Evidence map›Paper›PMID 18453543›Full record

ArticleCarcinogenesis2008

Abi1 gene silencing by short hairpin RNA impairs Bcr-Abl-induced cell adhesion and migration in vitro and leukemogenesis in vivo.

Weidong Yu, Xiaolin Sun, Nancy Clough, Everardo Cobos, Yunxia Tao, Zonghan Dai

Open access · hybridAbstract read
In one paragraph

Article in Carcinogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Acetylation and Deacetylation of Cytoskeleton-Associated Proteins.Results and problems in cell differentiation · 2025
    Review
  2. Adaptor protein Abelson interactor 1 in homeostasis and disease.Cell communication and signaling : CCS · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Acetylation of Abelson interactor 1 at K416 regulates actin cytoskeleton and smooth muscle contraction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. CRISPR/CAS9-mediated knockout of Abi1 inhibits p185Journal of hematology & oncology · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
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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

6 authors at 4 institutions in 2 countries.

Weidong YuDepartment of Internal Medicine, Texas Tech University Health Sciences Center, 1400 Wallace Boulevard, Amarillo, TX 79106, USA.
Xiaolin Sun
Nancy Clough
Everardo Cobos
Yunxia Tao
Zonghan Dai
Texas Tech University · USPeking University · CNTexas Tech University Health Sciences Center · USUniversity of Colorado Denver · US

Funding

AbI-Abi signaling in neoplastic hematopoiesisR01CA094921 · NCI · UNIVERSITY OF COLORADO DENVER · PI DAI, ZONGHAN · 2003 to 2007
$1.3M
THE ROLE OF VEGF ON PDPKD DISEASE PROGRESSIONK01DK067191 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI TAO, YUNXIA · 2005 to 2010
$651k
NCI NIH HHS R01 CA094921NIDDK NIH HHS K01 DK067191
6 · The paper itself

Abstract

Abl interactor (Abi) 1 was first identified as the downstream target of Abl tyrosine kinases and was found to be dysregulated in leukemic cells expressing oncogenic Bcr-Abl and v-Abl. Although the accumulating evidence supports a role of Abi1 in actin cytoskeleton remodeling and growth factor/receptor signaling, it is not clear how it contributes to Bcr-Abl-induced leukemogenesis. We show here that Abi1 gene silencing by short hairpin RNA attenuated the Bcr-Abl-induced abnormal actin remodeling, membrane-type 1 metalloproteinase clustering and inhibited cell adhesion and migration on fibronectin-coated surfaces. Although the knock down of Abi1 expression did not affect growth factor-independent growth of Bcr-Abl-transformed Ba/F3 cells in vitro, it impeded competitive expansion of these cells in non obese diabetic (NOD)/ severe combined immuno-deficiency (SCID) mice. Remarkably, the knock down of Abi1 expression in Bcr-Abl-transformed Ba/F3 cells impaired the leukemogenic potential of these cells in NOD/SCID mice. Abi1 contributes to Bcr-Abl-induced leukemogenesis in part through Src family kinases, as the knock down of Abi1 expression attenuates Bcr-Abl-stimulated activation of Lyn. Together, these data provide for the first time the direct evidence that supports a critical role of Abi1 pathway in the pathogenesis of Bcr-Abl-induced leukemia.

Indexed as

Gene SilencingAdaptor Proteins, Signal TransducingAnimalsBlotting, WesternCell AdhesionCell MovementCell Transformation, NeoplasticCytoskeletal ProteinsFemaleFlow CytometryFusion Proteins, bcr-ablImmunoprecipitationLeukemiaMatrix Metalloproteinase 14MiceMice, Inbred NODAbi1 protein, mouseAdaptor Proteins, Signal TransducingCytoskeletal ProteinsFusion Proteins, bcr-abllyn protein-tyrosine kinaseMatrix Metalloproteinase 14Mmp14 protein, mouseRNA, MessengerRNA, Small Interferingsrc-Family KinasesTyrosine

Identifiers

PMID18453543
PMCPMC2527646
OpenAlexW2153220877

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.