Monoclonal Antibodies to Signal Transduction Raf-1, anti-human, Format Aff. pur., Host Mouse, ISO Type IgG1,k, Clone Number 410
- Known as:
- Monoclonal Antibodies Signal Transduction Raf-1, (anti-) to-H. sapiens, Format Aff. pur., Host Mouse, ISO Type IgG1,k, Clone Number 410
- Catalog number:
- MO-M40091E
- Product Quantity:
- 0.5 mg
- Category:
- -
- Supplier:
- Anogen
- Gene target:
- Monoclonal Antibodies Signal Transduction Raf-1 anti-human Format Aff. pur. Host Mouse ISO Type IgG1 Clone Number 410
Related genes to: Monoclonal Antibodies to Signal Transduction Raf-1, anti-human, Format Aff. pur., Host Mouse, ISO Type IgG1,k, Clone Number 410
- 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: Monoclonal Antibodies to Signal Transduction Raf-1, anti-human, Format Aff. pur., Host Mouse, ISO Type IgG1,k, Clone Number 410
Related articles to: Monoclonal Antibodies to Signal Transduction Raf-1, anti-human, Format Aff. pur., Host Mouse, ISO Type IgG1,k, Clone Number 410
- 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 - - Source: PubMed
Publication date: 2026/08/05
Kim SujinKim BoyoonLim AhjinKim HoonCho Jeonghee - Ivabradine (IVA), a broad-spectrum hyperpolarization-activated cyclic nucleotide-gated (HCN) channel inhibitor, improves cardiac function in cardiovascular diseases and may protect against drug-induced cardiotoxicity. This study investigated the cardioprotective effects of IVA against cisplatin (Cis)-induced cardiac injury and explored the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/08/12
Aldabaan Nayef AAbdel-Wahab Basel AEl-Shoura Ehab A MAlqahtani Saad MisferBakir Marwa BSaad Hebatallah MMahmoud Omar Zainab MohammedZaafar Dalia