ArticleThe EMBO journal2010
Tyrosine dephosphorylation is required for Bak activation in apoptosis.
Article in The EMBO journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- Inhibition of tyrosine kinase BMX increases cell death in response to existing chemotherapeutic agents overcoming apoptotic resistance in cancer.Cell death & disease · 2025Article
- Mathematical modelling of Alzheimer's disease biomarkers: Targeting Amyloid beta, Tau protein, Apolipoprotein E and Apoptotic pathways.American journal of translational research · 2024Review
- Kinase signalling adaptation supports dysfunctional mitochondria in disease.Frontiers in molecular biosciences · 2024Review
- Mitochondrial Kinases and the Role of Mitochondrial Protein Phosphorylation in Health and Disease.Life (Basel, Switzerland) · 2021Review
- Structural and biophysical insights into the mode of covalent binding of rationally designed potent BMX inhibitors.RSC chemical biology · 2020Article
- The expression patterns and the diagnostic/prognostic roles of PTPN family members in digestive tract cancers.Cancer cell international · 2020Article
- Article
- Micro-Economics of Apoptosis in Cancer: ncRNAs Modulation of BCL-2 Family Members.International journal of molecular sciences · 2018Review
- Perturbing mitosis for anti-cancer therapy: is cell death the only answer?EMBO reports · 2018Review
- Article
- Bik reduces hyperplastic cells by increasing Bak and activating DAPk1 to juxtapose ER and mitochondria.Nature communications · 2017Article
- Role of Notch signaling pathway in pancreatic cancer.American journal of cancer research · 2017Review
- Targeting cell death signalling in cancer: minimising 'Collateral damage'.British journal of cancer · 2016Review
- Mitochondria-Judges and Executioners of Cell Death Sentences.Molecular cell · 2016Review
- Key role of MEK/ERK pathway in sustaining tumorigenicity and in vitro radioresistance of embryonal rhabdomyosarcoma stem-like cell population.Molecular cancer · 2016Article
- Molecular underpinnings of neurodegenerative disorders: striatal-enriched protein tyrosine phosphatase signaling and synaptic plasticity.F1000Research · 2016Review
- BMX Negatively Regulates BAK Function, Thereby Increasing Apoptotic Resistance to Chemotherapeutic Drugs.Cancer research · 2015Article
- Cancer chemoresistance and BAK.Oncoscience · 2015Article
- Identification of novel focal adhesion kinase substrates: role for FAK in NFκB signaling.International journal of biological sciences · 2015Article
- Chk1 activity is required for BAK multimerization in association with PUMA during mitochondrial apoptosis.Cell communication and signaling : CCS · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
Abstract
Activation of the cell-death mediator Bak commits a cell to mitochondrial apoptosis. The initial steps that govern Bak activation are poorly understood. To further clarify these pivotal events, we have investigated whether post-translational modifications of Bak impinge on its activation potential. In this study, we report that on apoptotic stimulation Bak undergoes dephosphorylation at tyrosine residue 108 (Y108), a critical event that is necessary but not sufficient for Bak activation, but is required both for early exposure of the occluded N-terminal domain and multimerisation. RNA interference (RNAi) screening identified non-receptor tyrosine phosphatases (PTPNs) required for Bak dephosphorylation and apoptotic induction through chemotherapeutic agents. Specifically, modulation of PTPN5 protein expression by siRNA and overexpression directly affected both Bak-Y108 phosphorylation and the initiation of Bak activation. We further show that MEK/ERK signalling directly affects Bak phosphorylation through inhibition of PTPN5 to promote cell survival. We propose a model of Bak activation in which the regulation of Bak dephosphorylation constitutes the initial step in the activation process, which reveals a previously unsuspected mechanism controlling the initiation of mitochondrial apoptosis.
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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.