ArticleThe EMBO journal2002
c-Abl is an effector of Src for growth factor-induced c-myc expression and DNA synthesis.
Article in The EMBO journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 120 citations in OpenAlex.
- Article
- Combating acquired resistance to MAPK inhibitors in melanoma by targeting Abl1/2-mediated reactivation of MEK/ERK/MYC signaling.Nature communications · 2020Article
- CDCP1 overexpression drives prostate cancer progression and can be targeted in vivo.The Journal of clinical investigation · 2020Article
- α-Synucleinopathy associated c-Abl activation causes p53-dependent autophagy impairment.Molecular neurodegeneration · 2020Article
- c-Abl regulates YAPY357 phosphorylation to activate endothelial atherogenic responses to disturbed flow.The Journal of clinical investigation · 2019Article
- Ponatinib: a novel multi-tyrosine kinase inhibitor against human malignancies.OncoTargets and therapy · 2019Review
- The HDAC6 inhibitor C1A modulates autophagy substrates in diverse cancer cells and induces cell death.British journal of cancer · 2018Article
- EnABLing Tumor Growth and Progression: Recent progress in unraveling the functions of ABL kinases in solid tumor cells.Current pharmacology reports · 2018Article
- Article
- Common and differential genetically pathways between ulcerative colitis and colon adenocarcinoma.Gastroenterology and hepatology from bed to bench · 2017Article
- Coordination of signalling networks and tumorigenic properties by ABL in glioblastoma cells.Oncotarget · 2016Article
- Somatically mutated ABL1 is an actionable and essential NSCLC survival gene.EMBO molecular medicine · 2016Article
- Multifunctional Abl kinases in health and disease.Journal of cell science · 2016Review
- C-Abl tyrosine kinase mediates neurotoxic prion peptide-induced neuronal apoptosis via regulating mitochondrial homeostasis.Molecular neurobiology · 2014Article
- Hypoxic conditioned medium from human amniotic fluid-derived mesenchymal stem cells accelerates skin wound healing through TGF-β/SMAD2 and PI3K/Akt pathways.International journal of molecular sciences · 2014Article
- Inhibition of c-Abl kinase activity renders cancer cells highly sensitive to mitoxantrone.PloS one · 2014Article
- Role of ABL family kinases in cancer: from leukaemia to solid tumours.Nature reviews. Cancer · 2013Review
- Transcriptome analyses of inhibitor-treated schistosome females provide evidence for cooperating Src-kinase and TGFβ receptor pathways controlling mitosis and eggshell formation.PLoS pathogens · 2013Article
- Functions and regulation of circular dorsal ruffles.Molecular and cellular biology · 2012Review
- Activation of abl family kinases in solid tumors.Genes & cancer · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism by which the ubiquitously expressed Src family kinases regulate mitogenesis is not well understood. Here we report that cytoplasmic tyrosine kinase c-Abl is an important effector of c-Src for PDGF- and serum-induced DNA synthesis. Inactivation of cytoplasmic c-Abl by the kinase-inactive Abl-PP-K(-) (AblP242E/P249E/K290M) or by microinjection of Abl neutralizing antibodies inhibited mitogenesis. The kinase-inactive SrcK295M induced a G(1) block that was overcome by the constitutively active Abl-PP (AblP242E/P249E). Conversely, the inhibitory effect of Abl-PP-K(-) was not compensated by Src. c-Src-induced c-Abl activation involves phosphorylation of Y245 and Y412, two residues required for c-Abl mitogenic function. Finally, we found that p53 inactivation and c-myc expression, two cell cycle events regulated by Src during mitogenesis, also implied c-Abl: c-Abl function was dispensable in cells deficient in active p53 and inhibition of c-Abl reduced mitogen-induced c-myc expression. These data identify a novel function of cytoplasmic c-Abl in the signalling pathways regulating growth factor-induced c-myc expression and we propose the existence of a tyrosine kinase signalling cascade (PDGFR/c-Src/c-Abl) important for mitogenesis.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.