Evidence map›Paper›PMID 23226578›Full record

ArticleGenes & cancer2012

Crk and ABI1: binary molecular switches that regulate abl tyrosine kinase and signaling to the cytoskeleton.

Sajjad Hossain, Patrycja M Dubielecka, Aleksander F Sikorski, Raymond B Birge, Leszek Kotula

Open access · bronzeAbstract read
In one paragraph

Article in Genes & cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. CRISPR/CAS9-mediated knockout of Abi1 inhibits p185Journal of hematology & oncology · 2020
    Article
  10. Article
  11. The Crk adapter protein is essential forMolecular biology of the cell · 2019
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

5 authors at 4 institutions in 2 countries.

Sajjad HossainNew York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA ; Current address: Stony Brook University, Stony Brook, NY, USA.
Patrycja M Dubielecka
Aleksander F Sikorski
Raymond B Birge
Leszek Kotula
New York State Office for People With Developmental Disabilities · USRutgers New Jersey Medical SchoolStony Brook University · USUniversity of Business in Wrocław · PL

Funding

Non-canonical Signal Pathway for Crk in Breast CancerR01CA165077 · NCI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI BIRGE, RAYMOND B. · 2012 to 2016
$1.7M
Regulation of Macropinocytosis by Hssh3bp1R01NS044968 · NINDS · NEW YORK BLOOD CENTER · PI KOTULA, LESZEK · 2003 to 2006
$1.0M
NCI NIH HHS R01 CA165077NINDS NIH HHS R01 NS044968
6 · The paper itself

Abstract

The nonreceptor tyrosine kinases Abl and Arg are among the most well-characterized tyrosine kinases in the human genome. The activation of Abl by N-terminal fusions with Bcr (Bcr-Abl) or Gag (v-Abl) is responsible for chronic myeloid leukemia or Ph+ acute lymphoblastic leukemia and mouse leukemia virus, respectively. In addition, aberrant Abl and Arg activation downstream of several oncogenic growth factor receptors contributes to the development and progression of a variety of human cancers, often associated with poor clinical outcome, drug resistance, and tumor invasion and metastasis. Abl activation can occur by a variety of mechanisms that include domain interactions involving structural remodeling of autoinhibited conformations as well as direct phosphorylation by upstream kinases and phosphatases. Constitutive activation of Abl plays a significant role in regulating the actin cytoskeleton by modulating cell adhesion, motility, and invadopodia. This review addresses the role of Abl and Arg in tumor progression with particular emphasis on the roles of Crk and Abi1 adapter proteins as distinct molecular switches for Abl transactivation. These insights, combined with new insights into the structure of these kinases, provide the rationale to envision that Crk and Abi1 fine-tune Abl regulation to control signaling to the cytoskeleton.

Indexed as

Abi1Abl kinaseCrkcytoskeletonWAVE complex

Identifiers

PMID23226578
PMCPMC3513786
OpenAlexW2023673608

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.