FADD & FASLG Protein Protein Interaction Antibody Pair
- Known as:
- FADD & FAS ligand Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0190
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- FADD & FASLG Protein Interaction Antibody Pair
Related genes to: FADD & FASLG Protein Protein Interaction Antibody Pair
- Gene:
- FADD NIH gene
- Name:
- Fas associated via death domain
- Previous symbol:
- -
- Synonyms:
- MORT1, GIG3
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-07
- Date modifiied:
- 2019-04-23
- Gene:
- FASLG NIH gene
- Name:
- Fas ligand
- Previous symbol:
- APT1LG1, TNFSF6
- Synonyms:
- FasL, CD178
- Chromosome:
- 1q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-09
- Date modifiied:
- 2019-04-23
Related products to: FADD & FASLG Protein Protein Interaction Antibody Pair
Related articles to: FADD & FASLG Protein Protein Interaction Antibody Pair
- In dogs diagnosed with pyometra, cervical patency status may influence the predominance of apoptosis or ferroptosis, two mechanistically distinct forms of regulated cell death. We evaluated the expression of selected transcripts related to apoptotic and ferroptotic pathways in the uterine tissuee of female dogs diagnosed with open- or closed-cervix pyometra. Twenty-four bitches were classified as healthy (n = 8), open-cervix pyometra (n = 8), or closed-cervix pyometra (n = 8). Uterine tissue samples from each dog were collected for the quantification of apoptotic- (BAX, BCL-2, TP53, and CASP3) and ferroptosis-related transcripts (GPX4, SLC7A11, and TFRC) via qPCR. Immunohistochemical analysis was conducted using antibodies specific to the proteins encoded by BAX, BCL2, TP53, CASP3, GPX4, SLC7A11, and TFRC genes. Furthermore, protein-protein interaction (PPI) and enrichment analyses for the same genes were conducted. Data were fitted in Kruskal-Wallis tests to fit the effect of healthy, open-cervix pyometra, or closed-cervix pyometra on gene expression profile and immunohistochemistry staining parameters. Compared to control, the expression of BAX, SLC7A11, TFRC, GPX were upregulated, BCL2 was downregulated in closed-cervix pyometra. Mild and strong immunopositivity in BAX, BCL2, TP53, CASP3 antibodies was observed in closed pyometra cases. In closed-cervix pyometra, severe inflammation was observed in the endometrium, with immunopositivity for SLC7A11 and GPX4 highlighted within the cytoplasm of mononuclear inflammatory cells, primarily located in the endometrial stroma. PPI analysis revealed proteins encoded by target genes, such as FADD, FASLG, and GSDME, considering maximum of 20 interactions per protein, resulting network highlights significant roles of proteins in various biological pathways, including apoptosis, ferroptosis, inflammation, cellular immunity. Apoptosis and ferroptosis are regulated in pyometra related cervical patency status and these pathways, more active in closed-cervix pyometra. This is the first study to identify apoptosis and ferroptosis pathways in pyometra, providing new insights into its pathophysiology and emphasizing prognostic relevance of both pathways, particularly in closed-cervix cases. - Source: PubMed
Publication date: 2025/08/07
Özkan HüseyinKeçeli Hasan HüseyinYazlik Murat OnurVural Sevil AtalayKaya UfukPascottini Osvaldo BogadoAltinbaş Yunus FurkanVural Mehmet Rıfat - This study aimed to investigate the role of Kindlin-2 in HCC and its underlying molecular mechanisms, focusing on its regulation of the Fas/FasL signaling pathway. - Source: PubMed
Publication date: 2025/05/20
Yu WeiweiWang YanWang Shugang - Although necroptosis is an emerging mechanism of multiple organ dysfunction in sepsis, data on the mechanistic link between necroptosis and sepsis are scarce. Bioinformatic analysis was performed to compare the gene profiles between the sepsis (n = 133) and healthy control (n = 12) groups and identify necroptosis-related differentially expressed genes (DEGs). The identified necroptosis-related DEGs were verified by three-step molecular experiments: (1) quantitative real-time PCR and enzyme-linked immunosorbent assay; (2) cell culture, transfection and Western blotting; and (3) cytokine array with apoptosis inhibition. Additionally, receiver-operating characteristic curve analyses were performed to evaluate the performance of the corresponding proteins to the necroptosis-related DEGs in diagnosing sepsis and in predicting in-hospital mortality of patients with sepsis. Eight necroptosis-related DEGs, including five upregulated (PYGL, TNF, CYLD, FADD and TLR3) and three downregulated (TP53, FASLG and NLRP6) DEGs, were identified. Moreover, the levels of the corresponding proteins to necroptosis-related DEGs showed excellent or considerable accuracy in diagnosing sepsis and in predicting the mortality of sepsis patients. In cell culture media transfected with plasma from the sepsis and control groups, Western blotting revealed that the levels of the corresponding proteins were increased in the upregulated DEGs and decreased in the downregulated DEGs. The cytokine array revealed cytokines in cell culture media transfected with plasma from patients with sepsis while preventing apoptosis by inhibiting the caspase-8 activity, wherein the transfected cells potentially underwent necroptosis. Eight necroptosis-related DEGs were identified in patients with sepsis by bioinformatic analysis and verified by molecular experiments, implying that necroptosis may be a key mechanism of sepsis. - Source: PubMed
