Evidence map›Paper›PMID 22802525›Full record

ArticleGenes & development2012

SPRED proteins provide a NF-ty link to Ras suppression.

Andrea I McClatchey, Karen Cichowski

Open access · diamondAbstract readComment
In one paragraph

Article in Genes & development, 2012. 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
–field-weighted citation impact
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, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Oncogenic KRAS engages an RSK1/NF1 pathway to inhibit wild-type RAS signaling in pancreatic cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  4. Article
  5. Frontiers in oncology · 2020
    Article
  6. Review
  7. The neurofibromin recruitment factor Spred1 binds to the GAP related domain without affecting Ras inactivation.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  8. Article
  9. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Andrea I McClatcheyMassachusetts General Hospital Center for Cancer Research, Department of Pathology, Harvard Medical School, Charlestown, Massachusetts 02129, USA. mcclatch@helix.mgh.harvard.edu
Karen Cichowski
Dana-Farber/Harvard Cancer Center · USMassachusetts General Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the SPRED1 (Sprouty-related protein with an EVH [Ena/Vasp homology] domain 1) and NF1 (neurofibromatosis 1) genes underlie clinically related human disorders. The NF1-encoded protein neurofibromin is a Ras GTPase-activating protein (GAP) and can directly limit Ras activity. Spred proteins also negatively regulate Ras signaling, but the mechanism by which they do so is not clear. In the July 1, 2012, issue of Genes & Development, Stowe and colleagues (pp. 1421-1426) present evidence that Spred1 recruits neurofibromin to the membrane, where it dampens growth factor-induced Ras activity, providing a satisfying explanation for the overlapping features of two human diseases.

Indexed as

AnimalsCafe-au-Lait SpotsHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsNeurofibromatosis 1Neurofibromin 1Repressor ProteinsIntracellular Signaling Peptides and ProteinsMembrane ProteinsNeurofibromin 1Repressor Proteins

Identifiers

PMID22802525
PMCPMC3404379
OpenAlexW2030298660

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.