Evidence map›Paper›PMID 25225292›Full record

ArticleThe Journal of biological chemistry2014

Cell cycle restriction is more important than apoptosis induction for RASSF1A protein tumor suppression.

Howard Donninger, Jennifer A Clark, Megan K Monaghan, M Lee Schmidt, Michele Vos, Geoffrey J Clark

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Review
  3. Detection of Endogenous RASSF1A Interacting Proteins.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  4. Article
  5. Article
  6. OncoTargets and therapy · 2020
    Article
  7. Review
  8. The Ambivalent Function of YAP in Apoptosis and Cancer.International journal of molecular sciences · 2018
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Ras signaling through RASSF proteins.Seminars in cell & developmental biology · 2016
    Review
  17. Article
  18. Article
  19. Article
  20. 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.

Howard DonningerFrom the Departments of Medicine.
Jennifer A ClarkFrom the Departments of Medicine.
Megan K MonaghanFrom the Departments of Medicine.
M Lee SchmidtBiochemistry and Molecular Biology, and.
Michele Vosthe Cell and Cancer Biology Branch, NCI, National Institutes of Health, Rockville, Maryland 20850.
Geoffrey J ClarkPharmacology and Toxicology, James Graham Brown Cancer Center, Molecular Targets Program, University of Louisville, Louisville, Kentucky 40202 and gjclar01@louisville.edu.
University of Louisville · US

Funding

PROJ 12: STEM CELL-BASED VACCINE FOR CANCER PROPHYLAXISP20RR018733 · NCRR · UNIVERSITY OF LOUISVILLE · PI TRENT, JOHN O · 2003 to 2011
$18.9M
The role of the Ras effector Nore1a in tumor suppressionR01CA133171 · NCI · UNIVERSITY OF LOUISVILLE · PI CLARK, GEOFFREY J. · 2010 to 2014
$1.3M
NCI NIH HHS R01 CA133171NCI NIH HHS R01 CA133171-01A2NCRR NIH HHS 1P20 RR18733NCRR NIH HHS P20 RR018733
6 · The paper itself

Abstract

The Ras association domain family protein 1A (RASSF1A) is arguably one of the most frequently inactivated tumor suppressors in human cancer. RASSF1A modulates apoptosis via the Hippo and Bax pathways but also modulates the cell cycle. In part, cell cycle regulation appears to be dependent upon the ability of RASSF1A to complex with microtubules and regulate their dynamics. Which property of RASSF1A, apoptosis induction or microtubule regulation, is responsible for its tumor suppressor function is not known. We have identified a short conserved motif that is essential for the binding of RASSF family proteins with microtubule-associated proteins. By making a single point mutation in the motif, we were able to generate a RASSF1A variant that retains wild-type apoptotic properties but completely loses the ability to bind microtubule-associated proteins and complex with microtubules. Comparison of this mutant to wild-type RASSF1A showed that, despite retaining its proapoptotic properties, the mutant was completely unable to induce cell cycle arrest or suppress the tumorigenic phenotype. Therefore, it appears that the cell cycle/microtubule effects of RASSF1A are key to its tumor suppressor function rather than its apoptotic effects.

Indexed as

ApoptosisCell CycleAmino Acid MotifsAmino Acid SequenceAnimalsCell Line, TumorChlorocebus aethiopsCOS CellsGreen Fluorescent ProteinsHEK293 CellsHumansMolecular Sequence DataMutationPhenotypePoint Mutationras ProteinsGreen Fluorescent Proteinsras ProteinsRASSF1 protein, humanTumor Suppressor ProteinsApoptosisCell CycleMicrotubule-associated Protein (MAP)OncogeneRasRas ProteinTumor Suppressor

Identifiers

PMID25225292
PMCPMC4223329
OpenAlexW2042318470

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.