PS338 [DPR/2/2A/3A] Raf1
- Known as:
- PS338 [DPR/2/2A/3A] Raf1
- Catalog number:
- mc-029
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- PS338 [DPR/2/2A/3A] Raf1
Related genes to: PS338 [DPR/2/2A/3A] Raf1
- 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: PS338 [DPR/2/2A/3A] Raf1
Related articles to: PS338 [DPR/2/2A/3A] Raf1
- This study aimed to elucidate the molecular mechanism underlying the anti-anxiety effects of flaxseed () by investigating its role in modulating the oxytocin (OXT) signaling pathway through protein-protein interaction (PPI) network analysis. - Source: PubMed
Publication date: 2025/11/01
Sadeghi Hajar SadatRezaei Tavirani MostafaAbrishami MelikaHamzeloo-Moghadam Maryam - While kinase-altered spindle cell tumours were classically recognised in paediatric superficial soft tissues, recent literature indicates an expanding clinicopathologic spectrum. This study investigates a cohort of -altered mesenchymal tumours to further characterise their presentations in adults, deep-seated/visceral locations, variable immunophenotypes and complex molecular evolution. - Source: PubMed
Publication date: 2026/06/03
Feng XiaolongHuang XianmingHao WeiweiWei JiacongLiu XiaoqiWen YaruCao QiJiang YuluGong Lihua - Adhesion G protein-coupled receptor F5 (ADGRF5) is widely expressed and is involved in various physiological and pathophysiological functions. ADGRF5 has been demonstrated to be expressed in glomerular endothelial cells and to maintain the integrity of the glomerular filtration barrier by regulating the expression of type IV collagens COL4A3 and COL4A4. However, the mechanisms underlying its activation remain unclear. Herein, we showed that ADGRF5 overexpression enhances ERK1/2 phosphorylation induced by laminar flow shear stress in human embryonic kidney PEAKrapid cells. Inhibitor and knockdown experiments revealed that the ADGRF5-mediated shear stress response proceeds via the Gαq/11-protein kinase C-RAF1-MEK1/2-ERK1/2 cascade. Mutagenesis analyses showed that shear flow-mediated activation of ADGRF5 requires the tethered agonist (Stachel) sequence and the C-terminal helix 8. Consistent with the overexpression analyses, endogenous ADGRF5 mediated shear stress-induced ERK1/2 signaling in human primary renal glomerular endothelial cells. Moreover, ADGRF5 knockdown attenuated shear flow-induced upregulation of the immediate early response genes and the type IV collagen genes COL4A3 and COL4A4. These results suggest that ADGRF5 mediates shear stress mechanotransduction in glomerular endothelial cells and regulates endothelial cell responses, with potential implications for glomerular filtration barrier homeostasis. - Source: PubMed
Publication date: 2026/06/03
Wang XiaoyangKato MasakoNagase MikiNakamura Nobuhiro - Clear cell renal cell carcinoma (ccRCC) is a highly aggressive malignancy with limited treatment options. Although RASD2, which encodes a Ras-related GTP-binding protein, has been linked to melanoma progression, its role in ccRCC remains unclear. In this study, we systematically investigated the oncogenic functions and mechanisms of RASD2 in ccRCC. Clinically, RASD2 was significantly overexpressed in tumor tissues compared with adjacent normal tissues and correlated with poor patient prognosis. Functional studies demonstrated that RASD2 promotes proliferation, migration, and invasion of the ccRCC cells in vitro, findings further supported by xenograft models in nude mice. Mechanistically, RASD2 activated the P38/ERK-MAPK pathway, and inhibition experiments confirmed its necessity for RASD2-driven oncogenesis. Through co-immunoprecipitation and LC-MS/MS, we identified RAF1 as a key binding partner. RASD2 enhanced RAF1 phosphorylation at Ser338, thereby activating the P38/ERK-MAPK pathway. RAF1 phosphorylation at Ser338 was critical for ccRCC cell growth, migration, and invasion. The RAF1 inhibitor BAY43-9006 reduced p-RAF1 (Ser338)/RAF1 levels, suppressed ccRCC proliferation, migration, and invasion in vitro, and significantly inhibited tumor growth in vivo. These findings identify RASD2 as a novel oncoprotein that promotes ccRCC tumorigenesis through p-RAF1 (Ser338)-mediated P38/ERK-MAPK activation, suggesting RAF1 inhibition as a promising therapeutic strategy for ccRCC patients. - Source: PubMed
Publication date: 2026/06/01
Yu JingxuanYu GangLiu YuanZhou YuLiu WeiWang LinLiu LideLiu YanPan TiejunLiu ZhenyuGao Lei - Pancreatic ductal adenocarcinoma (PDAC) has one of the lowest cancer survival rates. Recent studies using RAS inhibitors have opened the door to more efficacious therapies although their beneficial effect is still limited mainly due to the rapid appearance of tumor resistance. Here, we demonstrate that genetic ablation of three independent nodes involved in downstream (RAF1), upstream (EGFR), and orthogonal (STAT3) KRAS signaling pathways leads to complete and permanent regression of orthotopic PDACs induced by / mutations. Likewise, a combination of selective inhibitors of KRAS (RMC-6236/daraxonrasib), EGFR family (afatinib), and STAT3 (SD36) induced the complete regression of orthotopic PDAC tumors with no evidence of tumor resistance for over 200 d posttreatment. This combination therapy also led to significant regression of genetically engineered mouse tumors as well as patient-derived tumor xenografts (PDX) in the absence of tumor relapses. Of importance, this combination therapy was well tolerated. In sum, these results should guide the development of new clinical trials that may benefit PDAC patients. - Source: PubMed
Publication date: 2026/06/01
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