Evidence map›Paper›PMID 17389688›Full record

ArticleJournal of cell science2007

Bcr-Abl induces abnormal cytoskeleton remodeling, beta1 integrin clustering and increased cell adhesion to fibronectin through the Abl interactor 1 pathway.

Yingzhu Li, Nancy Clough, Xiaolin Sun, Weidong Yu, Brian L Abbott, Christopher J Hogan, Zonghan Dai

Open access · greenAbstract read
In one paragraph

Article in Journal of cell science, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

31 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. [Role of Abelson interactor 2 in progression and prognosis of gastric cancer and its regulatory mechanisms].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. CRISPR/CAS9-mediated knockout of Abi1 inhibits p185Journal of hematology & oncology · 2020
    Article
  15. Review
  16. Article
  17. Article
  18. Phosphoregulation of the WAVE regulatory complex and signal integration.Seminars in cell & developmental biology · 2013
    Review
  19. Structure and dynamic regulation of Abl kinases.The Journal of biological chemistry · 2013
    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

7 authors at 1 institution in 1 country.

Yingzhu LiDepartment of Medicine, University of Colorado at Denver and Health Sciences Center, Aurora, CO 80045, USA.
Nancy Clough
Xiaolin Sun
Weidong Yu
Brian L Abbott
Christopher J Hogan
Zonghan Dai
University of Colorado Denver · US

Funding

HUMAN HEMATOPOIETIC PRECURSOR CELLSR01HL061382 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI HOGAN, CHRISTOPHER J · 1999 to 2005
$1.8M
AbI-Abi signaling in neoplastic hematopoiesisR01CA094921 · NCI · UNIVERSITY OF COLORADO DENVER · PI DAI, ZONGHAN · 2003 to 2007
$1.3M
NCI NIH HHS R01 CA094921NCI NIH HHS R01 CA94921NHLBI NIH HHS R01 HL061382NHLBI NIH HHS R01 HL61382
6 · The paper itself

Abstract

Hematopoietic cells isolated from patients with Bcr-Abl-positive leukemia exhibit multiple abnormalities of cytoskeletal and integrin function. These abnormalities are thought to play a role in the pathogenesis of leukemia; however, the molecular events leading to these abnormalities are not fully understood. We show here that the Abi1 pathway is required for Bcr-Abl to stimulate actin cytoskeleton remodeling, integrin clustering and cell adhesion. Expression of Bcr-Abl induces tyrosine phosphorylation of Abi1. This is accompanied by a subcellular translocation of Abi1/WAVE2 to a site adjacent to membrane, where an F-actin-enriched structure containing the adhesion molecules such as beta1-integrin, paxillin and vinculin is assembled. Bcr-Abl-induced membrane translocation of Abi1/WAVE2 requires direct interaction between Abi1 and Bcr-Abl, but is independent of the phosphoinositide 3-kinase pathway. Formation of the F-actin-rich complex correlates with an increased cell adhesion to fibronectin. More importantly, disruption of the interaction between Bcr-Abl and Abi1 by mutations either in Bcr-Abl or Abi1 not only abolished tyrosine phosphorylation of Abi1 and membrane translocation of Abi1/WAVE2, but also inhibited Bcr-Abl-stimulated actin cytoskeleton remodeling, integrin clustering and cell adhesion to fibronectin. Together, these data define Abi1/WAVE2 as a downstream pathway that contributes to Bcr-Abl-induced abnormalities of cytoskeletal and integrin function.

Indexed as

Cell AdhesionCell LineCytoskeletonFibronectinsFusion Proteins, bcr-ablHumansIntegrin beta1FibronectinsFusion Proteins, bcr-ablIntegrin beta1

Identifiers

PMID17389688
PMCPMC1950936
OpenAlexW2148056757

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.