Choi HayoungLee Jin YoungYoo HongseokJeon Kyeongman - Autoimmune lymphoproliferative syndrome (ALPS) is a primary disorder of lymphocyte homeostasis, leading to chronic lymphoproliferation, autoimmune cytopenia, and increased risk of lymphoma. The genetic landscape of ALPS includes mutations in FAS, FASLG, and FADD, all associated with apoptosis deficiency, while the role of CASP10 defect in the disease remains debated. In this study, we aimed to assess the impact of CASP10 variants on ALPS pathogenesis. We benefit from thousands of genetic analysis datasets performed in our Institute's genetic platform to identify individuals carrying CASP10 variants previously suspected to be involved in ALPS outcome: p.C401LfsX15, p.V410I and p.Y446C, both at heterozygous and homozygous state. Clinical and laboratory features of the six included subjects were variable but not consistent with ALPS. Two individuals were healthy. Comprehensive analyses of CASP10 protein expression and FAS-mediated apoptosis were conducted and compared to healthy controls and ALPS patients with FAS mutations. Missense CASP10 variants (p.V410I and p.Y446C), which are common in the general population, did not disrupt CASP10 expression, nor FAS-mediated apoptosis. In contrast, homozygous p.C401LfsX15 CASP10 variant lead to a complete abolished CASP10 expression but had no impact on FAS-mediated apoptosis function. At heterozygous state, this p.C401LfsX15 variant lead to a reduced CASP10 protein levels but remained associated with a normal FAS-mediated apoptosis function. These findings demonstrate that CASPASE 10 is dispensable for FAS-mediated apoptosis. In consequences, CASP10 defect unlikely contribute to ALPS pathogenesis, since they did not result in an impairment of FAS-mediated apoptosis nor in clinical features of ALPS in human. Moreover, the absence of FAS expression up-regulation in subjects with CASP10 variants rule out any compensatory mechanisms possibly involved in the normal apoptosis function observed. In conclusion, this study challenges the notion that CASP10 variants contribute to the development of ALPS. - Source: PubMed
Publication date: 2024/05/04
Consonni FilippoMoreno SolangeVinuales Colell BlancaStolzenberg Marie-ClaudeFernandes AliciaParisot MélanieMasson CécileNeveux NathalieRosain JérémieBamberger SarahVigue Marie-GabrielleMalphettes MarionQuartier PierrePicard CapucineRieux-Laucat FrédéricMagerus Aude - Human Inborn Errors of Immunity (IEIs) encompass a clinically and genetically heterogeneous group of disorders, ranging from mild cases to severe, life-threatening types. Among these, Primary Immune Regulatory Disorders (PIRDs) constitute a subset of IEIs characterized by diverse clinical phenotypes, prominently featuring severe atopy, autoimmunity, lymphoproliferation, hyperinflammation, autoinflammation, and susceptibility to malignancies. According to the latest report from the International Union of Immunological Societies (IUIS), PIRDs arise from mutations in various genes including LYST, RAB27A, AP3B1, AP3D1, PRF1, UNC13D, STX11, STXBP2, FAAP24, SLC7A7, RASGRP1, CD70, CTPS1, RLTPR, ITK, MAGT1, PRKCD, TNFRSF9, SH2DIA, XIAP, CD27 (TNFRSF7), FAS (TNFRSF6), FASLG (TNFSF6), CASP10, CASP8, FADD, LRBA, STAT3, AIRE, ITCH, ZAP70, TPP2, JAK1, PEPD, FOXP3, IL2RA, CTLA4, BACH2, IL2RB, DEF6, FERMT1, IL10, IL10RA, IL10RB, NFAT5, TGFB1, and RIPK1 genes. We designed a targeted next-generation sequencing (TNGS) workflow using the Ion AmpliSeq™ Primary Immune Deficiency Research Panel to sequence 264 genes associated with IEIs on the Ion S5™ Sequencer. In this study, we report the identification of 38 disease-causing variants, including 16 novel ones, detected in 40 patients across 15 distinct PIRD genes. The application of next-generation sequencing enabled rapid and precise diagnosis of patients with PIRDs. - Source: PubMed
Publication date: 2024/04/22
Aykut AycaDurmaz AsudeKaraca NeslihanGulez NesrinGenel FerahCelmeli FatihCogurlu M TubaAkcan MedihaCicek DilekCipe Funda ErolKiykim AycaYıldıran AlisanUnluhizarci KursadKilic Sara SebnemAksu GuzideArdeniz OmurKutukculer Necil