ArticleProceedings of the National Academy of Sciences of the United States of America1999
Posttranslational modification of Galphao1 generates Galphao3, an abundant G protein in brain.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed.
- Selective protection of murine cerebral GJournal of molecular medicine (Berlin, Germany) · 2020Article
- Wnt-5a/Frizzled9 Receptor Signaling through the Gαo-Gβγ Complex Regulates Dendritic Spine Formation.The Journal of biological chemistry · 2016Article
- Lack of Gαi2 leads to dilative cardiomyopathy and increased mortality in β1-adrenoceptor overexpressing mice.Cardiovascular research · 2015Article
- Insulin secretion stimulated by L-arginine and its metabolite L-ornithine depends on Gα(i2).American journal of physiology. Endocrinology and metabolism · 2014Article
- Gαi2- and Gαi3-deficient mice display opposite severity of myocardial ischemia reperfusion injury.PloS one · 2014Article
- Primary cilium migration depends on G-protein signalling control of subapical cytoskeleton.Nature cell biology · 2013Article
- Gαi2- and Gαi3-specific regulation of voltage-dependent L-type calcium channels in cardiomyocytes.PloS one · 2011Article
- Molecular mechanisms of go signaling.Neuro-Signals · 2009Review
- An obligatory requirement for the heterotrimeric G protein Gi3 in the antiautophagic action of insulin in the liver.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Molecular diversity of rat brain proteins as revealed by proteomic analysis.Molecular diversity · 2005Article
- Sphingomyelin-enriched microdomains at the Golgi complex.Molecular biology of the cell · 2001Article
- Protein identification by in-gel digestion, high-performance liquid chromatography, and mass spectrometry: peptide analysis by complementary ionization techniques.Journal of the American Society for Mass Spectrometry · 2001Article
- The neuronal monoamine transporter VMAT2 is regulated by the trimeric GTPase Go(2).The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Galphao, the most abundant G protein in mammalian brain, occurs at least in two subforms, i.e., Galphao1 and Galphao2, derived by alternative splicing of the mRNA. A third Galphao1-related isoform, Galphao3, has been purified, representing about 30% of total Go in brain. Initial studies revealed distinct biochemical properties of Galphao3 as compared with other Galphao isoforms. In matrix-assisted laser desorption/ionization peptide mass mapping of gel-isolated Galphao1 and Galphao3, C-terminal peptides showed a difference of +1 Da for Galphao3. Nanoelectrospray tandem mass spectrometry sequencing revealed an Asp instead of an Asn at position 346 of Galphao3. Gel electrophoretic analysis of recombinant Galphao3 showed the same mobility as native Galphao3 but distinct to Galphao1. The conversion of 346Asn-->Asp changed the signaling properties, including the velocity of the basal guanine nucleotide-exchange reaction, which points to the involvement of the C terminus in basal guanosine 5'-[gamma-thio]triphosphate binding. No cDNA coding for Galphao3 was detected, suggesting an enzymatic deamidation of Galphao1 by a yet-unidentified activity. Therefore, Galpha heterogeneity is generated not only at the DNA or RNA levels, but also at the protein level. The relative amount of Galphao1 and Galphao3 differed from cell type to cell type, indicating an additional principle of G protein regulation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.