Matches in SemOpenAlex for { <https://semopenalex.org/work/W2068753896> ?p ?o ?g. }
Showing items 1 to 85 of
85
with 100 items per page.
- W2068753896 endingPage "68" @default.
- W2068753896 startingPage "63" @default.
- W2068753896 abstract "Recent studies indicate that the intracellular C-terminus of Group I metabotropic glutamate receptors (mGlu(1) and mGlu(5) receptor) is important in G protein coupling. To determine the necessity of the C-tail, a deletion mutant of mGlu(1) receptor was constructed, which included the first 840 amino acids of the rat mGlu(1a) receptor (mGlu(1)-dCT). G protein coupling of the receptors was assessed by measuring glutamate mediated inhibition of native calcium currents when each receptor was expressed in isolated sympathetic neurons from the rat superior cervical ganglion. Wild type mGlu(1) receptor activates both the Galpha(i/o) and Galpha(q/11) protein families. Each pathway can be detected in superior cervical ganglion neurons as voltage dependent and voltage independent inhibition of the calcium currents, respectively. While wild type mGlu(1) receptor gave rise to a strong, mixed voltage dependent and independent calcium current inhibition, mGlu(1)-dCT exhibited a weaker inhibition that was strongly voltage dependent, indicating activation of Galpha(i/o) was predominant. Further, pertussis toxin treatment reduced the inhibition by wild type mGlu(1) receptor to a smaller, voltage independent inhibition as expected, but completely abolished signaling through mGlu(1)-dCT. Finally, to test whether mGlu(1)-dCT could produce any activation of Galpha(q/11), inhibition of the native superior cervical ganglion M-type potassium currents was examined. M-channels, inhibited by PIP(2) depletion, were strongly inhibited by glutamate in cells expressing wild type mGlu(1) receptor, but no inhibition was detectable in neurons expressing mGlu(1)-dCT. These data indicate that C-terminal deletion of mGlu(1) receptor selectively abolishes Galpha(q/11) coupling." @default.
- W2068753896 created "2016-06-24" @default.
- W2068753896 creator A5005137674 @default.
- W2068753896 date "2010-02-01" @default.
- W2068753896 modified "2023-10-16" @default.
- W2068753896 title "C-terminal deletion of metabotropic glutamate receptor 1 selectively abolishes coupling to Gαq" @default.
- W2068753896 cites W1575439657 @default.
- W2068753896 cites W1790229448 @default.
- W2068753896 cites W1896163591 @default.
- W2068753896 cites W1913636106 @default.
- W2068753896 cites W1950417202 @default.
- W2068753896 cites W1965058020 @default.
- W2068753896 cites W1966418219 @default.
- W2068753896 cites W1969762570 @default.
- W2068753896 cites W1972211504 @default.
- W2068753896 cites W1973027891 @default.
- W2068753896 cites W1974152360 @default.
- W2068753896 cites W1982797011 @default.
- W2068753896 cites W1996143170 @default.
- W2068753896 cites W2023247734 @default.
- W2068753896 cites W2048894410 @default.
- W2068753896 cites W2053882680 @default.
- W2068753896 cites W2058205481 @default.
- W2068753896 cites W2064748241 @default.
- W2068753896 cites W2073251105 @default.
- W2068753896 cites W2078316320 @default.
- W2068753896 cites W2078935283 @default.
- W2068753896 cites W2084544813 @default.
- W2068753896 cites W2092819390 @default.
- W2068753896 cites W2112430429 @default.
- W2068753896 cites W2170912183 @default.
- W2068753896 cites W2171553829 @default.
- W2068753896 cites W2268202880 @default.
- W2068753896 cites W2417987987 @default.
- W2068753896 cites W2913636289 @default.
- W2068753896 doi "https://doi.org/10.1016/j.ejphar.2009.10.051" @default.
- W2068753896 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19879871" @default.
- W2068753896 hasPublicationYear "2010" @default.
- W2068753896 type Work @default.
- W2068753896 sameAs 2068753896 @default.
- W2068753896 citedByCount "6" @default.
- W2068753896 countsByYear W20687538962014 @default.
- W2068753896 countsByYear W20687538962016 @default.
- W2068753896 countsByYear W20687538962017 @default.
- W2068753896 countsByYear W20687538962021 @default.
- W2068753896 crossrefType "journal-article" @default.
- W2068753896 hasAuthorship W2068753896A5005137674 @default.
- W2068753896 hasConcept C170493617 @default.
- W2068753896 hasConcept C26702167 @default.
- W2068753896 hasConcept C49051014 @default.
- W2068753896 hasConcept C49773422 @default.
- W2068753896 hasConcept C55493867 @default.
- W2068753896 hasConcept C61174792 @default.
- W2068753896 hasConcept C80631254 @default.
- W2068753896 hasConcept C86803240 @default.
- W2068753896 hasConceptScore W2068753896C170493617 @default.
- W2068753896 hasConceptScore W2068753896C26702167 @default.
- W2068753896 hasConceptScore W2068753896C49051014 @default.
- W2068753896 hasConceptScore W2068753896C49773422 @default.
- W2068753896 hasConceptScore W2068753896C55493867 @default.
- W2068753896 hasConceptScore W2068753896C61174792 @default.
- W2068753896 hasConceptScore W2068753896C80631254 @default.
- W2068753896 hasConceptScore W2068753896C86803240 @default.
- W2068753896 hasIssue "1-3" @default.
- W2068753896 hasLocation W20687538961 @default.
- W2068753896 hasLocation W20687538962 @default.
- W2068753896 hasOpenAccess W2068753896 @default.
- W2068753896 hasPrimaryLocation W20687538961 @default.
- W2068753896 hasRelatedWork W1493473330 @default.
- W2068753896 hasRelatedWork W1845103358 @default.
- W2068753896 hasRelatedWork W1868301535 @default.
- W2068753896 hasRelatedWork W1991242725 @default.
- W2068753896 hasRelatedWork W2002877168 @default.
- W2068753896 hasRelatedWork W2014828654 @default.
- W2068753896 hasRelatedWork W2035055320 @default.
- W2068753896 hasRelatedWork W2064542078 @default.
- W2068753896 hasRelatedWork W2148091233 @default.
- W2068753896 hasRelatedWork W2330433164 @default.
- W2068753896 hasVolume "627" @default.
- W2068753896 isParatext "false" @default.
- W2068753896 isRetracted "false" @default.
- W2068753896 magId "2068753896" @default.
- W2068753896 workType "article" @default.