Evidence map›Paper›PMID 11940661›Full record

ArticleMolecular and cellular biology2002

Kinase suppressor of Ras (KSR) is a scaffold which facilitates mitogen-activated protein kinase activation in vivo.

AnhCo Nguyen, W Richard Burack, Jeffrey L Stock, Robert Kortum, Oleg V Chaika, Maryam Afkarian, William J Muller, Kenneth M Murphy, Deborah K Morrison, Robert E Lewis and 2 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

145 citing papers in PubMed, 273 citations in OpenAlex.

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  9. KSR1 Knockout Mouse Model Demonstrates MAPK Pathway's Key Role in Cisplatin- and Noise-induced Hearing Loss.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  10. Article
  11. SOS1 and KSR1 modulate MEK inhibitor responsiveness to target resistant cell populations based on PI3K and KRAS mutation status.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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  20. Polyvalent design in the cGAS-STING pathway.Seminars in immunology · 2021
    Review

85 more citing papers are in PubMed but not listed here.

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

12 authors at 4 institutions in 2 countries.

AnhCo NguyenDepartment of Pathology and Immunology, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
W Richard Burack
Jeffrey L Stock
Robert Kortum
Oleg V Chaika
Maryam Afkarian
William J Muller
Kenneth M Murphy
Deborah K Morrison
Robert E Lewis
John McNeish
Andrey S Shaw
Howard Hughes Medical Institute · USPfizer (United States) · USFrederick National Laboratory for Cancer Research · USMcMaster University · CA

Funding

KSR, a Modifier of Ras-Mediated Cell TransformationR01CA090400 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI LEWIS, ROBERT E. · 2002 to 2012
$2.7M
Intracellular Regulators of Insulin SignalingR01DK052809 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI LEWIS, ROBERT E. · 1997 to 2009
$2.3M
NCI NIH HHS CA90400NCI NIH HHS R01 CA090400NIDDK NIH HHS DK52809NIDDK NIH HHS R01 DK052809Wellcome Trust
6 · The paper itself

Abstract

While scaffold proteins are thought to be key components of signaling pathways, their exact function is unknown. By preassembling multiple components of signaling cascades, scaffolds are predicted to influence the efficiency and/or specificity of signaling events. Here we analyze a potential scaffold of the Ras/mitogen-activated protein kinase (MAPK) pathway, kinase suppressor of Ras (KSR), by generating KSR-deficient mice. KSR-deficient mice were grossly normal even though ERK kinase activation was attenuated to a degree sufficient to block T-cell activation and inhibit tumor development. Consistent with its role as a scaffold, high-molecular-weight complexes containing KSR, MEK, and ERK were lost in the absence of KSR. This demonstrates that KSR is a bona fide scaffold that is not required for but enhances signaling via the Ras/MAPK signaling pathway.

Indexed as

AnimalsBreast NeoplasmsCell DivisionEnzyme ActivationFibroblastsFlow CytometryGene DeletionGene TargetingInterferon-gammaInterleukin-2Interleukin-4Lymphocyte ActivationLymphocytesMAP Kinase Kinase 1MAP Kinase Signaling SystemMiceInterferon-gammaInterleukin-2Interleukin-4KSR-1 protein kinaseMap2k1 protein, mouseMAP Kinase Kinase 1Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesProtein KinasesProtein Serine-Threonine Kinases

Identifiers

PMID11940661
PMCPMC133772
OpenAlexW2116669977

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.