RASH_RAT Hras ELISA tesk kit
- Known as:
- RASH_RAT Hras Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16672
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- RASH_RAT Hras ELISA tesk kit
Related genes to: RASH_RAT Hras ELISA tesk kit
- Gene:
- HRAS NIH gene
- Name:
- HRas proto-oncogene, GTPase
- Previous symbol:
- HRAS1
- Synonyms:
- -
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
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- Clinically, acute kidney injury (AKI) is one of the most frequent complications of Naja atra (N. atra) envenomation, primarily attributed to snake venom phospholipase A (SVPLA). Although the SVPLA inhibitor varespladib shows great therapeutic promise, the underlying mechanisms remain incompletely understood. Herein, we integrated multi-omics and molecular biology approaches to investigate the critical role of SVPLA in N. atra venom-induced AKI, as evidenced by pharmacological inhibition with varespladib. Proteomic profiling identified HRAS and CCND1 as key mediators of SVPLA-induced nephrotoxicity. Mechanistically, SVPLA disrupts lipid raft integrity, impairing HRAS palmitoylation-dependent plasma membrane localization and GTPase activity. This defect suppresses phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling, causing apoptosis and cell cycle arrest in renal tubular epithelial cells, enforced activation of PI3K-AKT signaling effectively rescued cells from injury. Beyond direct cytotoxicity, SVPLA profoundly remodels the renal immune microenvironment. SVPLA enhances glycolysis by upregulating hexokinase 2 (HK2) while suppressing fatty acid oxidation through downregulation of carnitine palmitoyltransferase IA, thereby metabolically driving M1 polarization. This metabolic shift impairs macrophage efferocytosis and sustains inflammatory injury. HK2 knockdown reverses these effects in macrophages. Taken together, this study reveals a dual epithelial-immune mechanism by which SVPLA activity critically contributes to N. atra venom-induced AKI, as evidenced by pharmacological inhibition with varespladib. These findings highlight PI3K-AKT signaling and HK2 as potential therapeutic targets for N. atra-triggered AKI. Supplementary key words. - Source: PubMed
Publication date: 2026/08/14
Liu JiahaoChen SitongWu JiajiaTang SunkunWen ZejingBi XiaowenYang YangHuang Chunhong - Hip resurfacing arthroplasty (HRA) is needed for certain patients, such as those with in situ metal work and abnormal anatomy, and/or other needs that are not well-served by total hip replacement (THR). Over the last 20 years, almost all HRAs have been performed using Metal-on-Metal (MoM) bearings, but metal wear debris generated over time has now ended their continued use. Cemented highly cross-linked polyethylene (XLPE) acetabular bearings have shown excellent survivorship for use in THR and the aim of this study is to determine if this also applied to HRA. - Source: PubMed
Publication date: 2026/06/15
Pritchett James W - : Upper tract urothelial carcinoma (UTUC) is a rare malignancy representing approximately 5-10% of all urothelial cancers. Key risk factors include smoking, chemical exposures, selected metabolic conditions, and hereditary cancer syndromes. This narrative review summarises current knowledge on UTUC molecular pathogenesis, major risk determinants, and contemporary therapeutic strategies. : This study was conducted as a narrative review with a structured literature search. PubMed, Web of Science, Embase, and Scopus were searched using predefined combinations of UTUC-related terms covering molecular pathogenesis, carcinogenic risk factors, and treatment strategies. The review was prepared according to SANRA principles to improve transparency and consistency; however, no formal systematic review methodology or meta-analysis was performed. : Available genomic studies indicate that UTUC has a molecular profile distinct from urothelial bladder carcinoma (UBC), with recurrent alterations involving FGFR3, HRAS, KMT2D, CDKN2A, KRAS, MYC, and BRIP1. Smoking, aristolochic acid exposure, Lynch syndrome, and possibly early-onset urolithiasis contribute to carcinogenesis through distinct but incompletely understood mechanisms. Surgical treatment remains the standard of care for high-risk localised disease, whereas perioperative chemotherapy, immunotherapy, and targeted agents are expanding treatment options, particularly in advanced disease. A substantial proportion of the therapeutic evidence, however, is derived from broader urothelial carcinoma populations rather than UTUC-specific studies. : UTUC is biologically heterogeneous and shaped by both molecular alterations and environmental exposures. Although substantial progress has been made, important gaps remain in understanding UTUC-specific carcinogenic mechanisms and in defining evidence-based personalised treatment strategies. Better integration of molecular, environmental, and clinical data is needed to improve risk stratification and treatment selection. - Source: PubMed
Publication date: 2026/07/25
Zawadzki DominikLibergal NataliaNowak JaśminaGrzanka HannaMikołajczyk MaksymilianKisiała MikołajTulski MichałKrajewski WojciechSzydełko TomaszMałkiewicz Bartosz - The RAS family of oncogenes (KRAS, HRAS, NRAS) is among the most frequently mutated genes in human cancer. Therapeutic development has largely focused on inhibitors for KRAS codon 12 mutations, while mutant-selective inhibitors for Q61 variants remain elusive. A common mechanistic feature of G12 and Q61 mutants is the reduced efficiency of GTP hydrolysis, which enriches RAS in its active, signaling-competent state. Here we report small molecules that accelerate GTP hydrolysis in KRAS-Q61 mutants as an alternative therapeutic strategy. These compounds compensate for the loss of the catalytic residue Gln61 by introducing a general base into the active site, selectively enhancing hydrolysis of KRAS-Q61X (X = H, L, K, R) mutants by up to 20-fold. In mutant cancer cell lines, these compounds reduce GTP-bound RAS levels and suppress downstream signaling. This work establishes a mechanistic foundation for small-molecule 'GTPase activators' and offers a new paradigm for targeting RAS-driven cancers. - Source: PubMed
Publication date: 2026/08/12
Wang Ye-ChengChen Si-CongCao YangWu YangShi ZhongdaWang Celine DNorinskiy Michael ACelik HasanZhang Ziyang - RAS mutations occur in patients with several types of vascular anomalies, but effective treatments remain limited. To address this need, we evaluated the RAS (ON) multi-selective inhibitor RMC-7977 in human endothelial cells (ECs) expressing the NRAS mutation found in kaposiform lymphangiomatosis (KLA). RMC-7977 was evaluated using in vitro and in vivo models. Doxycycline-inducible NRAS and NRAS human ECs were treated with RMC-7977 (3.12-100 nM) or vehicle. We assessed signalling pathways, proliferation, migration, morphology, and angiopoietin-2 (ANG-2) production. NRAS ECs in a 3D angiogenesis assay were also treated with RMC-7977. For in vivo studies, NRAS ECs were injected into flanks of nude mice on a doxycycline diet to generate xenografts. Mice received oral RMC-7977 or vehicle, and xenografts were collected after 11 days. RMC-7977 inhibited NRAS-induced ERK phosphorylation and reduced proliferation, migration, spindle-like morphology, and ANG-2 production in a dose-dependent manner. RMC-7977 reduced vascular area in the angiogenesis assay. In vivo, RMC-7977 reduced xenograft weight, vascular area, and p-ERK staining. Overall, RMC-7977 suppressed NRAS-mediated signalling, aberrant EC behaviour, and ANG-2 production in vitro and reduced vascular overgrowth in angiogenesis assays and mouse xenografts. Therefore, RMC-7977 may be a promising therapeutic candidate for RAS-driven vascular anomalies, including KLA. - Source: PubMed
Alharbi SaraMerkle SvatavaPastura PatriciaMcDaniel C GriffinZaky George SWaters Andrew MLe Cras Timothy D