Ask about this productRelated genes to: RRAS2 antibody
- Gene:
- RRAS2 NIH gene
- Name:
- RAS related 2
- Previous symbol:
- -
- Synonyms:
- TC21
- Chromosome:
- 11p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-30
- Date modifiied:
- 2017-08-02
Related products to: RRAS2 antibody
Related articles to: RRAS2 antibody
- Distinct effector-binding preferences among RAS family GTPases challenge the longstanding view that canonical RAS proteins uniformly bind and activate RAF, PI3Kα, RalGDS, and other downstream effectors. Quantitative binding data, supported by structural insights into effector recognition, instead reveal a division of labor: the canonical RAS subfamily (KRAS, HRAS, NRAS) binds RAF kinases with high affinity, the RRAS subfamily (RRAS2 and MRAS) preferentially engages PI3Kα, and the RAP subfamily (RAP1A and RAP1B) shows the strongest binding to RalGDS. These intrinsic preferences, encoded in the switch regions and further shaped by isoform and effector expression, as well as subcellular localization, establish a hierarchy in which canonical RAS, RRAS2/MRAS, and RAP1A/B primarily activate RAF, PI3Kα, and RalGDS, respectively, in normal cells. Oncogenic mutations at codons G12, G13, or Q61 disrupt this hierarchy by driving sustained accumulation of GTP-bound canonical RAS, enabling engagement of lower-affinity effectors such as PI3Kα and RalGDS. In addition, certain mutations, including KRAS-G12D and -G12V, modestly enhance PI3Kα binding, representing a neomorphic expansion of effector engagement. Together, these effects bypass intrinsic effector selectivity, allowing canonical RAS to co-opt effectors normally associated with other RAS subfamilies and broaden downstream signaling. This framework explains how inherent effector preferences govern normal signaling and how oncogenic mutations override these constraints to expand effector engagement in RAS-driven cancers. - Source: PubMed
Simanshu Dhirendra KMcCormick Frank - Luminal breast cancer has a high incidence and significant heterogeneity. Exosomes, as key mediators of intercellular communication, are involved in the tumor process, but the related genes in Luminal breast cancer regarding prognosis and mechanism remain unclear. - Source: PubMed
Publication date: 2026/04/13
Huang JianTang XiulingSu QiyuanFang DalangWang JinLuo Zhizhai - Both short and long sleep duration have been associated with poor glycemic control and an increased risk of developing type 2 diabetes mellitus. Although sleep duration may differentially modify the effects of genetic risk factors for type 2 diabetes, this has not been systematically investigated. In the present study, we conducted genome-wide gene by sleep duration meta-analyses, separately assessing interactions of short and long sleep, for fasting glucose, fasting insulin, and hemoglobin A1c in up to 489,309 individuals without diabetes from seven different population groups. In total, 16 loci were identified to interact with sleep duration - six with short sleep and ten with long sleep. Of these, four loci were identified through cross-population meta-analysis. Mapped genes exhibit pathway connections to pericyte apoptosis, NMDA receptor activity, the GLUT1 receptor, neurological health, and sleep architecture. Eleven loci () have not been reported in previous glycemic trait genome-wide association studies. Interaction loci identify divergent biological mechanisms for short and long sleep duration influencing glycemic control, suggesting specific pathways of intervention for precision medicine approaches to diabetes prevention and management. - Source: PubMed
Publication date: 2026/03/03
Wang HemingNagarajan PavithraMiller Clint LBentley Amy RNoordam RaymondWesterman Kenneth EBrown Michael RKraja Aldi TO'Connell Jeffrey RSchwander KarenLi ChangweiSanghvi Mihir MSong YipeiBartz Traci MBraunack-Mayer VincentChen LingDu JiawenDunca DianaFeitosa Mary FGudmundsdottir ValborgGuo XiuqingHarris Sarah EHighland Heather MHuang ZhijieKang ChanghoonLakka Timo ALefevre ChristopheLuan Jian'anLyytikäinen Leo-PekkaMissikpode CelestinMorrison John LPalmer Nicholette DRichmond AnneShahisavandi MinaTang Jingxianvan der Most Peter JWeiss StefanYu ChenglongZhu WanyingAnsari Md Abu YusufAnugu PramodAschard HuguesAshok KaavyaAttia John RBazzano Lydia ACade Brian ECampbell ArchieDimitrov Latchezar MDo AnhFaquih TariqFinesilverSmith Sandy LFisher-Hoch Susan PFretts Amanda MGharib Sina AGoodarzi Mark OGraff MariaelisaGu CharlesHanson PaulHe JiangHeikkinen SamiHixson JamesHsu SarahKähönen MikaKho MinjungKim HyunjuKomulainen PirjoLauner Lenore JLemaitre Rozenn N McNeil John JMcCormick Joseph BNolte Ilja MRaffield Laura MRaitakari Olli TRamírez JuliaRiha Renata LRisch MartinRisch LorenzRuss Tom CSarnowski ChloéSchram Miranda TScott Rodney JSofer TamarSun QuanVölker UweVölzke HenryWang Yujievan Dijk Ko WillemsWood Alexis CYoung Kristin LZhang RuiyuanZhu XiaofengBelow Jennifer EConen DavidCox Simon RFox Ervin RFranceschini NoraGhanbari MohsenGrabe Hans JörgenGudnason VilmundurHayward CarolineHolliday Elizabeth GJaquish Cashell ELacaze PaulLee SeunggeunLehtimäki TerhoLiu Ching-TiMorrison Alanna CNorth Kari EPeyser Patricia AProvince Michael APsaty Bruce MRauramaa RainerRosendaal Frits RRotter Jerome ISnieder HaroldWagenknecht Lynne EWareham Nicholas JGiri AyushKelly Tanika NMunroe Patricia BGauderman JamesWinkler Thomas Wde Vries Paul SRao Dabeeru CManning Alisa KChen Hande Las Fuentes LisaRedline SusanMeigs James B - - Source: PubMed
Publication date: 2026/03/20
Legro Nicole RHaizler-Cohen LylachGenthe WilliamGreenberg Victoria - Colorectal cancer (CRC) demonstrates substantial clinical and biological diversity across age groups, ancestral backgrounds, and treatment settings, alongside a rising incidence of early-onset disease (EOCRC). The mitogen-activated protein kinase (MAPK) pathway is a major driver of CRC development and therapy response; however, the distribution and prognostic value of MAPK alterations across distinct patient subgroups remain unclear. - Source: PubMed
Publication date: 2026/01/17
Diaz Fernando CWaldrup BrigetteCarranza Francisco GManjarrez SophiaVelazquez-Villarreal Enrique