Evidence map›Paper›PMID 11238945›Full record

ArticleMolecular and cellular biology2001

Ras binding triggers ubiquitination of the Ras exchange factor Ras-GRF2.

C L de Hoog, J A Koehler, M D Goldstein, P Taylor, D Figeys, M F Moran

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. 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
2.0field-weighted citation impact, top 14% 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, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. RasGRF2 Rac-GEF activity couples NMDA receptor calcium flux to enhanced synaptic transmission.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  6. Article
  7. Insulin-induced phosphorylation of FKHR (Foxo1) targets to proteasomal degradation.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
  8. Article
  9. 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

6 authors at 1 institution in 1 country.

C L de HoogBanting and Best Department of Medical Research, University of Toronto, Toronto, Ontario M5G 1X5, Canada.
J A Koehler
M D Goldstein
P Taylor
D Figeys
M F Moran
University of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ras is a small GTPase that is activated by upstream guanine nucleotide exchange factors, one of which is Ras-GRF2. GRF2 is a widely expressed protein with several recognizable sequence motifs, including a Ras exchanger motif (REM), a PEST region containing a destruction box (DB), and a Cdc25 domain. The Cdc25 domain possesses guanine nucleotide exchange factor activity and interacts with Ras. Herein we examine if the DB motif in GRF2 results in proteolysis via the ubiquitin pathway. Based on the solved structure of the REM and Cdc25 regions of the Son-of-sevenless (Sos) protein, the REM may stabilize the Cdc25 domain during Ras binding. The DB motif of GRF2 is situated between the REM and the Cdc25 domains, tempting speculation that it may be exposed to ubiquitination machinery upon Ras binding. GRF2 protein levels decrease dramatically upon activation of GRF2, and dominant-negative Ras induces degradation of GRF2, demonstrating that signaling downstream of Ras is not required for the destruction of GRF2 and that binding to Ras is important for degradation. GRF2 is ubiquitinated in vivo, and this can be detected using mass spectrometry. In the presence of proteasome inhibitors, Ras-GRF2 accumulates as a high-molecular-weight conjugate, suggesting that GRF2 is destroyed by the 26S proteasome. Deleting the DB reduces the ubiquitination of GRF2. GRF2 lacking the Cdc25 domain is not ubiquitinated, suggesting that a protein that cannot bind Ras cannot be properly targeted for destruction. Point mutations within the Cdc25 domain that eliminate Ras binding also eliminate ubiquitination, demonstrating that binding to Ras is necessary for ubiquitination of GRF2. We conclude that conformational changes induced by GTPase binding expose the DB and thereby target GRF2 for destruction.

Indexed as

Amino Acid MotifsAmino Acid SequenceBinding SitesCells, CulturedCysteine EndopeptidasesCysteine Proteinase InhibitorsHumansIonomycinIonophoresLeupeptinsMass SpectrometryMolecular Sequence DataMultienzyme ComplexesMutationPhosphorylationProteasome Endopeptidase Complexbenzyloxycarbonylleucyl-leucyl-leucine aldehydeCysteine EndopeptidasesCysteine Proteinase InhibitorsIonomycinIonophoresLeupeptinsMultienzyme ComplexesProteasome Endopeptidase Complexras-GRF1RASGRF2 protein, humanras Guanine Nucleotide Exchange Factorsras ProteinsSon of Sevenless ProteinsUbiquitins

Identifiers

PMID11238945
PMCPMC86827
OpenAlexW2080158743

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.