mProX™ Human MAP2K1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 Western blot analysis of parental.
In the cetuximab-sensitive CRC cell line DiFi, expression of MAP2K1/MEK1 P124S and wild-type MAP2K1/MEK1 demonstrated that the mutation restored ERK phosphorylation and validated it as a novel driver of acquired cetuximab resistance.
Ref: Knebel, Franciele H., et al. "Circulating Tumour DNA Sequencing Identifies a Genetic Resistance-Gap in Colorectal Cancers with Acquired Resistance to EGFR-Antibodies and Chemotherapy." Cancers 12.12 (2020): 3736.
Pubmed: 33322618
DOI: 10.3390/cancers12123736
Research Highlights
These findings suggest that further genetic abnormalities in the RAS-RAF-MEK pathway may be present in LCH cells. These alterations, in the instance of MAP2K1, may be the cause of ERK activation in a BRAF wild type context. Clinical consequences for the co-administration of RAF and MEK inhibitors in LCH may arise from the resistance of certain variations to trametinib.
Nelson, David S., et al. "MAP2K1 and MAP3K1 mutations in Langerhans cell histiocytosis." Genes, Chromosomes and Cancer 54.6 (2015): 361-368.
Pubmed:
25899310
DOI:
10.1002/gcc.22247
A proliferation of Langerhans cells, commonly linked to lymphocytes, eosinophils, macrophages, and giant cells, is known as Langerhans cell histiocytosis (LCH). Between 40% and 70% of cases have been found to have BRAF mutations, typically V600E. More recently, individuals that tested negative for BRAF have been shown to have MAP2K1 mutations.
Alayed, Khaled, et al. "BRAF and MAP2K1 mutations in Langerhans cell histiocytosis: a study of 50 cases." Human Pathology 52 (2016): 61-67.
Pubmed:
26980021
DOI:
10.1016/j.humpath.2015.12.029
