WormBase gene description for asna-1 (worm)
Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Electronic Gene Ontology annotations created by transferring manual GO annotations between related proteins based on shared sequence features
Combined Automated Annotation using Multiple IEA Methods
A map of the interactome network of the metazoan C. elegans.
ASNA-1 positively regulates insulin secretion in C. elegans and mammalian cells.
-
asna-1 null mutants arrest reversibly at L1, are reduced in DAF-28/insulin secretion, and asna-1 is expressed in sensory neurons and intestinal cells.
"asna-1 mutants are reduced in insulin secretion while overexpression of asna-1 mimics the effects of insulin overexpression."
Caenorhabditis elegans expresses a functional ArsA.
-
Purified MBP-ASNA-1 has ATPase activity stimulated by As(III) and Sb(III), and asna-1 mutants are hypersensitive to these metalloids.
"The ATPase activity of the ASNA-1 protein was dependent on the presence of As(III) or Sb(III)."
Empirically controlled mapping of the Caenorhabditis elegans protein-protein interactome network.
A novel sphingolipid-TORC1 pathway critically promotes postembryonic development in Caenorhabditis elegans.
-
asna-1(ok938) is used only as a control L1-arrest mutant. Branched-chain lipid supplements do not rescue its arrest, placing it outside the mmBCFA/sphingolipid/TORC1 pathway.
"Neither C17ISO nor d17iso-SPA permits asna-1(−) animals to bypass L1 arrest."
Alternative redox forms of ASNA-1 separate insulin signaling from tail-anchored protein targeting and cisplatin resistance in C. elegans.
-
ASNA-1 is required for ER targeting of the TA protein SEC-61beta, binds SEC-61beta and the ER receptor WRB-1, and exists in reduced and oxidized redox states. The reduced form is needed for TA targeting and cisplatin resistance.
"We conclude that ASNA-1 exists in two alternative redox states, where formation of the oxidized state requires two conserved cysteines."
Identification of C. elegans ASNA-1 domains and tissue requirements that differentially influence platinum sensitivity and growth control.
-
Point mutants dHis164 and A63V are TA-targeting defective and cisplatin sensitive but secrete insulin normally. Depleting ASNA-1 in both neurons and intestine causes L1 arrest.
"Somatic depletion of ASNA-1 as well as simultaneous depletion of ASNA-1 in neurons and intestines resulted in an L1 arrest."
A proinsulin-dependent interaction between ENPL-1 and ASNA-1 in neurons is required to maintain insulin secretion in C. elegans.
-
ASNA-1 acts in neurons to promote DAF-28 secretion, interacts with ENPL-1/GRP94 (likely in its oxidized chaperone form) and localizes to neuronal Golgi.
"We conclude that ASNA-1 is found in the Golgi and its localization there depends on ENPL-1."
ASNA-1 activity modulates sensitivity to cisplatin.
-
asna-1 null mutants are hypersensitive to cisplatin, and human ASNA1 can substitute for the worm gene.
"Human ASNA1 can substitute for the worm gene, indicating a conserved function."
UniProt entry P30632 (ASNA_CAEEL)
Manual literature research for asna-1