Resistance of Short Term Activated T Cells to CD95-Mediated Apoptosis Correlates with De Novo Protein Synthesis of c-FLIPshort1
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Summary
C-FLIPshort, rather than c-FLIPlong, confers resistance of T cells to CD95-mediated apoptosis in the context of immune responses, and is suggested to be a more effective inhibitor than caspase-8 activation and apoptosis.
- Type
- article
- Published
- 2004-02-15
- Cited by
- 102
- References
- 44
- Access
- Open access
- OpenAlex
- https://openalex.org/W1932089347
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:43034204
Keywords
Apoptosis, Cycloheximide, Fas receptor, Flip, Cell biology
References
- c‐FLIPL is a dual function regulator for caspase‐8 activation and CD95‐mediated apoptosis
- Maturation of dendritic cells leads to up-regulation of cellular FLICE-inhibitory protein and concomitant down-regulation of death ligand-mediated apoptosis.
- Modulation of caspase-8 and FLICE-inhibitory protein expression as a potential mechanism of Epstein-Barr virus tumorigenesis in Burkitt's lymphoma.
- Transition of Apoptotic Resistant Vascular Smooth Muscle Cells to Troptotic Sensitive State Is Correlated with Downregulation of c-FLIP
- Tumoricidal activity of tumor necrosis factor–related apoptosis–inducing ligand in vivo
- Expression of c-FLIP(L) and resistance to CD95-mediated apoptosis of monocyte-derived dendritic cells: inhibition by bisindolylmaleimide.
- TCR-Mediated Up-Regulation of c-FLIPshort Correlates with Resistance Toward CD95-Mediated Apoptosis by Blocking Death-Inducing Signaling Complex Activity1
- CD95's deadly mission in the immune system
- Cytotoxicity‐dependent APO‐1 (Fas/CD95)‐associated proteins form a death‐inducing signaling complex (DISC) with the receptor.
- Metabolic inhibitors sensitize for CD95 (APO-1/Fas)-induced apoptosis by down-regulating Fas-associated death domain-like interleukin 1-converting enzyme inhibitory protein expression.
- Two CD95 (APO‐1/Fas) signaling pathways
- Biochemical mechanisms of IL-2-regulated Fas-mediated T cell apoptosis.
- The Role of c-FLIP in Modulation of CD95-induced Apoptosis*
- Monoclonal antibody-mediated tumor regression by induction of apoptosis.
- Endothelial Cell Apoptosis Induced by Oxidized LDL Is Associated with the Down-regulation of the Cellular Caspase Inhibitor FLIP*
- Expression level of c-FLIP versus Fas determines susceptibility to Fas ligand-induced cell death in murine thymoma EL-4 cells.
- Differential Modulation of Apoptosis Sensitivity in CD95 Type I and Type II Cells*
- Cellular FLICE-inhibitory Protein Splice Variants Inhibit Different Steps of Caspase-8 Activation at the CD95 Death-inducing Signaling Complex*
- DNA fragmentation and cell death is selectively triggered in activated human lymphocytes by Fas antigen engagement.
- The Long Form of FLIP Is an Activator of Caspase-8 at the Fas Death-inducing Signaling Complex*
Cited by
- Tissue-dependent T Cell Apoptosis and Transcriptional Regulation of Memory CD8+T Cell Differentiation During Viral Infections: A Dissertation
- Role of the ubiquitin-like modifier FAT10 in protein degradation and immunity
- c-FLIP-Proteine - von der Struktur zur Funktion in Immunantwort und Tumorgenese
- Cellular‐FLIP, Raji isoform (c‐FLIPR) modulates cell death induction upon T‐cell activation and infection
- Effector CD4+ T Cells Generate Intermediate Caspase Activity and Cleavage of Caspase-8 Substrates1
- Regulation of cell death by c-FLIP phosphorylation.
- Fever-Like Hyperthermia Controls T Lymphocyte Persistence by Inducing Degradation of Cellular FLIPshort1
- Prevalence of Newly Generated Naive Regulatory T Cells (Treg) Is Critical for Treg Suppressive Function and Determines Treg Dysfunction in Multiple Sclerosis1
- Anti-TOSO antibody treatment promotes T cell activation-induced cell death (AICD) in vitro and in vivo
- Switch in Fas-activated death signaling pathway as result of keratin 8/18-intermediate filament loss
- The role of apoptosis in the development and function of T lymphocytes
- Loss of Caspase-9 Provides Genetic Evidence for the Type I/II Concept of CD95-mediated Apoptosis*
- Upregulation of c-FLIP-short in response to TRAIL promotes survival of NSCLC cells, which could be suppressed by inhibition of Ca2+/calmodulin signaling
- A functional role of flip in conferring resistance of Crohn's disease lamina propria lymphocytes to FAS-mediated apoptosis.
- Mechanism underlying oxidative stress-mediated lipotoxicity: exposure of J774.2 macrophages to triacylglycerols facilitates mitochondrial reactive oxygen species production and cellular necrosis.
- The role of c-FLIP splice variants in urothelial tumours
- Viral FLICE inhibitory protein of Rhesus monkey rhadinovirus inhibits apoptosis by enhancing autophagosome formation
- Transgenic overexpression of the Caspase‐8 inhibitor FLIPshort leads to impaired T cell proliferation and an increased memory T cell pool after staphylococcal enterotoxin B injection
- Apoptosis by IL-2 deprivation in human CD8+ T cell blasts predominates over death receptor ligation, requires Bim expression and is associated with Mcl-1 loss.
- Up-regulation of c-FLIPS+R upon CD40 stimulation is associated with inhibition of CD95-induced apoptosis in primary precursor B-ALL.
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