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
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Publication date: 2026/04/30
Long ShengrongXiao KeweiHao Zhipeng - Sex is an important determinant for various immune system-related pathologies and sex steroids might possess immunomodulatory properties. - Source: PubMed
Publication date: 2026/04/01
Sertons YaëlCollet SarahVervalcke JeroenDefreyne JustineMueller Sven CHofmans MattiasBonroy CarolienD'Onofrio ValentinoSnaterse GidoT'Sjoen GuyLapauw Bruno - We sought to determine changes in the expression of immune response-related genes occurring in surgical necrotizing enterocolitis (NEC) tissues from infants with necrosis severity and survival status. - Source: PubMed
Publication date: 2026/03/24
Garg Parvesh MohanRiddick RobinZhang PengboShenberger JeffreyVarshney NehaSawaya DavidGarg Padma - Glioblastoma (GBM) is one of the most aggressive and treatment-refractory brain tumors. Temozolomide (TMZ) remains the standard chemotherapeutic agent but is frequently compromised by DNA-repair mechanisms, whereas tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induces apoptosis only in a subset of tumors due to strong intrinsic resistance. Here, we identify the Mu-2-related death-inducing gene (MUDENG/MuD) as the µ-subunit of adaptor protein complex 5 (AP5M1). TurboID-based proximity labeling revealed reproducible interactions with AP5B1 and AP5M1 subunits, as well as additional associations with AP1-3 complexes and nuclear proteins involved in cell-cycle regulation. These findings establish MuD as a multifunctional component of the AP5 complex that modulates cell-fate signaling in a context-dependent manner. Using MuD-mutant GBM cell lines, we demonstrate that MuD suppresses TRAIL-induced apoptosis by interfering with extrinsic and intrinsic pathways downstream of Bid, whereas it promotes TMZ-induced cytotoxicity through p53-dependent cell-cycle control and DNA-damage responses. Gene set enrichment analysis (GSEA) and functional profiling further revealed distinct MuD-associated interactomes linked to receptor endocytosis and genotoxic-stress pathways. Together, these results uncover opposing roles of MuD in TRAIL- and TMZ-mediated cell death, with MuD suppressing apoptotic signaling in response to TRAIL while modulating p53-dependent genotoxic stress responses that influence TMZ-induced cytotoxicity in glioblastoma. - Source: PubMed
Publication date: 2026/03/31
Shin JuhyunLee Yoon-MiJung SooHyunHan SuminNile ArtiKim Su-JinLee Sang-WonOh Jae-Wook - Severe aortic stenosis (SAS) requires timely intervention to prevent irreversible myocardial damage. This study evaluated echocardiographic strain parameters and serum biomarkers in SAS patients and explored their value for qualifying patients for aortic valve replacement (AVR). - Source: PubMed
Publication date: 2026/02/03
Gozdzik AnnaCzapla MichałKarolko BożenaObremska Marta