ArticleCellular signalling2007
c-Cbl is not required for ERK1/2-dependent degradation of BimEL.
Article in Cellular signalling, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Anoikis and cancer cell differentiation: novel modes of shikonin derivatives anticancer action in vitro.Molecular biology reports · 2024Article
- The role of Ubiquitination in Apoptosis and Necroptosis.Cell death and differentiation · 2022Review
- Delineating Crosstalk Mechanisms of the Ubiquitin Proteasome System That Regulate Apoptosis.Frontiers in cell and developmental biology · 2018Review
- Targeting Cdc20 as a novel cancer therapeutic strategy.Pharmacology & therapeutics · 2015Review
- The BCL2 Family: Key Mediators of the Apoptotic Response to Targeted Anticancer Therapeutics.Cancer discovery · 2015Review
- Potential roles of Centipede Scolopendra extracts as a strategy against EGFR-dependent cancers.American journal of translational research · 2015Article
- Targeting the regulatory machinery of BIM for cancer therapy.Critical reviews in eukaryotic gene expression · 2012Article
- Identification of a novel Bcl-2-interacting mediator of cell death (Bim) E3 ligase, tripartite motif-containing protein 2 (TRIM2), and its role in rapid ischemic tolerance-induced neuroprotection.The Journal of biological chemistry · 2011Article
- Bim and Mcl-1 exert key roles in regulating JAK2V617F cell survival.BMC cancer · 2011Article
- Contracting the 'mus cells'--does down-sizing suit us for diving into the memory pool?Immunological reviews · 2010Review
- The role of the ubiquitin proteasome system in ischemia and ischemic tolerance.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2009Review
- betaTrCP- and Rsk1/2-mediated degradation of BimEL inhibits apoptosis.Molecular cell · 2009Article
- Transforming growth factor beta (TGFbeta)-induced apoptosis: the rise & fall of Bim.Cell cycle (Georgetown, Tex.) · 2009Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Bim(EL) the most abundant Bim splice variant, is subject to ERK1/2-catalysed phosphorylation, which targets it for ubiquitination and proteasome-dependent destruction. In contrast, inactivation of ERK1/2, following withdrawal of survival factors, promotes stabilization of Bim(EL). It has been proposed that the RING finger protein Cbl binds to Bim(EL) and serves as its E3 ubiquitin ligase. However, this is controversial since most Cbl substrates are tyrosine phosphoproteins and yet Bim(EL) is targeted for destruction by ERK1/2-catalysed serine phosphorylation. Consequently, a role for Cbl could suggest a second pathway for Bim(EL) turnover, regulated by direct tyrosine phosphorylation, or could suggest that Bim(EL) is a coincidence detector, requiring phosphorylation by ERK1/2 and a tyrosine kinase. Here we show that degradation of Bim(EL) does not involve its tyrosine phosphorylation; indeed, Bim(EL) is not a tyrosine phosphoprotein. Furthermore, Bim(EL) fails to interact with Cbl and growth factor-stimulated, ERK1/2-dependent Bim(EL) turnover proceeds normally in Cbl-containing or Cbl-/- fibroblasts. These results indicate that Cbl is not required for ERK1/2-dependent Bim(EL) turnover in fibroblasts and epithelial cells and any role it has in other cell types is likely to be indirect.
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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.