Evidence map›Paper›PMID 8524290›Full record

ArticleMolecular and cellular biology1996

Differential activation of the Ras/extracellular-signal-regulated protein kinase pathway is responsible for the biological consequences induced by the Axl receptor tyrosine kinase.

Y W Fridell, Y Jin, L A Quilliam, A Burchert, P McCloskey, G Spizz, B Varnum, C Der, E T Liu

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

79 citing papers in PubMed, 168 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Article
  6. AXL Inhibitors: Status of Clinical Development.Current oncology reports · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. A FBXO7/EYA2-SCFMolecular cell · 2022
    Article
  12. Review
  13. AXL, an Important Host Factor for DENV and ZIKV Replication.Frontiers in cellular and infection microbiology · 2021
    Review
  14. Targeting AXL in NSCLC.Lung Cancer (Auckland, N.Z.) · 2021
    Review
  15. AXL Mediates Cetuximab and Radiation Resistance Through Tyrosine 821 and the c-ABL Kinase Pathway in Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

19 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

9 authors at 2 institutions in 1 country.

Y W FridellLineberger Comprehensive Cancer Center, Department of Pharmacology, University of North Carolina at Chapel Hill 27599-7295, USA.
Y Jin
L A Quilliam
A Burchert
P McCloskey
G Spizz
B Varnum
C Der
E T Liu
University of North Carolina at Chapel Hill · USAmgen (United States) · US

Funding

MOLECULAR DETERMINANTS IN LEUKEMIC PROGRESSIONR01CA049240 · NCI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI EARP, HENRY SHELTON · 1989 to 1999
–
NCI NIH HHS CA49240-06
6 · The paper itself

Abstract

To understand the mechanism of Axl signaling, we have initiated studies to delineate downstream components in interleukin-3-dependent 32D cells by using a chimeric receptor containing the recombinant epidermal growth factor (EGF) receptor extracellular and transmembrane domains and the Axl kinase domain (EAK [for EGF receptor-Axl kinase]). We have previously shown that upon exogenous EGF stimulation, 32D-EAK cells are capable of proliferation in the absence of interleukin-3. With this system, we determined that EAK-induced cell survival and mitogenesis are dependent upon the Ras/extracellular-signal-regulated protein kinase (ERK) cascade. Although the phosphatidylinositol-3 kinase pathway is activated upon EAK signaling, it appears to be dispensable for the biological actions of the Axl kinase. Furthermore, we demonstrated that different threshold levels of Ras/ERK activation are needed to induce a block to apoptosis or proliferation in 32D cells. Recently, we have identified an Axl ligand, GAS6. Surprisingly, GAS6-stimulated 32D-Axl cells exhibited no blockage to apoptosis or mitogenic response which is correlated with the absence of Ras/ERK activation. Taken together, these data suggest that different extracellular domains dramatically alter the intracellular response of the Axl kinase. Furthermore, our data suggest that the GAS6-Axl interaction does not induce mitogenesis and that its exact role remains to be determined.

Indexed as

Adaptor Proteins, Signal TransducingAdaptor Proteins, Vesicular TransportIntercellular Signaling Peptides and ProteinsMitogen-Activated Protein KinasesAnimalsAxl Receptor Tyrosine KinaseBase SequenceCalcium-Calmodulin-Dependent Protein KinasesCell DivisionCell LineDNA PrimersEnzyme ActivationErbB ReceptorsGRB2 Adaptor ProteinGrowth Arrest-Specific Protein 6MiceAdaptor Proteins, Signal TransducingAdaptor Proteins, Vesicular TransportAxl Receptor Tyrosine KinaseAXL receptor tyrosine kinase, mouseCalcium-Calmodulin-Dependent Protein KinasesDNA PrimersErbB ReceptorsGRB2 Adaptor ProteinGrb2 protein, mouseGrowth Arrest-Specific Protein 6Intercellular Signaling Peptides and ProteinsMitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesOncogene ProteinsPhosphatidylinositol 3-KinasesPhosphotransferases (Alcohol Group Acceptor)ProteinsProto-Oncogene Proteinsras ProteinsReceptor Protein-Tyrosine KinasesRecombinant Fusion ProteinsShc1 protein, mouseShc Signaling Adaptor ProteinsSrc Homology 2 Domain-Containing, Transforming Protein 1

Identifiers

PMID8524290
PMCPMC230987
OpenAlexW2164779212

What Socratic 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 Socratic graph.