TNFSF10 Blocking Peptide
- Known as:
- Tumor necrosis factor superfamily member 10 Blocking Peptide
- Catalog number:
- 33r-1684
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- TNFSF10 Blocking Peptide
Related genes to: TNFSF10 Blocking Peptide
- Gene:
- TNFSF10 NIH gene
- Name:
- TNF superfamily member 10
- Previous symbol:
- -
- Synonyms:
- TRAIL, Apo-2L, TL2, CD253
- Chromosome:
- 3q26
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2017-03-02
Related products to: TNFSF10 Blocking Peptide
Related articles to: TNFSF10 Blocking Peptide
- Sacituzumab govitecan (SG) is an antibody drug conjugate targeting trophoblast cell surface antigen 2 (Trop2) that is approved for treatment of patients with metastatic triple negative breast cancer (TNBC). Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) agonists are antitumor agents that interact with death receptors on the cell surface to induce apoptosis in cancer cells, often sparing normal cells. In this study, we investigated whether combination treatment with SG and TRAIL agonists inhibit TNBC cell growth. - Source: PubMed
Publication date: 2026/08/14
Addissie Yonit AGreer Yoshimi ENair JayakumarLipkowitz Stanley - Type 2 diabetes mellitus (T2DM) and major depressive disorder (MDD) are reciprocal risk factors, and both elevate dementia risk. Dysregulation of programmed cell death is implicated in T2DM, MDD, and neurodegeneration, but proteomic markers of apoptosis have yet to be studied as dementia predictors in people with T2DM and/or MDD. This study examines apoptosis markers in comorbid T2DM and MDD, and their associations with cognitive, dementia, and neuroimaging outcomes. The retrospective sample (n = 15,765) consisted of UK Biobank participants (MDD only n = 1230; T2DM only n = 3644; comorbid T2DM + MDD n = 721). Individuals with T2DM + MDD comorbidity had poorer cognitive performance, and a higher 15-year dementia incidence (HR = 4.44, 95% CI = [3.23,6.11]). Among 60 apoptosis-related proteins identified by Kyoto Encyclopedia of Genes and Genomes pathway enrichment, 41 were significantly up-regulated in comorbid T2DM + MDD relative to controls, and 4 were higher in the comorbid group than both T2DM alone and MDD alone. Tumor necrosis factor ligand superfamily member 10 (TNFSF10), growth arrest and DNA damage-inducible protein GADD45 beta, tumor necrosis factor ligand superfamily member 6, and RAC-gamma serine/threonine-protein kinase were associated with dementia risk. Nine proteins (e.g. apoptosis-inducing factor 1, mitochondrial, caspase-2, mitogen-activated protein kinase kinase kinase 5, TNFSF10), were associated with white matter hyperintensity volumes in comorbid T2DM + MDD after FDR correction, but none were associated with cognitive performance, atrophy, or white matter microstructural changes. These findings identify peripheral apoptosis markers that were further elevated in comorbid T2DM + MDD compared to either alone, pointing to an important pathophysiological element underlying adverse outcomes in the context of mood and metabolic comorbidity. - Source: PubMed
Publication date: 2026/08/05
Perfetto Sofia ERuthirakuhan MyuriWong Yuen YanRyoo Si WonHuang Celine H LFan FanChenoweth Meghan JNestor Sean MAndreazza Ana CGoubran MagedRabin Jennifer SJiang GuochengBlack Sandra ECogo-Moreira HugoMacIntosh Bradley JSwardfager Walter - Psoriasis is a chronic immune-mediated inflammatory skin disease characterized by epidermal dysfunction, aberrant keratinocyte activation, and complex immune remodeling. Although lipid dysregulation has increasingly been implicated in psoriasis, the role of palmitoylation-associated genes in cutaneous inflammation remains insufficiently defined. - Source: PubMed
Publication date: 2026/07/21
