RHEB also known as Ras homolog enriched in brain (RHEB) is a GTP-binding protein that is ubiquitously expressed in humans and other mammals. The protein is largely involved in the mTOR pathway and the regulation of the cell cycle.

研究结论：Rheb泛素化需要TSC复合物的GAP活性，其中TSC2可能主要促进Rheb的单泛素化。另外，Rheb的泛素化与其失活密切相关，而EGF处理会抑制Rheb的泛素化。 2.RNF152是Rheb的E3泛素连接酶. 作者筛选了一组E3连接酶，以确定催化Rheb泛素化的特异性E3连接酶。

小分子 GTP 酶 Rheb，在与 GTP 结合的状态下，是 mTORC1 激酶活性所需的强效刺激剂，并且受到其 GAP（即结节性硬化异二聚体 TSC1/2）的负性调控。绝大多数上游输入信号通过 Akt 和 TSC1/2 来调节 Rheb 的核苷酸负载状态。

2024年12月25日 · RHEB (Ras Homolog, MTORC1 Binding) is a Protein Coding gene. Diseases associated with RHEB include Focal Cortical Dysplasia, Type Ii and Isolated Focal Cortical Dysplasia Type Ii. Among its related pathways are Translation Insulin regulation of translation and PIP3 activates AKT signaling.

2017年12月13日 · Here we present the 3.0 ångström cryo-electron microscopy structure of mTORC1 and the 3.4 ångström structure of activated RHEB–mTORC1. RHEB binds to mTOR distally from the kinase active site,...

Rheb是一种小H-Ras-like GTPase，是溶酶体表面 雷帕霉素 复合物1（mTORC1）机制靶点的直接和必要激活剂。在研究Rheb在突触信号传导和细胞分化中的作用是，发现Rheb与丙酮酸代谢的能量调节中的线粒体调节有关。

RHEB is an important small GTPase that acts as an allosteric activator of the mTORC1 complex, a key nutrient sensor that controls cell growth and biomass production. In response to signals such as nutrients and growth factors, RHEB activates the MTOR kinase within mTORC1 by inducing conformational changes.

2018年2月7日 · Here, we report the discovery of a small molecule (NR1) that binds Rheb in the switch II domain and selectively blocks mTORC1 signaling. NR1 potently inhibits mTORC1 driven phosphorylation of...

研究细致地解析了细胞氨基酸水平变化可特异地调控mTORC1对转录因子TEFB磷酸化，揭示了Birt–Hogg–Dubé syndrome背后的致病机制。 mTORC1分别通过TSC-Rheb和Rag GTPase响应生长因子和氨基酸水平的变化。 mTORC1对TFEB磷酸化，后者滞留于胞质中，实现了对其的负调控。 生长条件改变时，mTORC1离开溶酶体，TEFB磷酸化抑制解除，TFEB来到细胞核，激活包括RagC/D基因在内的相关基因的转录。 与其它底物S6K和4E-BP不同的是，只有氨基酸缺乏可 …

RHEB is a potential therapeutic target in T cell acute lymphoblastic leukemia. Translation initiation factor eIF3a regulates glucose metabolism and cell proliferation via promoting small GTPase Rheb synthesis and AMPK activation. miR-199a-3p/5p regulate tumorgenesis via targeting Rheb in non-small cell lung cancer.