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- W2152911928 abstract "During development of the Caenorhabditis elegans hermaphrodite, the gonadal anchor cell induces nearby Pn.p cells to adopt vulval fates. The response to this signal is mediated by a receptor tyrosine kinase signal transduction pathway that has been remarkably well conserved during metazoan evolution. Because mitogen-activated protein (MAP) kinases are activated by receptor tyrosine kinase pathways in vertebrate cells, we hypothesized that C. elegans MAP kinase homologs may play a role in vulval induction. Two C. elegans MAP kinase genes, mpk-1 and mpk-2 (mpk, MAP kinase), were cloned using degenerate oligonucleotide primers and PCR amplification; in parallel, genes involved in vulval induction were identified by screening for mutations that suppress the vulval defects caused by an activated let-60 ras gene. One such suppressor mutation is an allele of mpk-1. We used a new type of mosaic analysis to show that mpk-1 acts cell autonomously in the Pn.p cells. Our results show that mpk-1 plays an important functional role as an activator in ras-mediated cell signaling in vivo." @default.
- W2152911928 created "2016-06-24" @default.
- W2152911928 creator A5037266029 @default.
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- W2152911928 creator A5071917788 @default.
- W2152911928 creator A5073965354 @default.
- W2152911928 creator A5075093223 @default.
- W2152911928 date "1994-01-01" @default.
- W2152911928 modified "2023-10-03" @default.
- W2152911928 title "A MAP kinase homolog, mpk-1, is involved in ras-mediated induction of vulval cell fates in Caenorhabditis elegans." @default.
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- W2152911928 doi "https://doi.org/10.1101/gad.8.2.160" @default.
- W2152911928 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8299936" @default.
- W2152911928 hasPublicationYear "1994" @default.
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