Human Polyclonal c-Myc Ab
- Known as:
- Human Polyclonal c-Myc Antibody
- Catalog number:
- a0309
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal c-Myc
Related products to: Human Polyclonal c-Myc Ab
Related articles to: Human Polyclonal c-Myc Ab
- Primary breast lymphoma (PBL) is a rare extranodal lymphoma of which diagnosis is challenging due to overlapping clinical and imaging features with breast carcinoma. While the existence of PBL is known, the diagnostic significance of specific sonographic patterns like the "grid-like echo" and the critical imperative for exhaustive systemic staging to differentiate primary from systemic lymphoma warrant emphasis. This case is unique as it demonstrates a diagnostic journey from a bilateral "grid-like echo" on ultrasound to a revised diagnosis of a systemic, high-grade lymphoma, highlighting key pitfalls and the necessity of comprehensive workup. - Source: PubMed
Publication date: 2026/04/30
Hao ZhihanZheng MinZhang Bo - Tumour progression towards dedifferentiated cell clusters plays a critical role in intratumour heterogeneity and therapy resistance. While tumour microenvironmental stress has been implicated, the underlying mechanisms remain poorly defined. Using mouse models of lung adenocarcinoma, we demonstrate that activation of the integrated stress response (ISR)-marked by phosphorylation of eIF2 (p-eIF2) and ATF4 induction-drives tumour heterogeneity. ISR activation facilitates the emergence of high-plasticity, undifferentiated and pre-epithelial-to-mesenchymal transition clusters characterized by elevated ATF4 and MYC activity. This process is MYC dependent and involves ISR-mediated repression of NKX2-1, a key determinant of alveolar identity, and induction of CHCHD10, a regulator of mitochondrial integrity and metabolic fitness. Disruption of the p-eIF2-ATF4 axis induces mitochondrial dysfunction, limits dedifferentiation and suppresses tumour growth. In human lung adenocarcinoma, ISR-driven dedifferentiation correlates with advanced disease and poor prognosis, identifying the ISR as a central driver of lineage reprogramming and metabolic fitness in tumour progression. - Source: PubMed
Publication date: 2026/06/15
Diao ShiqiZou Jia YiWang ShuoChan Jason EKortlever Roderik MPoulain NicolasGhaddar NourKim HyungdongEvan Gerard IKoumenis ConstantinosHatzoglou MariaWalter PeterSonenberg NahumLe Quesne JohnTammela TuomasKoromilas Antonis E - Naive B cells diversify via clonal expansion, immunoglobulin isotype switching, phenotypic variation and somatic hypermutation (SHM). Diversity in antigenic targets, functional classes and the production kinetics of antibodies affects immunity to malaria. Here we show that individual clones diversify over time during Plasmodium infection. During the first week, amid widespread bystander activation, isotype switching initiates soon after Myc upregulation and overlaps with clonal expansion, resulting in isotype variegation among clones. During the second week, expanded clones seeding germinal centers (GC) bifurcate into extrafollicular plasmablasts, exhibit isotype variegation and initiate SHM, indicating substantial intraclonal diversification. Over the following month, GC clones exhibit SHM at approximately four mutations per week. Antimalarial intervention does not impede SHM, instead exerting quantitative limits on GC size, plasma cell emergence, circulating antibody levels and protection against reinfection. Finally, contemporaneous B cell development relocates from bone marrow to spleen. Thus, multiple temporally overlapping mechanisms combine in vivo to diversify and safeguard humoral immune responses. - Source: PubMed
Publication date: 2026/06/15
Skinner Oliver PAsad SabaMoreira Marcela LLee Hyun JaeWilliams Cameron GRuan ZhengLim JoreneKerr Ashlyn SLi ShihanZhu ChenJin WangSteiner Thiago MAsatsuma TakahiroWanrooy Brooke JLiu ZihanTong Marcus Z WSoon Megan S FEngel Jessica AShobhana KalyanUldrich Adam PKhoury David STuong Zewen KelvinKing Hamish WHaque Ashraful - Mitochondrial protein import machineries are essential for organelle homeostasis. Metaxin-2 (Mtx2) is an evolutionarily conserved component of the mitochondrial sorting and assembly machinery, and its mutations are associated with a progeroid syndrome, named mandibuloacral dysplasia associated to Mtx2 (MADaM). To investigate the pathologic mechanisms of MADaM, we developed genetic models in . null mutants are lethal at a preadult stage, and this phenotype can be rescued by expression of either Mtx2 (dMtx2) or its human ortholog, demonstrating functional conservation across species. Tissue-specific conditional knockout and transgene rescue experiments pinpoint muscle as a critical tissue requiring dMtx2 function. Loss of dMtx2 impairs myofibril assembly and induces structural and functional abnormalities in muscle mitochondria. Notably, Mtx2 deficiency significantly reduces the expression of myogenic, mitochondrial, and ribosomal proteins. Overexpression of Myc, a master regulator of ribosome biogenesis and cell growth, successfully rescues the preadult lethality caused by deficiency, and partially restores sarcomere and mitochondrial defects. Our results reveal an interaction between Mtx2-related mitochondrial and ribosomal homeostasis, and elucidate potential Myc-dependent pharmaceutic mechanisms underlying MADaM pathologies. - Source: PubMed
Publication date: 2026/06/15
Shou XinyiFan XiaoyuLi LingRuan YinaLi WeiShang WeinaMao JianhuaXie Xiaojun - Aging is increasingly viewed as a pathological process and a principal driver of diverse age-related diseases (ARDs). Framing aging as a disease offers an opportunity to identify therapeutic targets capable of modifying multiple chronic disorders simultaneously. Here, we developed an artificial intelligence (AI)-driven target discovery framework that integrates large-scale multi-omic datasets to prioritize therapeutic targets shared between aging and 12 ARDs spanning four major disease areas: neurological, inflammatory, metabolic, and fibrotic disorders. We identified 29 high-confidence and 16 previously unrecognized aging-associated targets implicated across the selected disease areas, together with convergent pathway perturbations characterized by robust upregulation of interferon and inflammatory signaling, alongside coordinated downregulation of MYC-driven proliferative programs, consistent with heightened inflammatory activation and reduced anabolic activity during aging. Age-dependent transcriptomic alterations across tissues were observed for all identified target genes. Hallmarks of aging assessment revealed chronic inflammation as the most enriched hallmark across aging and ARDs. Mendelian randomization analyses provided genetic causal support for IL6, IL6R, NLRP3, NOS2, TLR4, and GLP1R in aging-related traits and multiple ARDs, highlighting potential opportunities for drug repurposing. Co-localization analyses suggested that the same genetic variants influencing IL6R expression are also associated with parental survival, a proxy for human lifespan, supporting a role for IL-6 signaling in longevity, and indicated a shared genetic signal at the NOS2 locus associated with rheumatoid arthritis risk. Together, our findings outline a scalable AI-guided multi-omic framework for identifying causal and repurposable therapeutic targets for aging and ARDs. - Source: PubMed
Publication date: 2026/06/12
Leung Geoffrey H DChen JianjiuErgun I AylinIzumchenko EvgenyAliper AlexRen FengPun Frank WZhavoronkov Alex