FADD (Ab-191) Antibody

1. results show that N-FADD is a more potent apoptotic inducer and VNP20009-mediated targeted expression of N-FADD provides a possible cancer gene therapeutic approach for the treatment of melanoma. PMID:27767039
2. these results demonstrated that RIPK3-mediated signaling in Tie-2 expressing cells was responsible for the embryonic lethality of Fadd-/- with cardiac failure. PMID:27584790
3. The study provides genetic evidence that different RIP1 kinase inactive mutations have distinct impacts on the embryogenesis of Fadd-deficient mice. PMID:28574501
4. Our findings reveal that MLKL and FADD play critical roles in preventing lymphoproliferative disease and activating the NLRP3 inflammasome PMID:27498868
5. miR-7a was a necessary mediator in FADD-regulated FAK expression. In contrast to its classical apoptotic role, FADD interference could reduce the rate of cell migration, which could be rescued by inhibiting miR-7a expression. PMID:27286445
6. In macrophages, ultraviolet radiation induced association of MyD88 with FADD and migration of FADD to the cell membrane PMID:27676214
7. The authors conclude that FADD is a master regulator of glucose and fat metabolism. PMID:27357657
8. Mice deficient in RIPK3 or doubly deficient in MLKL and FADD, but not MLKL alone, are more susceptible to influenza A virus than their wild-type counterparts, revealing an important role for RIPK3-mediated apoptosis in antiviral immunity. PMID:27321907
9. Wild-type cells can execute apoptosis via both, the mitochondrial and the receptor-mediated pathway whereas FADD-deficient cells can only activate the intrinsic pathway. There is a difference in UVC radiation response between two cell lines indicating the role of FADD in the selection of cell death modality. PMID:27258329
10. This study reveals an essential role of SUMOylated FADD in Drp1- and caspase-10-dependent necrosis. PMID:27799292
11. Deletion of FADD in macrophages and granulocytes results in RIP3- and MyD88-dependent systemic inflammation. PMID:25874713
12. A constitutively phosphoryl-mimicking mutation of Fas-associated death domain (FADD-D) enhances Notch-1 signaling and compromises Wnt signaling in both cultured myoblasts and regenerating muscles. PMID:26303234
13. Beta amyloid-induced upregulation of death receptor 6 accelerates the toxic effect of N-terminal fragment of amyloid precursor protein PMID:25150572
14. Phosphorylation of FADD by the kinase CK1alpha promotes KRASG12D-induced lung cancer. PMID:25628462
15. This study evaluated the role of FADD in pancreatic islets and insulin secretion. PMID:25641109
16. depletion of alphaNAC in multiple types of cancer cells induce typical apoptotic cell death. This anti-apoptotic function is mediated by the FADD/c-Jun N-terminal kinase pathway. PMID:24901053
17. These data suggest that as a death receptor, FADD is also required for cell survival in beta-selection as a regulator of Notch1 expression. PMID:24901044
18. using T-cell specific deletion mice, we observed that FADD deficiency in thymocytes led to increased apoptosis and reduced cell numbers, which may be attributed to the reduction of Glut1 expression and correspondingly decreased glucose uptake PMID:25078620
19. FADD deficiency protects against myocardial ischemia/reperfusion injury in a heart failure mouse model. PMID:24058479
20. glycogen synthesis, glycolysis, and gluconeogenesis were dysregulated because of FADD phosphorylation, both in MEFs and liver tissue of the mice bearing phosphorylation-mimicking mutation form of FADD. PMID:23828893
21. FADD regulates the fate determination of cycling satellite cells. PMID:24375410
22. p45 forms a complex with FADD and diminishes Fas-FADD mediated death signaling. PMID:23935974
23. Used proteomics and bioinformatic analysis to study proteins differentially expressed in three cell lines containing FADD and its mutant, FADD-A and FADD-D. PMID:23744592
24. Impaired mitochondrial function and proteolysis may play pivotal roles in the dysfunction associated with FADD deficiency-induced disorders, probably including embryonic lethality. PMID:23689606
25. FADD Protects Cells from IFN-gamma-Activated Necrosis by Preventing Formation of the RIP1-RIP3 Necrosome. PMID:23898178
