ArticleApoptosis : an international journal on programmed cell death2008
Changes in FADD levels, distribution, and phosphorylation in TNFalpha-induced apoptosis in hepatocytes is caspase-3, caspase-8 and BID dependent.
Article in Apoptosis : an international journal on programmed cell death, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 21 citations in OpenAlex.
- Impaired FADD/BID signaling mediates cross-resistance to immunotherapy in Multiple Myeloma.Communications biology · 2023Article
- Upregulated FADD is associated with poor prognosis, immune exhaustion, tumor malignancy, and immunotherapy resistance in patients with lung adenocarcinoma.Frontiers in oncology · 2023Article
- rCsHscB Derived fromPathogens (Basel, Switzerland) · 2022Article
- FADD as a key molecular player in cancer progression.Molecular medicine (Cambridge, Mass.) · 2022Review
- Review
- Relationship between gut microbiota and type 2 diabetic erectile dysfunction in Sprague-Dawley rats.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2017Article
- Role of apoptosis-inducing factor, proline dehydrogenase, and NADPH oxidase in apoptosis and oxidative stress.Cell health and cytoskeleton · 2012Article
- DRO1 sensitizes colorectal cancer cells to receptor-mediated apoptosis.Oncology letters · 2011Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
FADD/MORT1 (The adaptor protein of Fas Associate Death Domain/Mediator of Receptor Induced Toxicity) is essential for signal transduction of death receptor signaling. We have previously shown that FADD is significantly up-regulated in TNFalpha/ActD induced apoptosis. Over-expression of FADD also induces death of lung cancer cells and primary hepatocytes. We hypothesize that the increase in detectable FADD levels require the proximal steps in apoptotic signaling and speculated that FADD would be redistributed in cells destined to undergo apoptosis. We show that monomeric non-phosphorylated FADD is up-regulated in hepatocytes treated with TNFalpha/ActD and that it accumulates in the cytoplasm. Nuclear phosphorylated FADD decreases with TNFalpha/ActD treatment. Dimeric FADD in the cytoplasm remains constant with TNFalpha/ActD. The change in FADD levels and distribution was dependent on caspase-3, caspase-8 activity and the presence of BID. Thus, changes in FADD levels and distribution are downstream of caspase activation and mitochondria changes that are initiated by the formation of the DISC complex. Changes in FADD levels and distribution may represent a novel feed-forward mechanism to propagate apoptosis signaling in hepatocytes.
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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.