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
- Nance-Horan syndrome-like protein 3 (NHSL3) has been implicated in hepatocellular carcinoma (HCC) progression, but its role in sorafenib response and related growth and motility phenotypes remains unclear. In this study, we examined NHSL3 loss in Huh-7 cells and selected phenotypes in Hep3B cells. - Source: PubMed
Publication date: 2026/09/18
Yıldız GökhanKarabulut SonerDinçer Tuba - Raf kinases are central to mitogenic signaling and cancer, yet the full complement of functionally important Raf-proximal proteins across subcellular compartments remains undefined. Here, proximity-dependent biotinylation (BioID) of Raf1 in Raf1-dependent cancer cells recovered proteins localized to the mitochondrial matrix. Mitochondrial purification and super-resolution microscopy confirmed that a pool of Raf1 resides within mitochondria. There, Raf1 associated with glutaminase (GLS) across diverse human cancers and enabled glutaminolysis, a major source of biosynthetic precursors in tumor cells. These effects required Raf1 kinase activity but were independent of canonical MAP kinase pathway signaling, and matrix-targeted kinase-dead Raf1 impaired both glutaminolysis and in vivo tumorigenesis. Raf1 therefore acts inside mitochondria, where it engages GLS to drive glutamine catabolism and support tumor growth, revealing a non-canonical, metabolic arm of Raf signaling. - Source: PubMed
Publication date: 2026/09/09
Shanderson Ronald LFerguson Ian DDucoli LucaMiao WeiliSrinivasan SuhasSiprashvili ZurabLi Albert MVelasco Mary GraceLi YangHoang Christine NYe JiangbinKhavari Paul A - Structural neuroimaging in youth with RASopathies has shown alterations in total brain volume (TBV) and subcortical structures. However, whether these subcortical differences scale proportionately with TBV or follow nonlinear allometric relationships remains unclear, limiting accurate interpretation of neuroanatomical findings and their relevance to cognition. Using an allometric framework, this study aimed to determine whether (1) subcortical volumes exhibit deviations from normative scaling in RASopathies and (2) methods used to account for TBV influence the detection of subcortical volume alterations. We examined youth with RASopathies (N=133), including Neurofibromatosis Type-1 (NF1, N=27), Noonan Syndrome (NS, N=100; : 72, : 22, : 6), and Noonan Syndrome with Multiple Lentigines (NSML, N=5), compared to 80 age- and sex-matched controls. Subcortical volumes were analyzed using an allometric framework, compared with linear TBV correction methods (normalization and covariation), and explored in sex-stratified analyses. Allometric analyses revealed deviations from normative scaling in the thalamus for NF1; the caudate, putamen, ventral striatum, and pallidum for ; and the ventral striatum for No significant deviations were observed for NSML or Exploratory sex-stratified analyses suggested similar directional scaling patterns across sexes, with greater deviations in females, although subgroup sizes were small. Comparisons across correction methods demonstrated that linear approaches may overestimate regional differences, whereas thalamic alterations in NF1 and striatal alterations in were consistent across methods, suggesting robust, region-specific genetic effects beyond scaling. These findings highlight genotype-specific deviations from normative allometric scaling and underscore the importance of nonlinear scaling frameworks to accurately characterize neuroanatomical differences in RASopathies. Neurofibromatosis Type-1 and Noonan spectrum disorders are associated with atypical brain size, yet most neuroimaging studies rely on linear correction methods that assume proportional brain scaling. Regional brain allometry poses an important but underappreciated methodological challenge for accurately characterizing neuroanatomical differences in these conditions. Here, we apply a normative allometric framework that reveals gene- and sex-specific deviations in subcortical scaling that are potentially overestimated by linear correction approaches. These findings refine the interpretation of brain structure differences in RASopathies and demonstrate the need to account for nonlinear scaling in neurodevelopmental research. Incorporating allometric approaches will improve the biological specificity of neuroimaging markers and inform future efforts toward personalized assessment and intervention. - Source: PubMed
Publication date: 2026/09/08
McGhee-Deakin Chloe ARusso OdeyaPlank Julia RGreen Tamar - Gastric cancer is a major global health issue, especially in advanced stages with metastasis. However, anti-angiogenic treatments such as ramucirumab target vascular endothelial growth factor, yet the exact mechanisms behind hematogenous metastasis remain unclear. This study analyzed RNA sequencing data from TCGA to identify angiogenesis-related genes in metastatic gastric cancer. - Source: PubMed
Publication date: 2026/08/31
Yoo JaeunKim Hyun MyongJeong KyoungyunYoo Yie-RiShin Ji-YeonLee SeunghoLee SeungbokLee Hye SeungPark Kyoung UnKong Seong-HoPark Do JoongLee Hyuk-JoonYang Han-Kwang - Noonan syndrome-associated hypertrophic cardiomyopathy (NS-HCM) occurs frequently in patients with RAF1 mutations, but the signaling mechanisms underlying the hypertrophic cardiomyocyte phenotype remain incompletely understood, and effective therapeutic targets remain to be defined. This study aimed to characterize MAPK signaling dysregulation in RAF1-mutant induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) and to determine whether berberine (BBR) attenuates the hypertrophic phenotype through modulation of ERK5-Cyclin D1 signaling. - Source: PubMed
Publication date: 2026/08/29
Chen HongfeiZhang YuleLai XiaoqiWang Shushui