Ask about this productRelated genes to: TRAF7 Blocking Peptide
- Gene:
- TRAF7 NIH gene
- Name:
- TNF receptor associated factor 7
- Previous symbol:
- RFWD1
- Synonyms:
- RNF119, DKFZp586I021, MGC7807
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-14
- Date modifiied:
- 2015-11-20
Related products to: TRAF7 Blocking Peptide
Related articles to: TRAF7 Blocking Peptide
- Tumor necrosis factor receptor-associated factors (TRAFs) are key signal transduction molecules in innate immunity and are involved in multiple immune pathways, such as TNF receptor and Toll-like receptor signaling. In this study, 16 were identified from the common carp genome, assigned to six subfamilies (/////), with no found. Significant paralogous expansion was observed in the / subfamilies. All CcTRAF proteins were predicted to be unstable and hydrophilic by ProtParam analysis; most contain conserved RING, TRAF and MATH domains, whereas CcTRAF7 carries seven WD40 domains. Gene structure and conserved motif analysis revealed high conservation of exon numbers and motif compositions within each subfamily, while the TRAF7 subfamily displayed distinct characteristics. Collinearity analysis further indicated that segmental duplication promotes family expansion. qRT-PCR showed that genes have tissue-specific expression patterns and are preferentially expressed in the liver, spleen, and kidney. Under CyHV-3 infection, the expression levels of /6/ in these tissues first increased and then decreased, peaking at 48 h post-challenge. In summary, genes, especially /6/, play important roles in the immune response of common carp against CyHV-3. This study provides a molecular basis for understanding innate immune regulation in teleost fish and the functional roles of TRAF genes. - Source: PubMed
Publication date: 2026/09/11
Di YaxinJiang XiaonaLi ChitaoHu XuesongGe YanlongShi XiaodanZhao XinyuJia Zhiying - The MAPK-ERK1/2 pathway plays a crucial role in neurodevelopment during embryogenesis, and the hyperactivation of this signaling cascade serves as a pathological hallmark for various neurodevelopmental disorders. Germline variants in , encoding a RING-type E3 ubiquitin ligase, are genetically associated with cardiac, facial, and digital anomalies with developmental delay (CAFDADD) syndrome; however, the downstream substrates of TRAF7 and the precise mechanism driving neurodevelopmental defects remain enigmatic. Here, we established a knock-in mouse model and patient-specific induced pluripotent stem cell (iPSC)-derived human cortical organoids (hCOs) carrying the recurrent mutation. Heterozygous mice exhibited remarkable growth retardation, skeletal abnormalities, and neurobehavioral deficits, whereas mutant hCOs displayed early cortical neurogenesis defects, characterized by premature neural differentiation and a depleted progenitor pool. Mechanistically, biochemical analyses revealed that TRAF7 interacts with KRAS and NRAS to promote their polyubiquitination and subsequent proteasomal degradation, maintaining physiological homeostatic control over the downstream MAPK cascade. CAFDADD-associated TRAF7 variants exert a dominant-negative effect, disrupting WT protein function and causing the posttranslational accumulation of KRAS and NRAS, which fundamentally drives constitutive MAPK-ERK1/2 pathway hyperactivation. Notably, pharmacological inhibition of MEK1/2 with selumetinib suppressed ERK1/2 hyperactivation, partially mitigated aberrant neuroepithelial morphology and neural differentiation in hCOs, and improved brain-to-body weight ratios in mice. Together, our findings identify TRAF7 as a critical posttranslational regulator of RAS proteostasis during development and uncover a pivotal mechanistic link between impaired RAS ubiquitination and CAFDADD pathogenesis, providing preliminary clinical-front evidence for targeting the MAPK pathway to manage ongoing developmental deficits in TRAF7-associated disorders. - Source: PubMed
Publication date: 2026/09/25
Xiao ManLiu YangSong XiaozhenLiu JingxuanTang XiaojunDou MaosenYu WeiZhang HongWeng WenhaoHan DingdingLan XiaopingZhao TingtingWang ChenjiMa LixiangXu Nan-JieWu Shengnan - Cell-cell interactions shape tumor growth, immune evasion, and therapeutic response, but systematically dissecting their genetic regulators in vivo remains challenging. Existing cell-cell interaction tracing technologies rely largely on protein labels or enzymatic reactions, limiting their information content and scalability. To overcome these limitations, we developed match-seq, an imaging-free, sequencing-based cell proximity tracing system that uses virus-like particles to transmit barcodes between neighboring cells. Barcoded mRNAs are transmitted from sender cells to nearby receiver cells, thereby establishing a spatial linkage that can be computationally reconstructed by barcode sequencing after tissue dissociation. We apply this system to an in vivo syngeneic murine tumor model, where we observe robust labeling of all immune cell lineages, and leverage barcode labeling to reconstruct cell type niches that recapitulate known tumor spatial biology. Furthermore, we couple this system with CRISPR perturbations and single-cell RNA sequencing to perform genetic screens in vivo on tumor-immune interactions at single-cell resolution. We use this method to infer cell-cell spatial relationships and uncover genetic dependencies in cancer cells that change the composition and cell state of their local microenvironments. By calculating a local immune activation signature, we are able to prioritize targets whose deletion enhances anti-tumor immunity through distinct effector cell types: loss of Tgfb1 engages CD8 T cells and macrophages, Traf7 loss elicits a CD4 T cell response, and Nectin3 loss promotes NK cell-mediated immunity, relationships that we validate by in vivo immune cell depletion. Notably, Tgfb1 and Nectin3 deletion had little effect on cancer cell fitness in the pooled screen yet suppressed tumor growth when deleted throughout the tumor, demonstrating the potential of match-seq to reveal functionally important tumor-immune interactions that would otherwise remain hidden. Together, these results establish a general framework for pooled genetic dissection of cell-cell interactions in vivo, extending CRISPR screening from cell-intrinsic phenotypes to the mechanisms by which cells shape and respond to their local microenvironments. - Source: PubMed
Publication date: 2026/09/18
Du PeterKohno SethWang MengchenPapanicolaou MichaelVaughan-Jackson AlunDaigh LeightonPeng QiangweiSpees KaitlynMcCormick AaronDiehl MarkusBintu LacramioaraQiu XiaojieSatpathy AnsumanBassik Michael - The authors aimed to systematically investigate the expression and subcellular localization of estrogen receptors ERα and GPER in meningioma and to evaluate the functional impact of estradiol on cell viability in common meningioma cell lines and primary patient-derived cultures. - Source: PubMed
Miyagishima Danielle FMcGuone DeclanBrooks AmosCoskun SuleymanGultekin BaturHenegariu OctavianMishra-Gorur KetuBarak TanyeriMoliterno JenniferGunel Murat - Molecular profiling is increasingly important for risk stratification and individualization of treatment recommendations for patients with meningioma. Prior investigations have established the genomic architecture of meningioma, but the distribution of meningioma copy number alterations (CNAs) and short somatic variants (SSVs) across demographic groups is incompletely understood. Here we define a prospective, consecutive benchmark for meningioma CNAs and SSVs across demographic groups. - Source: PubMed
Publication date: 2026/08/19
Braman Brooke CNguyen Minh PMirchia KanishMorshed Ramin AOberheim Bush Nancy AnnArum ZoraVillanueva-Meyer Javier EChen William CVan Ziffle JessicaRajkovic AleksandarChang Susan MDevine Walter PatrickPerry ArieRaleigh David R