ArticleEMBO reports2022
Bclaf1 regulates c-FLIP expression and protects cells from TNF-induced apoptosis and tissue injury.
Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- BCLAF1 restrains stress responses in hematopoietic stem cells to support expansion and repopulation.Blood advances · 2025Article
- Phosphoproteome Reveals the Role of Baicalin in Alleviating rPVL-Induced Cell Cycle Arrest in BMECs.Microorganisms · 2025Article
- p85β acts as a transcription cofactor and cooperates with BCLAF1 in the nucleus.Nature communications · 2025Article
- BCLAF1 Regulates Osteoarthritic Cartilage Degradation Through Interaction with LAMTOR2.International journal of biological sciences · 2025Article
- The Characteristic Function of Blood-Derived Exosomes and Exosomal circRNAs Isolated from Dairy Cattle during the Dry Period and Mid-Lactation.International journal of molecular sciences · 2023Article
- Covalent Organic Framework Nanobowls as Activatable Nanosensitizers for Tumor-Specific and Ferroptosis-Augmented Sonodynamic Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Phosphoproteomic and proteomic profiling in post-infarction chronic heart failure.Frontiers in pharmacology · 2023Article
- Bclaf1 regulates c-FLIP expression and protects cells from TNF-induced apoptosis and tissue injury.EMBO reports · 2022Article
- The Pharmacological Mechanism of Xiyanping Injection for the Treatment of Novel Coronavirus Pneumonia (COVID-19): Based on Network Pharmacology Strategy.Evidence-based complementary and alternative medicine : eCAM · 2022Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TNF stimulation generates pro-survival signals through activation of NF-κB that restrict the build-in death signaling triggered by TNF. The competition between TNF-induced survival and death signals ultimately determines the fate of a cell. Here, we report the identification of Bclaf1 as a novel component of the anti-apoptotic program of TNF. Bclaf1 depletion in multiple cells sensitizes cells to TNF-induced apoptosis but not to necroptosis. Bclaf1 exerts its anti-apoptotic function by promoting the transcription of CFLAR, a caspase 8 antagonist, downstream of NF-κB activation. Bclaf1 binds to the p50 subunit of NF-κB, which is required for Bclaf1 to stimulate CFLAR transcription. Finally, in Bclaf1 siRNA administered mice, TNF-induced small intestine injury is much more severe than in control mice with aggravated signs of apoptosis and pyroptosis. These results suggest Bclaf1 is a key regulator in TNF-induced apoptosis, both in vitro and in vivo.
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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.