N_ras
- Known as:
- N_ras
- Catalog number:
- 000372A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- N_ras
Related genes to: N_ras
- Gene:
- NRAS NIH gene
- Name:
- NRAS proto-oncogene, GTPase
- Previous symbol:
- -
- Synonyms:
- N-ras
- Chromosome:
- 1p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: N_ras
kinase suppressor of ras (KSR) polyclonal antibody24KG,Rab11,Rab-11,Rab11a,Ras-related protein Rab-11A,Rat,Rattus norvegicus40 kDa BINP-binding protein,Brain-specific binding protein,p40BBP,Ras-induced senescence protein 1,Rat,Rattus norvegicus,Ris1,Tmem158,Transmembrane protein 15840 kDa BINP-binding protein,HBBP,Homo sapiens,Human,p40BBP,Ras-induced senescence protein 1,RIS1,TMEM158,Transmembrane protein 15840 kDa BINP-binding protein,Mbbp,Mouse,Mus musculus,p40BBP,Ras-induced senescence protein 1,Ris1,Tmem158,Transmembrane protein 15896-Well Ras Activation ELISA Kit (Chemiluminescent)96-Well Ras Activation ELISA Kit (Colorimetric)Activator of G-protein signaling 1,AGS1,Dexamethasone-induced Ras-related protein 1,DEXRAS1,Homo sapiens,Human,RASD1Active H-Ras Expression Vector SetActive H-Ras Expression Vector SetAD037,Homo sapiens,Human,Ras association domain-containing protein 4,RASSF4Adenovirus E3 14.7 kDa-interacting protein 1,FIP-1,Homo sapiens,Human,Rag A,RagA,Ras-related GTP-binding protein A,RRAGAAF6 is a Ras target that regulates cell-cell adhesions downstream of Ras activation. It is fused with MLL in leukemias caused by t (6;11) translocations.AF6-RBDGST (residues 1-141) GTP-H-Ras binding cytoplasmic protein, Afadin - Ras-binding domain human, recombinant, E. coliAF6-RBDGST (residues 1-141) GTP-H-Ras binding cytoplasmic protein, Afadin - Ras-binding domainhuman, recombinant, E. coli Related articles to: N_ras
- Monogenic lupus is a rare, early-onset form of lupus caused by high-penetrance genetic variants, with diverse clinical features and a central role for type I interferon (IFN-I) in its pathogenesis. Standard treatments are lacking, but Janus kinase (JAK) inhibitors show promise, especially in refractory cases. - Source: PubMed
Publication date: 2026/02/04
Al-Mayouf Sulaiman MAlAsmari AliAl-Saleem Alhanouf - [This corrects the article DOI: 10.1039/D4CB00233D.]. - Source: PubMed
Publication date: 2026/05/05
Rennella EnricoHenry ChrystèleDickson Callum JGeorgescauld FlorianWales Thomas EErdmann DirkCotesta SimonaMaira MichelSedrani RichardBrachmann Saskia MOstermann NilsEngen John RKay Lewis EBeyer Kim SWilcken RainerJahnke Wolfgang - Current approved KRAS inhibitors covalently bind the inactive GDP-bound (OFF) form of KRAS . Recently, KRAS inhibitors that selectively bind to the GTP-bound (ON) form of both KRAS (ON) and (OFF) forms have been reported and entered clinical testing. In principle, KRAS (ON) inhibitors may be less susceptible to adaptive mechanisms that promote resistance to (OFF) inhibitors, however the specific mechanisms that differentiate the activity of (ON) versus (OFF) inhibition are not well understood. We profiled the activity of BBO-8520, a covalent dual inhibitor of GTP-bound (ON) and GDP-bound (OFF) KRAS , in -mutant non-small cell lung cancer models. BBO-8520 exerted more potent and sustained inhibition of KRAS and anti-tumor activity and compared with sotorasib, a KRAS (OFF)-only inhibitor. While cells treated with BBO-8520 or sotorasib both exhibited feedback reactivation of MAPK signaling driven by wild-type HRAS/NRAS isoforms, more durable suppression of KRAS by BBO-8520 was associated with decreased PI3Kα-AKT activation . Disruption of the interaction between RAS and PI3Kα using a novel protein:protein interaction inhibitor suppressed PI3Kα-AKT activation and increased the tumor response to sotorasib to a similar level as BBO-8520. Moreover, in some contexts, disruption of RAS-PI3Kα further increased the anti-tumor activity of BBO-8520 monotherapy. These results reveal mechanistic differences between KRAS (ON) and (OFF) inhibitors, highlight the importance of PI3Kα-AKT signaling in driving resistance to KRAS inhibition in lung cancer, and suggest combination strategies that suppress PI3Kα-AKT to improve the response to KRAS inhibitors. - Source: PubMed
Publication date: 2026/04/30
Parker KatherineGhorbanpoor SamarMalik WafaHighfield LaurenWang JamieHensley EmilyKelley GraceClark SarahRanieri MichelaSahu SoumyadipZhang CathyPloszaj MagdalenaAndrussier DanielHuang Hsin-YiChen TingWang BinXu RuiSetoodeh SamanLin KenMaciag Anna EMcCormick FrankBeltran Pedro JWong Kwok-KinStice James PSinkevicius Kerstin WHata Aaron N - Colorectal cancer is one of the most common cancers in Aotearoa New Zealand. Evidence supports that right colon cancer (RCC) and left colon cancer (LCC) represent distinct entities, with RCC associated with a poorer prognosis, despite accounting for stage. Oncogenic mutations in MMR protein expression, BRAF V600E, and RAS genes have been shown to differ significantly between RCC and LCC, influencing tumour behaviour and prognosis. - Source: PubMed
Publication date: 2026/05/06
Petrie ACarson D ACribb B - BRAF V600 inhibitors are clinically approved for the treatment of BRAF-mutant melanoma in combination with a MEK inhibitor, but are ineffective in other melanoma subtypes. Moreover, pan-RAF inhibitors, such as belvarafenib, when combined with MEK inhibitors (cobimetinib), have promising but limited efficacy in non-BRAF-mutant melanomas. Here, we report that the mTOR inhibitor sapanisertib improves the efficacy of combined belvarafenib and cobimetinib therapy in NRAS, NF1, and KIT-mutant melanomas. Mechanistically, sapanisertib combined with belvarafenib and cobimetinib suppressed ATF4 expression and its target gene MTHFD2 while inducing DNA damage, revealing a previously underappreciated role of the ATF4-MTHFD2 axis in DNA damage repair and drug response. Human and murine models resistant to combined belvarafenib and cobimetinib exhibited elevated levels of ATF4 and MTHFD2 and were sensitive to sapanisertib. This study provides promising treatment opportunities for patients with non-BRAF-mutant melanomas, or those who relapse following belvarafenib and cobimetinib combination therapy. - Source: PubMed
Publication date: 2026/05/06
Cai FeiyangHuang FanGoncalves ChristopheSrikannan HarineeGagnon NataschaGuettler Elizabeth MMukeba-Harchies LéaMaxwell JenniferSu JieBijian KrikorJourne FabriceRose April A NOrthwein AlexandreDel Rincón Sonia VictoriaMiller Wilson H