Evidence map›Paper›PMID 26473374›Full record

ArticleOncotarget2015

Reciprocal regulation of Abl kinase by Crk Y251 and Abi1 controls invasive phenotypes in glioblastoma.

Sushil Kumar, Bin Lu, Updesh Dixit, Sajjad Hossain, Yongzhang Liu, Jing Li, Peter Hornbeck, Weiming Zheng, Adam G Sowalsky, Leszek Kotula and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Adaptor protein Abelson interactor 1 in homeostasis and disease.Cell communication and signaling : CCS · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Overexpression of CrkL as a novel biomarker for poor prognosis in gastric cancer.Cancer biomarkers : section A of Disease markers · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

11 authors at 8 institutions in 2 countries.

Sushil KumarDepartment of Microbiology, Biochemistry and Molecular Genetics, Cancer Center, Rutgers New Jersey Medical School, Newark, New Jersey, USA.
Bin LuInstitute of Biophysics, School of Life Sciences, Wenzhou Medical University, Wenzhou, China.
Updesh DixitDepartment of Microbiology, Biochemistry and Molecular Genetics, Cancer Center, Rutgers New Jersey Medical School, Newark, New Jersey, USA.
Sajjad HossainDepartments of Urology and Biochemistry and Molecular Biology, SUNY Upstate Medical University, New York, NY, USA.
Yongzhang LiuInstitute of Biophysics, School of Life Sciences, Wenzhou Medical University, Wenzhou, China.
Jing LiCell Signaling Technology, Danvers, MA, USA.
Peter HornbeckCell Signaling Technology, Danvers, MA, USA.
Weiming ZhengDepartment of Neurosurgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Adam G SowalskyDepartment of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Leszek KotulaDepartments of Urology and Biochemistry and Molecular Biology, SUNY Upstate Medical University, New York, NY, USA.
Raymond B BirgeDepartment of Microbiology, Biochemistry and Molecular Genetics, Cancer Center, Rutgers New Jersey Medical School, Newark, New Jersey, USA.
Cell Signaling Technology (United States) · USRutgers New Jersey Medical SchoolSUNY Upstate Medical University · USFirst Affiliated Hospital of Wenzhou Medical University · CNHarvard University · USInstitute of Biophysics · CNRutgers, The State University of New Jersey · USWenzhou Medical University · CN

Funding

Mechanism of PIN development in Abi1/Hssh3bp1 KO mouseR01CA161018 · NCI · UPSTATE MEDICAL UNIVERSITY · PI KOTULA, LESZEK · 2013 to 2017
$1.7M
NCI NIH HHS R01 CA161018PHS HHS NIH R01 161018PHS HHS NIH R01165077
6 · The paper itself

Abstract

Crk is the prototypical member of a class of Src homology 2 (SH2) and Src homology 3 (SH3) domain-containing adaptor proteins that positively regulate cell motility via the activation of Rac1 and, in certain tumor types such as GBM, can promote cell invasion and metastasis by mechanisms that are not well understood. Here we demonstrate that Crk, via its phosphorylation at Tyr251, promotes invasive behavior of tumor cells, is a prominent feature in GBM, and correlating with aggressive glioma grade IV staging and overall poor survival outcomes. At the molecular level, Tyr251 phosphorylation of Crk is negatively regulated by Abi1, which competes for Crk binding to Abl and attenuates Abl transactivation. Together, these results show that Crk and Abi1 have reciprocal biological effects and act as a molecular rheostat to control Abl activation and cell invasion. Finally, these data suggest that Crk Tyr251 phosphorylation regulate invasive cell phenotypes and may serve as a biomarker for aggressive GBM.

Indexed as

Cell MovementAdaptor Proteins, Signal TransducingApoptosisBinding SitesBiomarkers, TumorBlotting, WesternCell ProliferationCytoskeletal ProteinsFemaleGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticGlioblastomaHumansImmunoenzyme TechniquesImmunoprecipitationMaleABI1 protein, humanAdaptor Proteins, Signal TransducingBiomarkers, TumorCytoskeletal ProteinsProto-Oncogene Proteins c-ablProto-Oncogene Proteins c-crkAbi1cell invasionglioblastoma multiformaenon-canonical Crk signaling

Identifiers

PMID26473374
PMCPMC4741966
OpenAlexW2282477053

What OpenQuestion holds

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LicenceCC BY
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.