Evidence map›Paper›PMID 25788415›Full record

ArticleStem cells (Dayton, Ohio)2015

Activated k-ras, but not h-ras or N-ras, regulates brain neural stem cell proliferation in a raf/rb-dependent manner.

R Hugh F Bender, Kevin M Haigis, David H Gutmann

Open access · bronzeAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Promotion of cancer cell stemness by Ras.Biochemical Society transactions · 2021
    Review
  9. Ras Variant Biology and Contributions to Human Disease.Methods in molecular biology (Clifton, N.J.) · 2021
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Contextual signaling in cancer.Seminars in cell & developmental biology · 2016
    Review
  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

3 authors at 2 institutions in 1 country.

R Hugh F BenderDepartment of Neurology, Washington University School of Medicine, St. Louis, Missouri, USA.
Kevin M HaigisDepartment of Medicine, Cancer Research Institute, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.
David H GutmannDepartment of Neurology, Washington University School of Medicine, St. Louis, Missouri, USA.
Washington University in St. Louis · USBeth Israel Deaconess Medical Center · US

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN · 2001 to 2026
$128.0M
TRAINING PROGRAM IN CELLULAR AND MOLECULAR BIOLOGYT32GM007067 · NIGMS · WASHINGTON UNIVERSITY · PI TRUE-KROB, HEATHER L · 1985 to 2020
$20.4M
NEUROFIBROMIN REGULATION OF NEURAL STEM CELL FUNCTION IN VITRO AND IN VIVOR01NS065547 · NINDS · WASHINGTON UNIVERSITY · PI GUTMANN, DAVID H · 2010 to 2014
$1.6M
Genetic and genomic analysis of Ras signaling in colorectal cancer progressionK01CA118425 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI HAIGIS, KEVIN · 2006 to 2010
$781k
NCI NIH HHS 1K01 CA118425NCI NIH HHS K01 CA118425NCI NIH HHS P30 CA091842NIGMS NIH HHS T32 GM007067NINDS NIH HHS NS065547-01NINDS NIH HHS R01 NS065547
6 · The paper itself

Abstract

Neural stem cells (NSCs) give rise to all the major cell types in the brain, including neurons, oligodendrocytes, and astrocytes. However, the intracellular signaling pathways that govern brain NSC proliferation and differentiation have been incompletely characterized to date. Since some neurodevelopmental brain disorders (Costello syndrome and Noonan syndrome) are caused by germline activating mutations in the RAS genes, Ras small GTPases are likely critical regulators of brain NSC function. In the mammalian brain, Ras exists as three distinct molecules (H-Ras, K-Ras, and N-Ras), each with different subcellular localizations, downstream signaling effectors, and biological effects. Leveraging a novel series of conditional-activated Ras molecule-expressing genetically engineered mouse strains, we demonstrate that activated K-Ras, but not H-Ras or N-Ras, expression increases brain NSC growth in a Raf-dependent, but Mek-independent, manner. Moreover, we show that activated K-Ras regulation of brain NSC proliferation requires Raf binding and suppression of retinoblastoma (Rb) function. Collectively, these observations establish tissue-specific differences in activated Ras molecule regulation of brain cell growth that operate through a noncanonical mechanism.

Indexed as

AnimalsBrainCell CycleCell DifferentiationCell ProliferationMiceNeural Stem Cellsras ProteinsRetinoblastoma ProteinSignal Transductionras ProteinsRetinoblastoma ProteinCell proliferationNeural stem cellsRaf kinasesRas proteinsRetinoblastoma protein

Identifiers

PMID25788415
PMCPMC4889217
OpenAlexW1902929441

What OpenQuestion holds

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LicenceTDM
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.