ArticleGenes & development1999
c-Abl is activated by growth factors and Src family kinases and has a role in the cellular response to PDGF.
Article in Genes & development, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 195 papers.
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.
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.
Who cites it
195 citing papers in PubMed, 423 citations in OpenAlex.
- An Itch Receptor Drives Melanoma.bioRxiv : the preprint server for biology · 2026Article
- Membrane Curvature Activates Src kinase and Promotes Metastatic Cancer Cell Survival.bioRxiv : the preprint server for biology · 2026Article
- Selective Targeting of Tip Endothelial Cells as a Therapeutic Strategy for Tumor Angiogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- c-Abl controls early embryonic morphogenesis through YAP/p73-dependent regulation of trophectoderm and inner cell mass lineages.Cell communication and signaling : CCS · 2026Article
- Detection of c-Abl and mTERT expression by DMBA-ınduced mouse model of premature ovarian ınsufficiency.Journal of molecular histology · 2025Article
- ABL1‒YAP1 axis in intestinal stem cell activated by deoxycholic acid contributes to hepatic steatosis.Journal of translational medicine · 2024Article
- The identification of c-Abl inhibitors as potential agents for Parkinson's disease: a preliminary in silico approach.Molecular diversity · 2024Article
- Wnt signaling couples G2 phase control with differentiation during hematopoiesis in Drosophila.Developmental cell · 2024Article
- Non-Receptor Tyrosine Kinases: Their Structure and Mechanistic Role in Tumor Progression and Resistance.Cancers · 2024Review
- A NanoCurvS platform for quantitative and multiplex analysis of curvature-sensing proteins.Biomaterials science · 2023Article
- Src stimulates Abl-dependent phosphorylation of the guanine exchange factor Net1A to promote its cytosolic localization and cell motility.The Journal of biological chemistry · 2023Article
- The phosphorylation of PHF5A by TrkA-ERK1/2-ABL1 cascade regulates centrosome separation.Cell death & disease · 2023Article
- ABL1/2 and DDR1 Drive MEKi Resistance in NRAS-Mutant Melanomas by Stabilizing RAF/MYC/ETS1 and Promoting RAF Homodimerization.Cancers · 2023Article
- Extracellular matrix regulates force transduction at VE-cadherin junctions.Molecular biology of the cell · 2022Article
- ABL kinases regulate translation in HER2+ cells through Y-box-binding protein 1 to facilitate colonization of the brain.Cell reports · 2022Article
- Circular dorsal ruffles disturb the growth factor-induced PI3K-AKT pathway in hepatocellular carcinoma Hep3B cells.Cell communication and signaling : CCS · 2022Article
- A JAM-A-tetraspanin-αvβ5 integrin complex regulates contact inhibition of locomotion.The Journal of cell biology · 2022Article
- Imatinib can act as an Allosteric Activator of Abl Kinase.Journal of molecular biology · 2022Article
- Computational Identification of BCR-ABL Oncogenic Signaling as a Candidate Target of Withaferin A and Withanone.Biomolecules · 2022Article
- Nonreceptor Tyrosine Kinase c-Abl-Mediated PHB2 Phosphorylation Aggravates Mitophagy Disorder in Parkinson's Disease Model.Oxidative medicine and cellular longevity · 2022Article
135 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The c-Abl tyrosine kinase localizes to the cytoplasm and plasma membrane in addition to the nucleus. However, there is little information regarding a role for c-Abl in the cytoplasm/plasma membrane compartments. Here we report that a membrane pool of c-Abl is activated by the growth factors PDGF and EGF in fibroblasts. The pattern and kinetics of activation are similar to growth factor activation of Src family kinases. To determine whether a link existed between activation of c-Abl and members of the Src family, we examined c-Abl kinase activity in cells that expressed oncogenic Src proteins. We found that c-Abl kinase activity was increased by 10- to 20-fold in these cells, and that Src and Fyn kinases directly phosphorylated c-Abl in vitro. Furthermore, overexpression of wild-type Src potentiated c-Abl activation by growth factors, and a kinase-inactive form of Src reduced this activation, showing that Abl activation by growth factors occurs at least in part via activation of Src kinases. Significantly, we show that c-Abl has a functional role in the morphological response to PDGF. Whereas PDGF treatment of serum-starved wild-type mouse embryo fibroblasts resulted in distinct linear or circular/dorsal membrane ruffling, c-Abl-null cells demonstrated dramatically reduced ruffling in response to PDGF, which was rescued by physiological re-expression of c-Abl. These data identify c-Abl as a downstream target of activated receptor tyrosine kinases and Src family kinases, and show for the first time that c-Abl functions in the cellular response to growth factors.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.