Evidence map›Paper›PMID 24421390›Full record

ReviewMolecular and cellular biology2014

The capable ABL: what is its biological function?

Jean Y J Wang

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 1 pooled it
7.9field-weighted citation impact, top 2% 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

115 citing papers in PubMed, 1 synthesis or guideline pooled it, 191 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. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Weighted Ensemble Simulations With the Drude Polarizable Model.Journal of computational chemistry · 2025
    Article
  8. Article
  9. Review
  10. Article
  11. Haploinsufficiency ofFrontiers in cell and developmental biology · 2025
    Article
  12. Acetylation and Deacetylation of Cytoskeleton-Associated Proteins.Results and problems in cell differentiation · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

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

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

1 author at 1 institution in 1 country.

Jean Y J WangDepartment of Medicine, Division of Hematology-Oncology, Moores Cancer Center, University of California, San Diego, La Jolla, California, USA.
University of California San Diego · US

Funding

STRUCTURE AND FUNCTION OF THE C-ABL PROTO-ONCOPROTEINR01CA043054 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI WANG, JEAN Y.J. · 1986 to 2018
$4.4M
NCI NIH HHS R01 CA043054NCI NIH HHS R01CA043054
6 · The paper itself

Abstract

The mammalian ABL1 gene encodes the ubiquitously expressed nonreceptor tyrosine kinase ABL. In response to growth factors, cytokines, cell adhesion, DNA damage, oxidative stress, and other signals, ABL is activated to stimulate cell proliferation or differentiation, survival or death, retraction, or migration. ABL also regulates specialized functions such as antigen receptor signaling in lymphocytes, synapse formation in neurons, and bacterial adhesion to intestinal epithelial cells. Although discovered as the proto-oncogene from which the Abelson leukemia virus derived its Gag-v-Abl oncogene, recent results have linked ABL kinase activation to neuronal degeneration. This body of knowledge on ABL seems confusing because it does not fit the one-gene-one-function paradigm. Without question, ABL capabilities are encoded by its gene sequence and that molecular blueprint designs this kinase to be regulated by subcellular location-dependent interactions with inhibitors and substrate activators. Furthermore, ABL shuttles between the nucleus and the cytoplasm where it binds DNA and actin--two biopolymers with fundamental roles in almost all biological processes. Taken together, the cumulated results from analyses of ABL structure-function, ABL mutant mouse phenotypes, and ABL substrates suggest that this tyrosine kinase does not have its own agenda but that, instead, it has evolved to serve a variety of tissue-specific and context-dependent biological functions.

Indexed as

Genes, ablAnimalsHumansMiceModels, BiologicalMutationNuclear Localization SignalsOncogene Proteins v-ablProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene MasProto-Oncogene Proteins c-ablSignal TransductionARG tyrosine kinaseMAS1 protein, humanNuclear Localization SignalsOncogene Proteins v-ablProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene MasProto-Oncogene Proteins c-abl

Identifiers

PMID24421390
PMCPMC3993570
OpenAlexW2133900563

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.