Evidence map›Paper›PMID 7777512›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1995

Phosphorylation of the human leukemia inhibitory factor (LIF) receptor by mitogen-activated protein kinase and the regulation of LIF receptor function by heterologous receptor activation.

W P Schiemann, L M Graves, H Baumann, K K Morella, D P Gearing, M D Nielsen, E G Krebs, N M Nathanson

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
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  4. Endosomes as Signaling Platforms for IL-6 Family Cytokine Receptors.Frontiers in cell and developmental biology · 2021
    Review
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  16. Article
  17. Inhibition of cytokines and JAK-STAT activation by distinct signaling pathways.Proceedings of the National Academy of Sciences of the United States of America · 1996
    Article
  18. Review
  19. IL-6 cytokine family and signal transduction: a model of the cytokine system.Journal of molecular medicine (Berlin, Germany) · 1996
    Review
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

8 authors at 2 institutions in 2 countries.

W P SchiemannDepartment of Pharmacology, University of Washington, Seattle 98195, USA.
L M Graves
H Baumann
K K Morella
D P Gearing
M D Nielsen
E G Krebs
N M Nathanson
University of Washington · USAmgen (United States) · US

Funding

MOLECULAR ANALYSIS OF NEURAL MUSCARINIC RECEPTORSR01NS026920 · NINDS · UNIVERSITY OF WASHINGTON · PI NATHANSON, NEIL MARC · 1989 to 2005
$1.8M
NCI NIH HHS CA26222NIGMS NIH HHS GM07750NINDS NIH HHS NS26920
6 · The paper itself

Abstract

We used a bacterially expressed fusion protein containing the entire cytoplasmic domain of the human leukemia inhibitory factor (LIF) receptor to study its phosphorylation in response to LIF stimulation. The dose- and time-dependent relationships for phosphorylation of this construct in extracts of LIF-stimulated 3T3-L1 cells were superimposable with those for the stimulation of mitogen-activated protein kinase (MAPK). Indeed, phosphorylation of the cytoplasmic domain of the low-affinity LIF receptor alpha-subunit (LIFR) in Mono Q-fractionated, LIF-stimulated 3T3-L1 extracts occurred only in those fractions containing activated MAPK; Ser-1044 served as the major phosphorylation site in the human LIFR for MAPK both in agonist-stimulated 3T3-L1 lysates and by recombinant extracellular signal-regulated kinase 2 in vitro. Expression in rat H-35 hepatoma cells of LIFR or chimeric granulocyte-colony-stimulating factor receptor (G-CSFR)-LIFR mutants lacking Ser-1044 failed to affect cytokine-stimulated expression of a reporter gene under the control of the beta-fibrinogen gene promoter but eliminated the insulin-induced attenuation of cytokine-stimulated gene expression. Thus, our results identify the human LIFR as a substrate for MAPK and suggest a mechanism of heterologous receptor regulation of LIFR signaling occurring at Ser-1044.

Indexed as

Interleukin-6Mitogen-Activated Protein Kinases3T3 CellsAnimalsCalcium-Calmodulin-Dependent Protein KinasesGrowth InhibitorsHumansLeukemia Inhibitory FactorLeukemia Inhibitory Factor Receptor alpha SubunitLymphokinesMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphorylationProtein Serine-Threonine KinasesProtein-Tyrosine KinasesCalcium-Calmodulin-Dependent Protein KinasesGrowth InhibitorsInterleukin-6Leukemia Inhibitory FactorLeukemia Inhibitory Factor Receptor alpha SubunitLIF protein, humanLif protein, mouseLIFR protein, humanLifr protein, mouseLifr protein, ratLymphokinesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesReceptors, CytokineReceptors, OSM-LIF

Identifiers

PMID7777512
PMCPMC41694
OpenAlexW2057043231

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.