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
- 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 - Colorectal cancer is a leading cause of cancer-related death worldwide. The role of immediate early response 5-like (IER5L) in colorectal cancer remains unknown. This study investigated IER5L expression, biological function, and molecular mechanism in colorectal cancer. IER5L was significantly overexpressed in tumor tissues and cell lines. High IER5L expression correlated with poor patient prognosis. Functional assays demonstrated that IER5L promoted proliferation, migration, invasion, epithelial-mesenchymal transition, and liver metastasis in vitro and in vivo. Mechanistically, IER5L bound directly to the E3 ubiquitin ligase TRAF7. This interaction facilitated K48-linked ubiquitination and proteasomal degradation of the tumor suppressor p53. Restoring p53 expression reversed IER5L-driven malignant phenotypes. TRAF7 knockdown or mutation of its lysine 451 residue, a critical IER5L binding site, abrogated IER5L effects. The IER5L-TRAF7-p53 axis represents a previously unrecognized driver of colorectal cancer progression. These findings provide mechanistic insight and suggest potential therapeutic targets for colorectal cancer. - Source: PubMed
Publication date: 2026/07/21
Guoyu-Li Xudong-Yang Qing-Feng Enshan-Zhu Lixing-Zhang Rong-Ding Xuan-Zhang Xiaoqiong-Chen Yunfeng-Li - Tumor necrosis factor receptor-associated factor 7 (TRAF7) is an atypical member of the TRAF family, with well-established roles in modulating vertebrate innate immunity, apoptosis, and intracellular signal transduction. In contrast, its functional repertoire in invertebrates, particularly among marine mollusks, remains poorly characterized. In this study, a TRAF7 ortholog from the Zhikong scallop (Chlamys farreri) was identified and designated as CfTRAF7. The cloned CfTRAF7 cDNA comprises a 1953-bp open reading frame encoding a 650-amino-acid polypeptide. Function domain prediction confirmed that the N-terminal RING finger domain and the C-terminal WD40 repeat region exhibit significant sequence homology with TRAF7 orthologs across metazoans. Phylogenetic analysis indicated that CfTRAF7 clusters with TRAF7 homologs from other mollusks. Quantitative real-time PCR assays demonstrated that CfTRAF7 mRNA was widely expressed in all tested scallop tissues, with the highest expression in hemocytes. After stimulation with lipopolysaccharide (LPS), polyinosinic-polycytidylic acid, and peptidoglycan, the mRNA expression of CfTRAF7 was significantly upregulated, with temporal differences in response to various pathogen-associated molecular patterns. Co-immunoprecipitation confirmed that CfTRAF7 interacted with C. farreri transforming growth factor beta-activated kinase 1 (CfTAK1). Western blot analysis revealed that overexpression of CfTRAF7 in HEK293T cells significantly enhanced the phosphorylation of mitogen-activated protein kinase (MAPK) proteins (e.g. JNK and Erk1/2), whereas RNA interference (RNAi) of CfTRAF7 suppressed MAPK phosphorylation levels in vivo following LPS challenge, but had no obvious effect on p38 phosphorylation. RNAi assays demonstrated that silencing of CfTRAF7 significantly altered the expression of several immune-related genes, including CfTAK1, CfRel, CfIL17A, CfIL17D, CfTNF-like, and CfSOD, following LPS challenge. Dual-luciferase reporter assay showed that overexpression of CfTRAF7 could activate immune-related reporter genes such as interleukin-6 (IL-6), interferon α/γ (IFNα/γ), activator protein-1 (AP-1), nuclear factor kappa B (NF-κB), and tumor necrosis factor α (TNFα), in a dose-dependent manner. This study not only enriches the functional research on TRAF7 in invertebrates but also provides a new perspective for understanding the evolutionary conservation and species specificity of molluscan innate immune signaling pathways. Additionally, it also offers important theoretical support for further comprehension of the molecular mechanism of scallop immune defense and promoting the green control of aquatic diseases in marine farming. - Source: PubMed
Publication date: 2026/07/08
Lin XiaoxueZhang ZihaoChu XiaolongLiu FengchenZhao KaixinJin QinghuaWang Xiaotong - Optic nerve sheath meningiomas (ONSMs) occupy a unique intersection between neuro-oncology and genetics. Although most cases arise in middle-aged women as solitary, slow-growing tumors, pediatric onset, bilateral disease, or rapid progression frequently signal an underlying germline alteration, most often in neurofibromatosis type II (NF2). This narrative review synthesizes the literature through May 2025, examining clinical behavior, imaging, pathology, hereditary syndromes, and the molecular drivers of ONSMs, with particular emphasis on NF2, SMARCB1, TRAF7, and recent copy-number and methylation studies. Classic sporadic ONSMs seldom exhibit loss of chromosome 22q. However, somatic alterations and occasional changes in chromatin-remodeling genes still converge on Hippo pathway output (Yes-associated protein/transcriptional coactivator with PDZ-binding motif (YAP/TAZ)-driven transcriptional activity), phosphoinositide 3-kinase-protein kinase B (PI3K-AKT), and MAPK signaling. Emerging multi-omics data indicate that optic nerve tumors represent a molecularly distinct subset within the meningioma spectrum. This finding may explain the associated characteristically indolent growth and favorable response to conformal radiotherapy. Genotyping refines risk stratification: early testing is warranted in children and in bilateral or atypical presentations, enabling timely surveillance and genetic counseling. While fractionated stereotactic radiotherapy remains the mainstay of therapy, pathway-targeted and gene-replacement strategies developed for -associated tumors may soon expand therapeutic options. Given the site-specific diagnostic and functional constraints of peri-optic tumors, larger collaborative cohorts and genotype-guided trials are essential to translate these biological insights into precision care for patients with ONSMs. - Source: PubMed
Zeppieri MarcoD'Esposito FabianaGagliano CaterinaBattista MarcoBarboni PieroNicolosi Simonetta GaiaCapobianco Matteo - Population-based studies have linked progestin exposure to increased meningioma risk. However, the molecular basis of meningiomas associated with depot medroxyprogesterone acetate (DMPA) - a common injectable contraceptive-remains undefined. - Source: PubMed
Publication date: 2026/06/08
Huq SakibulGatesman Taylor AAbou-Al-Shaar HussamRaleigh David RHadjipanayis Constantinos GBayley James CZenonos Georgios APearce Thomas MMarker Daniel FAgnihotri SameerGardner Paul A