ArticleCell death and differentiation2011
TAK1 regulates SCF expression to modulate PKBα activity that protects keratinocytes from ROS-induced apoptosis.
Article in Cell death and differentiation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- TAK1 activates PANoptosis through the NF-κB signalling pathway to delay diabetic wound healing.Burns & trauma · 2026Article
- Screening of Mediterranean Plant-Derived Extracts for Antioxidant Effect in Cell-Free and Human Cell Line Models.Antioxidants (Basel, Switzerland) · 2025Article
- ROS induced pyroptosis in inflammatory disease and cancer.Frontiers in immunology · 2024Review
- Skin wound closure delay in metabolic syndrome correlates with SCF deficiency in keratinocytes.Scientific reports · 2020Article
- Deficiency in fibroblast PPARβ/δ reduces nonmelanoma skin cancers in mice.Cell death and differentiation · 2020Article
- Multifaceted roles of TAK1 signaling in cancer.Oncogene · 2020Review
- Mesenchymal stem cells restore the sperm motility from testicular torsion-detorsion injury by regulation of glucose metabolism in sperm.Stem cell research & therapy · 2019Article
- Article
- Angiopoietin-like 4 Mediates Colonic Inflammation by Regulating Chemokine Transcript Stability via Tristetraprolin.Scientific reports · 2017Article
- Cancer-associated fibroblasts enact field cancerization by promoting extratumoral oxidative stress.Cell death & disease · 2017Article
- Multikinase Inhibitors Induce Cutaneous Toxicity through OAT6-Mediated Uptake and MAP3K7-Driven Cell Death.Cancer research · 2016Article
- Differential roles of ASK1 and TAK1 in Helicobacter pylori-induced cellular responses.Infection and immunity · 2013Article
- Loss of TAK1 increases cell traction force in a ROS-dependent manner to drive epithelial-mesenchymal transition of cancer cells.Cell death & disease · 2013Article
- Enhancement of wound closure in diabetic mice by ex vivo expanded cord blood CD34+ cells.Cellular & molecular biology letters · 2013Article
- FIH-1/c-kit signaling: a novel contributor to corneal epithelial glycogen metabolism.Investigative ophthalmology & visual science · 2013Article
- Nox4-dependent ROS modulation by amino endoperoxides to induce apoptosis in cancer cells.Cell death & disease · 2013Article
- Transforming growth factor beta-activated kinase 1 (TAK1)-dependent checkpoint in the survival of dendritic cells promotes immune homeostasis and function.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- TAK1 negatively regulates NF-κB and p38 MAP kinase activation in Gr-1+CD11b+ neutrophils.Immunity · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated reactive oxygen species (ROS) generation contributes to many human pathologies, including cancer and diabetes. During normal wound repair, inflammation-induced ROS production must be tightly controlled, but the mechanisms reining their generation remain unclear. Herein, we show that transforming growth factor β-activated kinase 1 (TAK1) directly regulates stem cell factor (SCF) expression, which activates the protein kinase B (PKB)α pro-survival pathway in a cell-autonomous manner to protect keratinocytes from ROS-mediated cell death. TAK1 is a pivotal inflammatory mediator whose expression was transiently elevated during wound healing, paralleling the ROS production profile. TAK1 deficiency in keratinocytes led to increased apoptosis in response to anoikis and TNF-α treatment and was associated with elevated ROS level as analyzed by FACS. Using organotypic skin co-culture and comparative growth factor array analysis, we revealed a cell-autonomous mechanism that involved the SCF/c-Kit/PKBα signaling cascade. Ectopic expression of TAK1 or treatment with exogenous recombinant SCF restored the increased ROS production and apoptotic cell death in TAK1-deficient keratinocytes. Conversely, normal keratinocytes treated with various inhibitors targeting the SCF/c-Kit/PKBα pathway exhibited increased ROS production and TNF-α- or anoikis-induced apoptosis. Our study reveals a novel anti-apoptotic role for SCF in keratinocytes and identifies TAK1 as a novel player uniting inflammation and ROS regulation in skin redox biology.
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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.