Matches in SemOpenAlex for { <https://semopenalex.org/work/W4213280542> ?p ?o ?g. }
- W4213280542 endingPage "111776" @default.
- W4213280542 startingPage "111776" @default.
- W4213280542 abstract "Mitosis is the process of cell division and is regulated by checkpoints in the cell cycle. G1-S, S, and G2-M are the three main checkpoints that prevent initiation of the next phase of the cell cycle phase until previous phase has completed. DNA damage leads to activation of the G2-M checkpoint, which can trigger a downstream DNA damage response (DDR) pathway to induce cell cycle arrest while the damage is repaired. If the DNA damage cannot be repaired, the replication stress response (RSR) pathway finally leads to cell death by apoptosis, in this case called mitotic catastrophe. Many cancer treatments (chemotherapy and radiotherapy) cause DNA damages based on SSBs (single strand breaks) or DSBs (double strand breaks), which cause cell death through mitotic catastrophe. However, damaged cells can activate WEE1 kinase (as a part of the DDR and RSR pathways), which prevents apoptosis and cell death by inducing cell cycle arrest at G2 phase. Therefore, inhibition of WEE1 kinase could sensitize cancer cells to chemotherapeutic drugs. This review focuses on the role of WEE1 kinase (as a biological macromolecule which has a molecular mass of 96 kDa) in the cell cycle, and its interactions with other regulatory pathways. In addition, we discuss the potential of WEE1 inhibition as a new therapeutic approach in the treatment of various cancers, such as melanoma, breast cancer, pancreatic cancer, cervical cancer, etc." @default.
- W4213280542 created "2022-02-24" @default.
- W4213280542 creator A5001374433 @default.
- W4213280542 creator A5011842204 @default.
- W4213280542 creator A5018840587 @default.
- W4213280542 creator A5021561644 @default.
- W4213280542 creator A5039909451 @default.
- W4213280542 creator A5041732327 @default.
- W4213280542 creator A5053089824 @default.
- W4213280542 creator A5057379777 @default.
- W4213280542 creator A5064003008 @default.
- W4213280542 creator A5073639155 @default.
- W4213280542 creator A5083649866 @default.
- W4213280542 date "2022-01-01" @default.
- W4213280542 modified "2023-10-11" @default.
- W4213280542 title "Cell cycle involvement in cancer therapy; WEE1 kinase, a potential target as therapeutic strategy" @default.
- W4213280542 cites W1268875343 @default.
- W4213280542 cites W136863196 @default.
- W4213280542 cites W1495609430 @default.
- W4213280542 cites W1553367038 @default.
- W4213280542 cites W1565539350 @default.
- W4213280542 cites W1620318121 @default.
- W4213280542 cites W1790548656 @default.
- W4213280542 cites W1845168065 @default.
- W4213280542 cites W1965239527 @default.
- W4213280542 cites W1967878199 @default.
- W4213280542 cites W1968563045 @default.
- W4213280542 cites W1979898579 @default.
- W4213280542 cites W1980130462 @default.
- W4213280542 cites W1981494266 @default.
- W4213280542 cites W1984283750 @default.
- W4213280542 cites W1991054314 @default.
- W4213280542 cites W1991199800 @default.
- W4213280542 cites W1991917259 @default.
- W4213280542 cites W1992689141 @default.
- W4213280542 cites W1993546170 @default.
- W4213280542 cites W1994107958 @default.
- W4213280542 cites W2001507329 @default.
- W4213280542 cites W2001997645 @default.
- W4213280542 cites W2002661091 @default.
- W4213280542 cites W2006043249 @default.
- W4213280542 cites W2006289717 @default.
- W4213280542 cites W2006705023 @default.
- W4213280542 cites W2010289373 @default.
- W4213280542 cites W2010468994 @default.
- W4213280542 cites W2015044019 @default.
- W4213280542 cites W2021278812 @default.
- W4213280542 cites W2021347119 @default.
- W4213280542 cites W2030618323 @default.
- W4213280542 cites W2030774185 @default.
- W4213280542 cites W2030864103 @default.
- W4213280542 cites W2032629746 @default.
- W4213280542 cites W2033086926 @default.
- W4213280542 cites W2039493713 @default.
- W4213280542 cites W2040091286 @default.
- W4213280542 cites W2040273468 @default.
- W4213280542 cites W2042097047 @default.
- W4213280542 cites W2046860085 @default.
- W4213280542 cites W2047114542 @default.
- W4213280542 cites W2047724766 @default.
- W4213280542 cites W2054261736 @default.
- W4213280542 cites W2054626432 @default.
- W4213280542 cites W2056658675 @default.
- W4213280542 cites W2060821036 @default.
- W4213280542 cites W2064221650 @default.
- W4213280542 cites W2068972095 @default.
- W4213280542 cites W2069881137 @default.
- W4213280542 cites W2074140569 @default.
- W4213280542 cites W2075176849 @default.
- W4213280542 cites W2075751250 @default.
- W4213280542 cites W2077548113 @default.
- W4213280542 cites W2078826308 @default.
- W4213280542 cites W2078909694 @default.
- W4213280542 cites W2084566512 @default.
- W4213280542 cites W2085388752 @default.
- W4213280542 cites W2086255242 @default.
- W4213280542 cites W2089353165 @default.
- W4213280542 cites W2091841161 @default.
- W4213280542 cites W2094980313 @default.
- W4213280542 cites W2100963721 @default.
- W4213280542 cites W2101601609 @default.
- W4213280542 cites W2103957625 @default.
- W4213280542 cites W2107495112 @default.
- W4213280542 cites W2107661677 @default.
- W4213280542 cites W2111222453 @default.
- W4213280542 cites W2112521155 @default.
- W4213280542 cites W2120459950 @default.
- W4213280542 cites W2122032760 @default.
- W4213280542 cites W2127806929 @default.
- W4213280542 cites W2129695021 @default.
- W4213280542 cites W2134175830 @default.
- W4213280542 cites W2137450457 @default.
- W4213280542 cites W2153655604 @default.
- W4213280542 cites W2155426995 @default.
- W4213280542 cites W2155638473 @default.
- W4213280542 cites W2160005077 @default.
- W4213280542 cites W2162730779 @default.
- W4213280542 cites W2163530629 @default.