LET‐23‐mediated signal transduction during Caenorhabditis elegans development
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References (37)
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The multivulva phenotype of certain Caenorhabditis elegans mutants results from defects in two functionally redundant pathways.
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The Caenorhabditis elegans locus lin-15, a negative regulator of a tyrosine kinase signaling pathway, encodes two different proteins.
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Multiple intercellular signalling systems control the development of the Caenorhabditis elegans vulva
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The lin-15 locus encodes two negative regulators of Caenorhabditis elegans vulval development.
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A MAP kinase homolog, mpk-1, is involved in ras-mediated induction of vulval cell fates in Caenorhabditis elegans.
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The let-60 locus controls the switch between vulval and nonvulval cell fates in Caenorhabditis elegans.
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Multiple functions of let-23, a Caenorhabditis elegans receptor tyrosine kinase gene required for vulval induction.
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Suppression of activated Let-60 ras protein defines a role of Caenorhabditis elegans Sur-1 MAP kinase in vulval differentiation.
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unc-101, a gene required for many aspects of Caenorhabditis elegans development and behavior, encodes a clathrin-associated protein.
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Characterization of a new member of the human /-adaptin gene family from chromosome 22q12, a candidate meningioma gene
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Mutations in the Caenorhabditis elegans let-23 EGFR-like gene define elements important for cell-type specificity and function.
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Splicing in Caenorhabditis elegans does not require an AG at the 3' splice acceptor site.
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The lin-3/let-23 pathway mediates inductive signalling during male spicule development in Caenorhabditis elegans
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Multiple cell interactions are required for fate specification during male spicule development in Caenorhabditis elegans
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The multivulva phenotype of certain C. elegans mutants results from defects in two functionally redundant pathways
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Cell fate patterning during C. elegans vulval development
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Deleted Work
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