ArticleThe Journal of biological chemistry2006
Opposite roles of FAP-1 and dynamin in the regulation of Fas (CD95) translocation to the cell surface and susceptibility to Fas ligand-mediated apoptosis.
Article in The Journal of biological chemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Regulation of TCR signalling by tyrosine phosphatases: from immune homeostasis to autoimmunity.Immunology · 2012Pooled it
- The Fas-FasL system: from apoptosis regulator to therapeutic target in autoimmunity, cancer, and transplantation.Immunologic research · 2026Review
- CPNE5 overexpression inhibits cardiomyocytes apoptosis by promoting the degradation of FAS receptor.iScience · 2025Article
- HSP70-Mediated Autophagy-Apoptosis-Inflammation Network and Neuroprotection Induced by Heat Acclimatization.Biology · 2025Review
- Mechano-inhibition of endocytosis sensitizes cancer cells to Fas-induced Apoptosis.Cell death & disease · 2024Article
- Pirin Inhibits FAS-Mediated Apoptosis to Support Colorectal Cancer Survival.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Therapeutic approaches targeting CD95L/CD95 signaling in cancer and autoimmune diseases.Cell death & disease · 2022Review
- Overexpression of cytoplasmic dynamin 2 is associated with worse outcomes in patients with clear cell renal cell carcinoma.Cancer biomarkers : section A of Disease markers · 2022Article
- A review of Dynamin 2 involvement in cancers highlights a promising therapeutic target.Journal of experimental & clinical cancer research : CR · 2021Review
- Heat Shock Protein 70 (HSP70) Induction: Chaperonotherapy for Neuroprotection after Brain Injury.Cells · 2020Review
- Heat shock protein signaling in brain ischemia and injury.Neuroscience letters · 2020Review
- Polyubiquitination of p62/SQSTM1 is a prerequisite for Fas/CD95 aggregation to promote caspase-dependent apoptosis in cadmium-exposed mouse monocyte RAW264.7 cells.Scientific reports · 2019Article
- Apoptotic signalling targets the post-endocytic sorting machinery of the death receptor Fas/CD95.Nature communications · 2019Article
- The Effect of Caffeic Acid on Spermatogonial Stem Cell-type A Cryopreservation.Reports of biochemistry & molecular biology · 2018Article
- The impact of phosphatases on proliferative and survival signaling in cancer.Cellular and molecular life sciences : CMLS · 2018Review
- Therapeutic hypothermia for ischemic stroke; pathophysiology and future promise.Neuropharmacology · 2018Review
- The Fas/Fap-1/Cav-1 complex regulates IL-1RA secretion in mesenchymal stem cells to accelerate wound healing.Science translational medicine · 2018Article
- The 70-kDa heat shock protein (Hsp70) as a therapeutic target for stroke.Expert opinion on therapeutic targets · 2018Review
- Computational Structural Biology ofFrontiers in oncology · 2018Review
- TRPC1 Deletion Causes Striatal Neuronal Cell Apoptosis and Proteomic Alterations in Mice.Frontiers in aging neuroscience · 2018Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Human melanoma is the most aggressive form of skin cancer and is extremely resistant to radiation and chemotherapy. One of the critical parameters of this resistance is down-regulation of Fas (CD95) cell-surface expression. Using TIG3 normal human fibroblasts and human melanoma cell lines, we investigated transcriptional regulation of FAP-1, a regulator of Fas translocation in the cell. Protein-tyrosine phosphatase FAP-1 (PTPN13, PTP-BAS) interacts with human Fas protein and prevents its export from the cytoplasm to the cell surface. In contrast, dynamin-2 facilitates Fas protein translocation from the Golgi apparatus via the trans-Golgi network to the cell surface. Suppression of dynamin functions by dominant negative dynamin K44A blocks Fas export, whereas the down-regulation of FAP-1 expression by specific RNA interference restores Fas export (a phenomenon that could still be down-regulated in the presence of dominant-negative dynamin). Based on the FAP-1- and dynamin-dependent regulation of Fas translocation, we have created human melanoma lines with different levels of surface expression of Fas. Treatment of these melanoma lines with soluble Fas ligand resulted in programmed cell death that was proportional to the pre-existing levels of surface Fas. Taking into consideration the well known observations that FAP-1 expression is often up-regulated in metastatic tumors, we have established a causal connection between high basal NF-kappaB transcription factor activity (which is a hallmark of many types of metastatic tumors) and NF-kappaB-dependent transcriptional regulation of FAP-1 gene expression that finally restricts Fas protein trafficking, thereby, facilitating the survival of cancer cells.
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