Raf1 (Dominant Negative) Recombinant Adenovirus
- Known as:
- Raf1 (Dominant Negative) Recombinant Adenovirus
- Catalog number:
- ADV-133
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Cell Biolabs
- Gene target:
- Raf1 (Dominant Negative) Recombinant Adenovirus
Related genes to: Raf1 (Dominant Negative) Recombinant Adenovirus
- Gene:
- RAF1 NIH gene
- Name:
- Raf-1 proto-oncogene, serine/threonine kinase
- Previous symbol:
- -
- Synonyms:
- Raf-1, c-Raf, CRAF
- Chromosome:
- 3p25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: Raf1 (Dominant Negative) Recombinant Adenovirus
Related articles to: Raf1 (Dominant Negative) Recombinant Adenovirus
- RASopathies constitute a group of rare genetic disorders caused by mutations in genes along the canonical RAS/mitogen-activated protein kinase (MAPK) signaling pathway, affecting cell growth and differentiation. These syndromes, which include Noonan syndrome (NS), are characterized by developmental delays, distinctive facial dysmorphia, and cardiac defects, notably hypertrophic cardiomyopathy (HCM). Despite their prevalence and impact, therapeutic options for RASopathies remain limited. Rigosertib, a novel dual RAS/MAPK and phosphatidylinositol 3-kinase (PI3K)/AKT pathway inhibitor, is currently in clinical trials for treatment of melanoma and recessive dystrophic epidermolysis bullosa. Here, we identify rigosertib as a candidate therapy for RAF1-associated HCM. - Source: PubMed
Publication date: 2026/08/18
Legler LeviMarchetti KatyaXu BingKeshavarz Shirazi TaraKurzum SereeneKessinger ChaseVredenburg IzabellaSun YanDinenno Frank ABohler DamianAleman Angelika GRodriguez Nelson ANg SimonGao SophieWang AngelaSuarez-Farinas MayteLin Hung-MoDas TirthaOcorr KarenCagan Ross LGelb Bruce DKontaridis Maria I - Osteoporotic fracture is the most severe complication of osteoporosis, and impaired bone regeneration and delayed healing after fracture remain major clinical challenges. Extracellular vesicles (EVs) derived from bone marrow mesenchymal stem cells (BMSCs) may play a critical role in promoting bone regeneration after osteoporotic fracture. Enhancing their osteogenic potential and elucidating the underlying mechanisms may contribute to accelerated fracture healing. In this study, resveratrol-stimulated BMSC-derived EVs (Res-EVs) were isolated using differential centrifugation combined with ultracentrifugation. We found that compared with EVs secreted by BMSCs under normal culture conditions (Nor-EVs), Res-EVs significantly enhanced BMSCs osteogenic differentiation capacity. Analysis of miRNA sequencing data identified miR-19a-3p as significantly downregulated and PC-3p-83,608 as significantly upregulated. The reliability of the sequencing data was validated by qPCR results. By transfecting BMSCs with inhibitor and mimic of miR-19a-3p, we found that miR-19a-3p was a negative regulator of osteogenic differentiation. Bioinformatics prediction and dual-luciferase reporter assays confirmed that miR-19a-3p directly targets Raf1. Western blot results indicated that miR-19a-3p regulates osteogenic differentiation of BMSCs by targeting Raf1. In vivo experiments further demonstrated that Res-EVs treatment enhanced repair at osteoporotic fracture sites and increased the expression of RUNX2 and RAF1. Collectively, these findings indicate that Res-EVs promote bone regeneration at osteoporotic bone defect sites in rats, with the miR-19a-3p/Raf1 axis representing a potential underlying mechanism. - Source: PubMed
Publication date: 2026/08/15
Lv YanDu YongjunPeng ZhiMa ChengjieLi ZhenggangXu RuiHou JianhongLu Sheng - Imatinib (IMA), a front-line targeted therapy, was demonstrated by our prior study to potentially cause premature ovarian insufficiency (POI) after long-term administration. Additionally, we found that quercetin (QUE) may ameliorate IMA-induced ovarian injury by regulating mitophagy. Previous studies have shown that mitochondrial dysfunction may be involved in various cell death pathways. PANoptosis is a recently identified form of cell death that exhibits characteristics of pyroptosis, apoptosis, and necroptosis simultaneously. The present study further investigates whether IMA induces PANoptosis via mitochondrial dysfunction and explores the underlying mechanisms and potential therapeutic targets. In vitro experiments on granulosa cells revealed that IMA induced PANoptosis, characterized by membrane blebbing and swelling, pyknosis, as well as rupture of the nuclear and plasma membranes observed via transmission electron microscopy and confocal microscopy. This was accompanied by increased lactate dehydrogenase release, an elevated proportion of propidium iodide positive cells, and activation of caspase-3 (apoptosis), gasdermin D (GSDMD, pyroptosis), and mixed lineage kinase domain-like protein (MLKL, necroptosis). Network pharmacology revealed that the related genes associated with IMA, QUE, mitochondrial function, and POI were enriched in the MAPK pathway, with RAF1 identified as a key target. Western blot analysis demonstrated that IMA upregulated phosphorylation of RAF1, its downstream effector ERK1/2, and the mitochondrial fission mediator Drp1 (Ser616) in granulosa cells and ovarian. GW5074 (a RAF1 inhibitor), Mdivi1 (a Drp1 inhibitor), and QUE restored mitochondrial membrane potential and mitochondrial superoxide levels in granulosa cells and oocytes, suppressed IMA-induced PANoptosis, and improved granulosa cell viability and oocyte quality. These findings provide new insights into potential strategies for protecting ovarian function during IMA treatment. - Source: PubMed
Publication date: 2026/08/11
Li Qing-HuiJi MinZhou YanWeng Shi-QiKong YaoXiao QinLuo TaoLiu Zhao-Xia - To investigate the regulatory effect of everolimus on biological behaviors of rdafitinib-resistant bladder cancer cells and the underlying mechanism. - Source: PubMed
Wu HaosongJiang YiZhang XiaolinWang Sheng - Constitutive activation of the MAPK pathway is a hallmark of melanoma, leading to aberrant cell proliferation and survival. Although oncogenic mutations in NRAS and BRAF are well established, the functional and therapeutic significance of RAF1 mutations remains incompletely defined. Here, we identify RAF1 S257L and S259F as recurrent hotspot mutations in melanoma by integrating our hospital cohort with TCGA-SKCM. These conserved region 2 mutations relieve CRAF autoinhibition by reducing inhibitory Ser259 phosphorylation, resulting in elevated ERK signalling in a dimerization-dependent manner. Both mutants exhibit oncogenic activity and transform melanocytes in vitro, and the resulting transformed cells display intrinsic resistance to the RAS(ON) inhibitor daraxonrasib. Subsequent RAF-isoform knockdown and ectopic expression further demonstrate that daraxonrasib-resistant ERK activation is primarily driven by mutant CRAF. Importantly, in human melanoma cells, combined treatment with daraxonrasib and the MEK inhibitor cobimetinib effectively overcomes this mutant CRAF-driven resistance, producing greater suppression of p-ERK and cell proliferation than either agent alone and demonstrating marked synergy. Our findings establish RAF1 S257L/S259F as critical determinants of MAPK pathway activation and cellular response under daraxonrasib, provide mechanistic insights into intrinsic resistance to RAS(ON) inhibition, and underscore a therapeutic framework for genotype-guided combination strategies in RAF1-mutant melanoma. - Source: PubMed
Publication date: 2026/08/07
Fu YihangAmiot MathildeKuzniak IsabelleJouenne FanélieMourah SamiaLebbé CélesteDumaz Nicolas