Raf1 (Phospho_Ser259) Antibody
- Known as:
- Raf1 (Phospho_Ser259) Antibody
- Catalog number:
- E011006-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- Raf1 (Phospho_Ser259) Antibody
Related genes to: Raf1 (Phospho_Ser259) Antibody
- 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 (Phospho_Ser259) Antibody
Related articles to: Raf1 (Phospho_Ser259) Antibody
- : Hepatocellular carcinoma (HCC) represents an extremely lethal malignancy on a global scale. The clinical significance and molecular mechanisms of the immune-related gene in HCC remain unclear. This study seeks to elucidate the clinical implications and diagnostic utility of in HCC, while further exploring its underlying molecular mechanisms. Expression differences of in pan-cancer and HCC were analyzed using the TCGA and GEO (GSE45267) databases. Its diagnostic efficacy was evaluated by Cox regression, Kaplan-Meier survival curves, and ROC curves. Potential functional pathways were explored through GO, KEGG, and GSEA enrichment analyses. The correlation between and immune cell infiltration, as well as immune checkpoint molecules, was analyzed using the ssGSEA algorithm and CIBERSORTx. In vitro, siRNA interference was employed to knock down expression in Huh-7 and MHCC97H cells. The effects on cell proliferation and RAF1 protein levels were assessed using a CCK-8 assay and Western blot, respectively. : was significantly overexpressed in HCC tissues and was closely associated with aggressive clinical features, including pathological T stage, histological grade, and AFP levels. Multivariate Cox regression analysis confirmed that was an independent risk factor for survival in HCC patients (HR = 1.871). The area under the ROC curve (AUC) was 0.939, demonstrating excellent diagnostic predictive value. Enrichment analysis revealed a significant association with the cell cycle, PPAR signaling pathway, and lipid metabolism pathways. Immune infiltration analysis further revealed that expression was significantly positively correlated with Th2 and TFH cells, as well as key immune checkpoint molecules such as PD-1, CTLA4, and LAG3, suggesting distinct features of immune polarization and an inhibitory microenvironment. In vitro cellular experiments demonstrated that knocking down significantly inhibited the proliferative capacity of HCC cells and reduced RAF1 protein expression. : may promote HCC progression by driving a multidimensional proliferation-metabolism-immunity mechanism. holds promise as a novel biomarker for diagnostic assessment and a potential therapeutic target for HCC patients. - Source: PubMed
Publication date: 2026/03/31
Qu TaimeiTian Lv - : RASopathies represent a clinically and genetically diverse group of syndromes resulting from germline mutations in genes regulating the RAS/mitogen-activated protein kinase (MAPK) signaling cascade. : The aim of this study was to describe the clinical features and genetic variants identified in patients with genetically confirmed Noonan syndrome (NS) in a limited cohort from Romania. A total of 25 patients with positive genetic testing for NS-associated genes were included. Genetic testing was performed primarily using next-generation sequencing. : A total of twenty-six variants were identified in twenty-five patients, as one patient carried two pathogenic variants in the gene (c.188A>G and c.922A>G). Of these variants, twenty-four (92.31%) were classified as pathogenic and two (7.69%) as variants of uncertain significance (VUS). Pathogenic variants were found in different genes, including , , , and , with being the most frequently affected gene. Males predominated (17/25), with a male-to-female ratio of approximately 2:1. Two patients inherited the pathogenic variant from an affected parent. Cardiovascular involvement was present in 21 patients (84%), with pulmonary valve stenosis (PVS) being the most common finding (48%), followed by hypertrophic cardiomyopathy (16%). Additional cardiac anomalies included atrial septal defect, valvular regurgitation, dysplastic valves, coarctation of the aorta, and sinotubular junction narrowing. Short stature was observed in 64% of patients, and craniofacial dysmorphism was present in 96%. Cutaneous, ectodermal, dental, ophthalmologic, and auditory manifestations were variably observed. : Although based on a limited cohort from Romania, this study provides insights into clinical features suggestive of NS. Our findings highlight the genetic heterogeneity of NS and emphasize the importance of comprehensive genetic testing for confirming diagnosis, guiding clinical management, and supporting family counseling. - Source: PubMed
Publication date: 2026/04/17