Luo QingqiongShi RongcanYang DandanTang YijieXie QinghuiShi YulingSun Fenyong - TRAIL is a TNF family ligand that trimerizes TRAIL-R1 (DR4) or TRAIL-R2 (DR5) to induce apoptosis, necroptosis, and/or NF-κB activation in receptor-bearing cells. We previously identified TRAILshort as a splice variant of TRAIL that lacks cysteine 230, cannot trimerize, and acts as a dominant-negative ligand that blocks TRAIL-mediated apoptosis. TRAILshort is expressed on cell surfaces and within extracellular vesicles, enabling it to confer TRAIL resistance to both producing and bystander cells. In this study, we showed that elevated TRAILshort levels were associated with chronic viral infections, cancer, and autoimmune diseases, suggesting a link to impaired immune regulation. Using unbiased phosphoproteomics and mechanistic studies, we demonstrated that TRAILshort binding to DR5 recruited and activated the phosphatase Src homology region 2 domain-containing phosphatase 1 (SHP-1), leading to zeta-chain-associated protein kinase 70 (ZAP-70) dephosphorylation, disruption of ZAP-70-CD3ζ interactions, and impaired T cell receptor signaling, thereby reducing T cell activation, proliferation, and cytokine production in response to antigen or CD3/CD28 ligation. Genetic or pharmacologic SHP-1 inhibition reverses these effects. In humanized mouse models, TRAILshort promoted the persistence of transformed mouse embryonic fibroblasts (MEFs) and L428 and antagonized CD19-directed CAR T cell activity, revealing TRAILshort as an immunomodulator of T cell function with therapeutic implications, including blocking TRAILshort to restore T cell immunity or delivering TRAILshort to enforce tolerance. - Source: PubMed
Publication date: 2026/08/03
Jalali ShahrzadNatesampillai SekarNie ZilinZhang YingCan IsmailChandrasekar Aswath PHameister Brianna MCorreia CristinaZhao Tuantuan VMun Dong-GiGarcia-Rivera EnriqueMatson RobertKrogman AshtonMaynes Mark ABatchelor RobinMonie Dileep DLi HuBehfar AttaKenderian Saad SPandey AkhileshAnsell Stephen MTaner TimucinWeyand CorneliaBilladeau Daniel DBadley Andrew D - Kashin-Beck disease (KBD) is a chronic, endemic osteoarticular disorder associated with T-2 toxin exposure, which is rapidly metabolized to HT-2 toxin in vivo. However, the role of zinc transporter ZIP6 in HT-2 toxin-induced extracellular matrix metabolic disturbance in chondrocytes remains unclear. This study established HT-2 toxin intervention and ZIP6 knockdown chondrocyte models, combined with quantitative reverse transcription polymerase chain reaction (qRT-PCR) and transcriptome sequencing, to investigate the regulatory mechanisms of ZIP6 in chondrocyte injury. Following HT-2 toxin exposure, altered chondrocyte morphology and reduced cell viability were observed; ZIP6, COL2A1, MTF1, and MTF2 expression were significantly downregulated, whereas MMP1, MMP13, and COL10A1 were upregulated. ZIP6 knockdown significantly upregulated COL2A1, MTF1, and MTF2, downregulated MMP1 and COL10A1, but did not alter MMP13 expression. Differentially expressed genes following ZIP6 knockdown were predominantly enriched in FoxO, cAMP, and TNF signaling pathways. qRT-PCR validation confirmed consistent expression changes in FOXO4, TNFSF10, COLEC10, UCA1, and LRRC17 with transcriptome sequencing results. Collectively, HT-2 toxin suppresses ZIP6, MTF1, and MTF2 expression, disrupting chondrocyte extracellular matrix metabolism; conversely, ZIP6 knockdown ameliorates matrix metabolic abnormalities through modulation of relevant signaling pathways. These findings reveal differential regulatory effects of HT-2 toxin and ZIP6 on cartilage matrix metabolism, providing experimental evidence for elucidating molecular mechanisms underlying cartilage injury-related diseases. - Source: PubMed
Liu YangZhang YuHuang RuitianBai LuluLiu LianWang ChaoweiQin YirongWang HuiGuo XiongWang XiNing Yujie