26. Fas (TNF receptor superfamily member CD95) activates interleukin (IL)-1beta and IL-18 in a caspase-8- and Fas-associated death domain (FADD) protein-dependent and receptor-interacting protein (Rip)3-independent pathway. PMID:23144495
27. show that epidermal keratinocyte-restricted deficiency of the adaptor protein FADD (FADD(E-KO)) induced severe inflammatory skin lesions in mice PMID:22000287
28. RIPK3 and FADD have opposing and complementary roles in promoting T-cell clonal expansion and homeostasis. PMID:21876153
29. tumor necrosis factor alpha-induced necroptosis requires the adaptor proteins FADD and NEMO. PMID:21746883
30. mechanisms preventing RIP3-mediated epithelial cell death are critical for maintenance of intestinal homeostasis and indicate that programmed necrosis of intestinal epithelial cells might be implicated in the pathogenesis of inflammatory bowel disease PMID:21804564
31. data demonstrate an unexpected cell-type-specific interplay between FADD and RIP1, which is critical for the regulation of apoptosis and necrosis during embryogenesis and lymphocyte function PMID:21368761
32. specific polymorphisms at Fas, FasL and Fadd genes that differentiate mouse strains exhibiting extreme differences in susceptibility to gamma radiation-induced T-cell lymphomas. PMID:20889682
33. FADD is critical for ODC apoptosis and the development of autoimmune demyelinating disease. PMID:21068410
34. molecular studies led to the discovery of a previously unappreciated HIF-1 binding site in the FADD promoter, which controls repression of FADD during hypoxia. PMID:20943999
35. FADD constitutes a mechanism to keep TCR-induced programmed necrotic signaling in check during early phases of T-cell clonal expansion. PMID:20615958
36. Importance in signaling in serum deprivation and hypoxia-induced cardiomyocyte apoptosis PMID:12063258
37. inhibition of FADD function blocks proliferation but not MAP kinase-activation and interleukin-2-production during primary stimulation of T cells PMID:12115619
38. MORT1/FADD is indispensable for Fas and TNF-mediated hepatic injury PMID:12500197
39. FADD acquired a domain during evolution, rendering it a "proliferation-apoptosis coupler" that balances cell proliferation and apoptosis. PMID:12705854
40. Loss of this protein's expression results in a biased Fas-signaling pathway and correlates with the development of tumoral status in thyroid follicular cells. PMID:12743602
41. In a highly regulated fashion, FADD can transduce either a signal for survival or one that leads directly to apoptosis; the balance between these opposing outcomes is crucial to adaptive immunity. PMID:12817005
42. RIP, TRAF2, and FADD are crucial in mediating ROS accumulation in TNF-induced necrotic cell death PMID:14701813
43. Modifications and intracellular trafficking of Mort1 after T-lymphocyte activation was studied. PMID:15017386
44. binding of Fas-associated death domain (FADD) to the tumor necrosis factor-related apoptosis-inducing ligand receptor DR5 is regulated by the death effector domain of FADD PMID:15173180
45. FasL induces NF-kappaB activation and IL-8 production by a novel mechanism, distinct from that of TNF-alpha and FADD had a dominant-negative effect on the FasL-induced NF-{kappa}B activation. PMID:15337758
46. Data suggest that the loss of FADD/caspase-8 function during development and/or in mature T cells selectively impacts on some but not other pathways of T-cell activation and maturation. PMID:15376191
47. mammalian cells lacking the death-domain-containing protein FADD are defective in intracellular dsRNA-activated gene expression, including production of type I (alpha/beta) interferons, and are thus very susceptible to viral infection PMID:15549108
48. A site is identified in the death domain of FADD that is essential for signal-specific binding to Fas and TRADD and for mediating apoptosis. PMID:16009710
49. Casein kinase Ialpha (CKIalpha) phosphorylates FADD at Ser194 both in vitro and in vivo. Phosphorylation of FADD by CKI is a crucial event during mitosis. PMID:16061179
50. FADD plays a dispensable role during thymocyte development, but is essential in maintaining peripheral T cell homeostasis. and regulating both apoptotic and proliferation signals. PMID:16116191

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UNIGENE: Mm.5126

KEGG: mmu:14082

STRING: 10090.ENSMUSP00000033394