Evidence map›Paper›PMID 12880183›Full record

ArticleCerebellum (London, England)2003

Distribution of regulator of G protein signaling 8 (RGS8) protein in the cerebellum.

Osamu Saitoh, Ikuo Masuho, Masayuki Itoh, Hideki Abe, Keiichiro Komori, Megumi Odagiri

Abstract read
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In one paragraph

Article in Cerebellum (London, England), 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.1field-weighted citation impact, top 54% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. RGS2 and female common diseases: a guard of women's health.Journal of translational medicine · 2023
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 5 institutions in 1 country.

Osamu SaitohDepartment of Molecular Cell Signaling, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan. osaito@tmin.ac.jp
Ikuo Masuho
Masayuki Itoh
Hideki Abe
Keiichiro Komori
Megumi Odagiri
Fuchu Hospital · JPChiba University · JPKanagawa Institute of Technology · JPTokyo Medical and Dental University · JPTokyo Metropolitan Institute of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The regulator of G protein signaling (RGS) proteins modulate heterotrimeric G protein signaling. RGS8 was identified as a brain-specific RGS protein of 180 amino acids. Biochemical studies indicated that RGS8 binds to Galphao and Galphai3, and that it functions as a GTPase-activating protein (GAP) for Galpha subunits. Physiological investigations demonstrated that RGS8 is not a simple negative regulator, but accelerates the G-protein-coupled responses. In situ hybridization analysis showed a highly dense expression of RGS8 mRNA in Purkinje cells of the cerebellum in rat brain. When the cellular distribution of RGS8 was examined in non-neural cells transfected with RGS8 cDNA, the protein was found to be concentrated in nuclei. Further, co-expression of constitutively active Galphao resulted in the translocation of RGS8 protein to the plasma membrane. The cellular distribution of the RGS8 protein in cerebellar Pukinje cells was also studied in detail. It was shown that the protein is excluded from the nuclei and distributed in the cell body and dendrites except the axons of Purkinje cells. Thus, it is evident that there is a novel mechanism controlling the distribution of RGS8 protein in cerebellar Purkinje cells.

Indexed as

AnimalsCell LineCerebellumDendritesHumansPurkinje CellsRGS ProteinsRNA, MessengerSignal TransductionTranscription, GeneticTransfectionRGS8 protein, humanRgs8 protein, ratRGS ProteinsRNA, Messenger

Identifiers

PMID12880183
OpenAlexW2006093100

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.