Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Combined Automated Annotation using Multiple IEA Methods
Systematic interactome mapping and genetic perturbation analysis of a C. elegans TGF-beta signaling network.
C. Elegans Fatty Acid Two-Hydroxylase Regulates Intestinal Homeostasis by Affecting Heptadecenoic Acid Production.
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The fath-1 RNAi growth defect is rescued by (R)- but not (S)-2-hydroxy palmitate, consistent with FATH-1 producing (R)-2-hydroxy fatty acids.
"The results showed that (R)-2-OH FA supplement nicely rescued the growth defect caused by fath-1 RNAi, while (S)-2-OH FA did not"
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FATH-1 is required mainly in the intestine for growth.
"When fath-1 was inactivated only in the intestine, it affected the worm growth in a similar degree as when systemic knockdown was applied."
A novel sphingolipid-TORC1 pathway critically promotes postembryonic development in Caenorhabditis elegans.
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fath-1 RNAi causes L1 arrest that is not rescued by d17iso-sphinganine and is suppressed by nprl-3(ku540), placing FATH-1 in the glucosylceramide branch upstream of TORC1 signalling.
"As shown above, RNAi of fath-1, or mutating both cgt-1 and cgt-3, caused larval arrest that could not be rescued by feeding with either mmBCFAs or d17iso-SPA"
Apicobasal domain identities of expanding tubular membranes depend on glycosphingolipid biosynthesis.
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C. elegans glucosylceramide is invariably 2-hydroxylated, and C25A1.5 knockdown causes the intestinal polarity phenotype shared with cgt-1/cgt-3 loss.
"Finally, our MS analysis characterized GlcCer as invariably hydroxylated, consistent with the identified sphingolipid fatty-acid hydroxylase, C25A1.5"
UniProt entry Q9XVS0 (fath-1)