Raf1 (constitutively active) Recombinant Adenovirus
- Known as:
- Raf1 (constitutively functionnal) Recombinant Adenovirus
- Catalog number:
- ADV-134
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Cell Biolabs
- Gene target:
- Raf1 (constitutively active) Recombinant Adenovirus
Related genes to: Raf1 (constitutively active) 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 (constitutively active) Recombinant Adenovirus
Related articles to: Raf1 (constitutively active) Recombinant Adenovirus
- Despite advancements in primary percutaneous coronary intervention (PCI), cardiac dysfunction remains a challenge in patients with ST-segment elevation myocardial infarction (STEMI). Although thymosin beta 4 has shown cardioprotective effects in preclinical MI models, its impact on chronic cardiac functional recovery post ischemia/reperfusion (I/R), especially in STEMI, warrants further investigation. This study aims to explore the therapeutic potential of recombinant human thymosin beta 4 (rhTB4) in both murine models subjected to I/R and in subjects with STEMI post-PCI. - Source: PubMed
Publication date: 2025/11/12
Zhang YuzeDong QiutingBian XiaohuiQiao ZhengCui ChuanjueYang NingLiu JincanFu RuiZhang JunJia LeiWu ChaoGuo JinchengLin WenhuaWang JingpingFan JiamaoLi YangLiu FanYang BinJia XinweiGao ChuanyuBai MingHe YiHan ChengquanYin DongDou Kefei - Pediatric low-grade gliomas (pLGGs) are the most common brain tumors in children with varying degrees of infiltration. Despite having a positive prognosis, if the standard treatment, gross total resection, is impossible due to tumor location or diffuseness, outcomes worsen. Development of targeted therapeutics for diverse subtypes of pLGGs is limited by a lack of genetic models. We generated five fly pLGG models using patient-derived fusion genes to investigate molecular subtype-specific pathology, and found glial overexpression of QKI::RAF1, associated with pilocytic astrocytomas and glioneuronal tumors, induced aberrant glial migration and infiltration. Both repulsive guidance signaling and GPR180/CG9304 mediated glial infiltration, which was suppressed by glial overexpression of Robo2 or PlexA/B, or knockdown of GPR180/CG9304. ROBO2 and GPR180/CG9304 were down and upregulated, respectively, in flies and patients with RAF fusions. Our study provides mechanistic insights into pLGG tumorigenesis and suggests targeting repulsive guidance signaling and GPR180/CG9304 as potential therapeutics for pLGG subtypes. - Source: PubMed
Publication date: 2025/11/11
Jung GeenaLiang ZizhuoJain PayalDeutsch Hannah MLi FengRathi Komal SSun ZhichuanChen XinStraka JoshuaKazerooni Anahita FathiSun YuqiKoptyra Mateusz PSanchez-Maldonado StephanieFamiliar ArianaWaanders Angela JNabavizadeh AliHuang XiResnick Adam CSong Yuanquan - Ribosome-binding protein 1 (RRBP1), a core regulator of endoplasmic reticulum-ribosome interactions, serves key roles in the development and progression of various cancer types by coordinating protein synthesis and organelle dynamic interactions. RRBP1 regulates the unfolded protein response by stabilizing glucose-regulated protein 78 and it enhances cancer cell adaptation to endoplasmic reticulum stress and chemotherapy. The stability of RRBP1 is regulated by N6-methyladenosine modification by methyltransferase-like 3 and deubiquitination by ubiquitin-specific processing protease 35. Furthermore, RRBP1 drives cellular anti-apoptosis mechanisms by activating pro-survival pathways such as TGF-β1/SMAD, PI3K/AKT and Notch or binding cyclic RNAs. By contrast, aberrant activation of kinase function and deubiquitination pathways by fusion genes [-anaplastic lymphoma kinase, -Raf1 proto-oncogene, serine/threonine kinase and -ubiquitin specific peptidase 6] exacerbates malignant progression. Furthermore, the pleiotropic regulation of RRBP1 in neurodegeneration, cardiovascular homeostasis and bone metabolism highlights its environment-dependent functions. The present review identified the multidimensional regulatory network of RRBP1 in cancer and non-cancer systems to enhance the understanding of its molecular mechanism, demonstrated its broad regulatory value and potentially provided a key entry point to analyze the disease and develop precision therapies. - Source: PubMed
Publication date: 2025/10/23
Huang HoOuyang Jia - This study aims to explore the lymphangiogenesis (LG)-related diagnostic markers of abdominal aortic aneurysm (AAA) through bioinformatics, as well as the alteration of the regional lymphatic system during the progression of AAA and the influence of lymphatic drainage obstruction on AAA progression. 2957 differentially expressed genes (DEGs) were identified between the AAA patient group and the healthy donor group in Gene Expression Omnibus microarray datasets. Subsequently, the DEGs and the LG gene were intersected, and 93 genes were obtained. Weighted gene co-expression network analysis (WGCNA) was performed to obtain module genes. Module genes intersected with the above 93 genes, and 26 genes were obtained. Five hub genes (HSPA5, RAB10, RAB1A, RAF1, SMAD4) identified by machine learning may serve as diagnostic candidates for AAA patients through nomogram and ROC evaluation. Gene set enrichment analysis (GSEA) and immune infiltration analysis were performed further to understand the function of these candidate genes and explore the effect of immunity in AAA, respectively. By establishing an AAA animal model, it was found that the iliac lymph nodes around the abdominal aorta were significantly enlarged, and the number and lumen size of lymphatic vessels in the vessel wall were both significantly increased during the progression of AAA. Additionally, AAA was significantly promoted by ligating lymphatic vessels, which caused lymphatic drainage obstruction around the abdominal aorta. Our findings have the potential to enhance knowledge about the development and diagnosis of AAA. - Source: PubMed
Publication date: 2025/11/01
Qin SuZhang JingCao MeifangJiang TaoJiang Baohong - The P2Y purinergic receptor (P2YR) plays a crucial role in the progression of liver fibrosis, and selective inhibition of this receptor has emerged as a promising therapeutic approach. In this study, an integrative computational pipeline identified a unique and highly flexible binding pocket within P2YR, which is divided into two quasi-symmetrical subdomains. Leveraging this structural feature, we designed and synthesized two novel families of inhibitors based on benzoxazole-urea and benzoxazole-squaramide scaffolds. The lead compound, (), demonstrates exceptional potency (IC = 0.026 nM) and superior metabolic stability. HDB-1 exhibited antihepatic fibrosis activity both and Mechanistically, inhibits P2YR-mediated signaling by suppressing the PKA/Raf1/MEK/ERK cascade, thereby preventing the activation of hepatic stellate cells-the central pathological event in fibrosis development. Taken together, represents a novel and potent P2YR inhibitor with strong potential as an available therapeutic for liver fibrosis driven by dysregulated P2YR signaling. - Source: PubMed
Publication date: 2025/11/03
Li ChenchengWang HuiLiu LiLiu ChunxiaoWang YiyunYin LiYang YalianTian ShengQian JialongZhou MengzeLi HuanqiuHu Qinghua