| http://purl.uniprot.org/citations/9247271 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/9247271 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/9247271 | http://www.w3.org/2000/01/rdf-schema#comment | "Mutations in the C. elegans egl-36 gene result in defective excitation of egg-laying and enteric muscles. Dominant gain-of-function alleles inhibit enteric and egg-laying muscle contraction, whereas a putative null mutation has no observed phenotype. egl-36 encodes a Shaw-type (Kv3) voltage-dependent potassium channel subunit. In Xenopus oocytes, wild-type egl-36 expresses noninactivating channels with slow activation kinetics. One gain-of-function mutation causes a single amino acid substitution in S6, and the other causes a substitution in the cytoplasmic amino terminal domain. Both mutant alleles produce channels dramatically shifted in their midpoints of activation toward hyperpolarized voltages. An egl-36::gfp fusion is expressed in egg-laying muscles and in a pair of enteric muscle motor neurons. The mutant egl-36 phenotypes can thus be explained by expression in these cells of potassium channels that are inappropriately opened at hyperpolarized potentials, causing decreased excitability due to increased potassium conductance."xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.org/dc/terms/identifier | "doi:10.1016/s0896-6273(00)80355-4"xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.org/dc/terms/identifier | "doi:10.1016/s0896-6273(00)80355-4"xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/author | "Butler A."xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/author | "Butler A."xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/author | "Thomas J.H."xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/author | "Thomas J.H."xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/author | "Wei A."xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/author | "Wei A."xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/author | "Salkoff L."xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/author | "Salkoff L."xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/author | "Johnstone D.B."xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/author | "Johnstone D.B."xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/date | "1997"xsd:gYear |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/date | "1997"xsd:gYear |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/name | "Neuron"xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/name | "Neuron"xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/pages | "151-164"xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/pages | "151-164"xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/title | "Behavioral defects in C. elegans egl-36 mutants result from potassium channels shifted in voltage-dependence of activation."xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/title | "Behavioral defects in C. elegans egl-36 mutants result from potassium channels shifted in voltage-dependence of activation."xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/volume | "19"xsd:string |
| http://purl.uniprot.org/citations/9247271 | http://purl.uniprot.org/core/volume | "19"xsd:string |