mProX™ Human CHEK2 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 CRISPR/Cas9-mediated CHEK2 gene inactivation in CRC cell lines.
Western blot analysis verified that CHEK2KO cells had completely lost the ability to produce Chk2. Following CHEK2 KO, there was no effect on cell proliferation. This suggested that the functional characterisation of CHEK2 may be investigated using this CRISPR cell model.
Ref: Xu, Pingping, et al. "Germline mutations in a DNA repair pathway are associated with familial colorectal cancer." JCI insight 6.18 (2021).
Pubmed: 34549727
DOI: 10.1172/jci.insight.148931
Research Highlights
Hereditary cancer risk has been linked to germline mutations in numerous genes that code for proteins mediating DNA repair and DNA damage response (DDR) to double-strand breaks (DDSB).
Stolarova, Lenka, et al. "CHEK2 germline variants in cancer predisposition: stalemate rather than checkmate." Cells 9.12 (2020): 2675.
Pubmed:
33322746
DOI:
10.3390/cells9122675
While CHEK2 PVs were linked to thyroid, kidney, and breast malignancies, they were not linked to colorectal cancer. The common p.I157T, p.S428F, and p.T476M alleles were not linked to nonbreast malignancies and had a less correlation with breast cancer when compared to other CHEK2 PVs. The treatment and genetic counseling provided to people with CHEK2 PVs may benefit from these data.
Bychkovsky, Brittany L., et al. "Differences in Cancer Phenotypes Among Frequent CHEK2 Variants and Implications for Clinical Care-Checking CHEK2." JAMA oncology 8.11 (2022): 1598-1606.
Pubmed:
36136322
DOI:
10.1001/jamaoncol.2022.4071