Evidence map›Paper›PMID 9677305›Full record

ArticleThe Biochemical journal1998

Prenylation of Rab8 GTPase by type I and type II geranylgeranyl transferases.

A L Wilson, R A Erdman, F Castellano, W A Maltese

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Protein Prenylation in Plant Stress Responses.Molecules (Basel, Switzerland) · 2019
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Protein geranylgeranyltransferase-I of Trypanosoma cruzi.Molecular and biochemical parasitology · 2008
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Rab geranylgeranyl transferase alpha mutation in the gunmetal mouse reduces Rab prenylation and platelet synthesis.Proceedings of the National Academy of Sciences of the United States of America · 2000
    Article
  18. Article
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

4 authors at 1 institution in 1 country.

A L WilsonHood Research Program, Weis Center for Research, Pennsylvania State University College of Medicine, 100 N. Academy Avenue, Danville, PA 17822-2616, USA.
R A Erdman
F Castellano
W A Maltese
Pennsylvania State University · US

Funding

STEROL SYNTHESIS, MEMBRANE LIPIDS AND TUMOR CELL GROWTHR01CA034569 · NCI · WEIS CENTER FOR RESEARCH-GEISINGER CLINC · PI MALTESE, WILLIAM A · 1985 to 2005
$1.5M
NCI NIH HHS CA34569
6 · The paper itself

Abstract

Rab GTPases are post-translationally modified by addition of geranylgeranyl moieties to carboxyl-terminal cysteine residues. For Rab proteins ending with xxCC xCxC and CCxx motifs this modification is catalysed by geranylgeranyltransferase type II (GGTaseII), and is entirely dependent on the Rab substrate being bound to Rab escort protein (REP). Several Rab proteins contain carboxyl-terminal CaaL prenylation motifs typical of members of the Rho family, which are modified in a REP-independent manner by geranylgeranyltransferase type I (GGTaseI). The present studies show that one such Rab protein (Rab8), which ends with a CVLL motif, is uniquely able to serve as a substrate for either REP/GGTaseII or GGTaseI in cell-free assays. The modification of Rab8 by GGTaseI did not require REP, indicating that a REP-induced conformational change is not essential for exposure of the Rab carboxyl-terminal cysteine prenylation site. To determine whether one enzyme plays a predominant role in Rab8 prenylation in vivo, the incorporation of [3H]mevalonate into Rab8 was measured in human embryonal kidney 293 cells under conditions where the activity of GGTaseI, but not GGTaseII, was blocked by the peptidomimetic inhibitor GGTI-298. The GGTaseI inhibitor did not prevent prenylation of either overexpressed Myc-tagged Rab8 or endogenous Rab8, whereas prenylation of a known GGTaseI substrate with the same carboxyl-terminal motif, Cdc42Hs, was completely blocked. To rule out the possibility that the apparent prenylation of Rab8 by GGTaseII occurs only when GGTaseI activity is eliminated, metabolic labelling studies were carried out in the absence of the GGTaseI inhibitor, using a REP-binding-deficient Rab8 construct (Y78D) that cannot serve as a substrate for GGTaseII, but is indistinguishable from wild-type Rab8 as a substrate for GGTaseI. Prenylation of the Y78D mutant was reduced by 60-70% in intact cells, consistent with the conclusion that the majority of Rab8 is prenylated by the REP/GGTaseII system in vivo.

Indexed as

Protein Prenylationrab GTP-Binding ProteinsAdaptor Proteins, Signal TransducingAlkyl and Aryl TransferasesCarrier ProteinsEnzyme InhibitorsGTP-Binding ProteinsGTP PhosphohydrolasesHumansMutationSubstrate SpecificityTransferasesAdaptor Proteins, Signal TransducingAlkyl and Aryl TransferasesCarrier ProteinsCHM protein, humanEnzyme Inhibitorsgeranylgeranyltransferase type-IGTP-Binding ProteinsGTP PhosphohydrolasesRAB8A protein, humanRab geranylgeranyl transferase beta-subunitrab GTP-Binding ProteinsTransferases

Identifiers

PMID9677305
PMCPMC1219609
OpenAlexW2213633897

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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.