Nazarie Florina VictoriaDobrescu Mihaela AmeliaLazea CeciliaDavid Ana AdrianaȘufană CrinaBucerzan SimonaCainap Simona SoranaRancea RalucaStănoiu-Pînzariu OanaPascanu Ionela MariaPopp Radu AnghelPop Laura AncutaLazăr CălinAlkhzouz CameliaMiclea DianaVulturar Romana - Developing cardiomyocytes grow by proliferative and hypertrophic pathways and can be mediated by the RAF/MEK/ERK (MAPK) pathway. Dysregulation of Raf-1 in late development causes murine myocardial hypertrophy, however, less is known about B-Raf. We hypothesized the loss of B-Raf (conditional knockout) would lead to reduced neonatal cardiomyocyte proliferation and accelerate maturation, resulting in impaired function in adulthood. We also determined sex differences to ensure complete interrogation of the model. Murine neonatal hearts undergo a proliferative to terminal differentiation switch that is complete by 2 weeks of age and thus studied hearts at four timepoints in that period (Days 1, 3, 8, 14). Primary cultures of knockout (KO) hearts revealed reduced B-Raf and phosphorylated ERK1/2 by postnatal day 3, even when stimulated with insulin growth factor 1. Histology revealed increased cardiomyocyte volume in KO hearts by 3d and elevated markers of hypertrophy and maturation by 8d (mTOR and SERC2A). There was also elevated cell cycle inhibitors p21, p27 and p53, accompanied with increased cyclin levels. Heart weight to body weight ratio was greater in 8d KO compared to age matched wildtype (WT) animals as well as other KO ages, whereas there was no difference among WT ages. Earliest signs of altered myocardium via echocardiographs were detected by 3 months. KO mice exhibited dilated cardiomyopathy, thinned myocardial walls, and enlarged left chamber volume. Deletion of B-Raf led to adaptive remodeling of male KO hearts. This adaptation maintains cardiac function however future studies will interrogate changes in the face of physiological stress. - Source: PubMed
Publication date: 2026/04/29
Chattergoon Natasha NRees Katherina PLescher SaraTakahashi MahoStork Philip J S - Knee osteoarthritis (KOA) is a common degenerative joint disease marked by progressive articular cartilage loss, pathological subchondral bone remodeling, and inflammation-associated disruption of extracellular matrix (ECM) homeostasis. Disease-modifying options remain scarce, despite advances in symptomatic management. Daidzein (DAI), a soy-derived isoflavone, has demonstrated anti-inflammatory and chondroprotective effects; however, its key targets and downstream mechanisms in KOA remain unclear. - Source: PubMed
Publication date: 2026/04/27
Dong XiaokunMa JinxinWang JiliMa LongfeiSong MingzheYuan BingsenLiu XinyanBan SaiboCheng ShaoWang Shangzeng - Noonan syndrome (NS) is the most common RASopathy, a developmental disorder that derives from dysregulation of the mitogen-activated protein kinase (MAPK) pathway. NS results from modestly activating mutations in proteins throughout the pathway. Trametinib, a MEK inhibitor, has shown promising results for certain NS complications, but NS-specific therapeutic options are lacking. CRAF activity, which is governed by the adaptor protein 14-3-3, represents a key NS regulatory node that has not been exploited. When phosphorylated (p) at CRAF S259, the 14-3-3/CRAF-pS259 complex adopts an inactive conformation in which CRAF does not fully bind to RAS or to other RAFs. NS mutations in CRAF occur at residues surrounding S259 (CRAF). Here, we quantify how these mutations impair 14-3-3/CRAF, both through decreased phosphorylation (64 to 97%) and decreased binding affinity to 14-3-3 (three- to >100-fold decrease). We also explore the potential of restoring homeostasis in NS using molecular glues (MGs) to enhance the 14-3-3/CRAF inhibitory complex. We report that MGs protect phosphorylation of CRAF-pS259 in CRAF-effector NS mutant backgrounds. They also stabilize 14-3-3/CRAF interactions and increase the levels of S259 phosphorylation up to 2.8-fold, leading to decreased association of CRAF with NRAS and decreased formation of the active CRAF kinase dimers. Ultimately, inhibition of CRAF activation leads to decreased phosphorylation of the downstream target ERK, similarly to trametinib, in three different NS variants (activation of the phosphatase SHOC2, CRAF, and CRAF). These results reveal a potential therapeutic strategy for NS and related RASopathies. They also demonstrate the scope and limitations of stabilizing mutation-weakened complexes with molecular glues. - Source: PubMed
Publication date: 2026/04/28
Virta Johanna MVickery Holly RKonstantinidou MarkellaCrawford Mckenna CPennings Marloes A MOttmann ChristianBrunsveld LucArkin Michelle R