W4387142675 cites W2784483500 @default.
• W4387142675 cites W2793600083 @default.
• W4387142675 cites W2809511022 @default.
• W4387142675 cites W2903449267 @default.
• W4387142675 cites W2946653431 @default.
• W4387142675 cites W2948817675 @default.
• W4387142675 cites W2952849134 @default.
• W4387142675 cites W2953679327 @default.
• W4387142675 cites W2981159647 @default.
• W4387142675 cites W2995654684 @default.
• W4387142675 cites W3006263696 @default.
• W4387142675 cites W3011361504 @default.
• W4387142675 cites W3011378589 @default.
• W4387142675 cites W3039779782 @default.
• W4387142675 cites W3046854097 @default.
• W4387142675 cites W3089297481 @default.
• W4387142675 cites W3118084285 @default.
• W4387142675 cites W3134972677 @default.
• W4387142675 cites W3154159901 @default.
• W4387142675 cites W3160242511 @default.
• W4387142675 cites W3167903794 @default.
• W4387142675 cites W3171501889 @default.
• W4387142675 cites W3196485964 @default.
• W4387142675 cites W3197809966 @default.
• W4387142675 cites W3214654448 @default.
• W4387142675 cites W4200252861 @default.
• W4387142675 cites W4220720306 @default.
• W4387142675 cites W4224210737 @default.

• next