Evidence map›Paper›PMID 20841568›Full record

ReviewScience signaling2010

ABL tyrosine kinases: evolution of function, regulation, and specificity.

John Colicelli

Erratum issuedAbstract readReview
In one paragraph

Review in Science signaling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 208 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
208citing papers in PubMed, 1 pooled it
10.1field-weighted citation impact, top 1% 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

208 citing papers in PubMed, 1 synthesis or guideline pooled it, 354 citations in OpenAlex.

  1. The Role of c-Abl in Alzheimer's Disease: Guilty or not Guilty?Cellular and molecular neurobiology · 2025
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Tyrosine phosphoproteome profiling identifies cell-intrinsic signals limiting the efficacy of tyrosine kinase inhibitor therapies.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  8. Article
  9. Article
  10. Review
  11. Activity of STAMP inhibitors inBlood neoplasia · 2025
    Article
  12. Article
  13. Bend it like BIN1: how a membrane-curving adaptor protein shapes cardiac physiology.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  14. Article
  15. Article
  16. Review
  17. Role of c-ABL in DENV-2 Infection and Actin Remodeling in Vero Cells.International journal of molecular sciences · 2025
    Article
  18. Current and future of targeted therapies against BCR::ABL kinases.Journal of the Egyptian National Cancer Institute · 2025
    Review
  19. Article
  20. Article

148 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

1 author at 1 institution.

John ColicelliDepartment of Biological Chemistry, Molecular Biology Institute and Jonsson Comprehensive Cancer Center, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA. colicelli@mednet.ucla.edu
UCLA Jonsson Comprehensive Cancer Center

Funding

A Novel Screen for Compounds that Outflank BCR-ABL Drug-ResistanceR01CA136699 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI COLICELLI, JOHN J. · 2009 to 2011
$937k
NCI NIH HHS CA136699NCI NIH HHS R01 CA136699
6 · The paper itself

Abstract

ABL-family proteins comprise one of the best conserved branches of the tyrosine kinases. Each ABL protein contains an SH3-SH2-TK (Src homology 3-Src homology 2-tyrosine kinase) domain cassette, which confers autoregulated kinase activity and is common among nonreceptor tyrosine kinases. This cassette is coupled to an actin-binding and -bundling domain, which makes ABL proteins capable of connecting phosphoregulation with actin-filament reorganization. Two vertebrate paralogs, ABL1 and ABL2, have evolved to perform specialized functions. ABL1 includes nuclear localization signals and a DNA binding domain through which it mediates DNA damage-repair functions, whereas ABL2 has additional binding capacity for actin and for microtubules to enhance its cytoskeletal remodeling functions. Several types of posttranslational modifications control ABL catalytic activity, subcellular localization, and stability, with consequences for both cytoplasmic and nuclear ABL functions. Binding partners provide additional regulation of ABL catalytic activity, substrate specificity, and downstream signaling. Information on ABL regulatory mechanisms is being mined to provide new therapeutic strategies against hematopoietic malignancies caused by BCR-ABL1 and related leukemogenic proteins.

Indexed as

Evolution, MolecularActinsAnimalsDNA DamageDNA RepairFusion Proteins, bcr-ablHematologic NeoplasmsHumansMicrotubulesNuclear Localization SignalsProtein BindingProtein Processing, Post-TranslationalProtein TransportProto-Oncogene Proteins c-ablsrc Homology DomainsActinsFusion Proteins, bcr-ablNuclear Localization SignalsProto-Oncogene Proteins c-abl

Identifiers

PMID20841568
PMCPMC2954126
OpenAlexW1990848928

What OpenQuestion holds

Textmetadata
LicenceTDM
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.