1. Signaling Pathways
  2. PI3K/Akt/mTOR
  3. mTOR

mTOR (哺乳动物雷帕霉素靶蛋白)

Mammalian target of Rapamycin

mTOR(哺乳动物雷帕霉素靶蛋白)是一种由人类 mTOR 基因编码的蛋白质。mTOR 是一种丝氨酸/苏氨酸蛋白激酶,可调节细胞生长、细胞增殖、细胞运动、细胞存活、蛋白质合成和转录。mTOR 属于磷脂酰肌醇 3-激酶相关激酶蛋白家族。mTOR 整合上游通路的输入,包括生长因子和氨基酸。mTOR 还能感知细胞营养、氧气和能量水平。mTOR 通路在人类疾病中失调,例如糖尿病、肥胖症、抑郁症和某些癌症。雷帕霉素通过与其细胞内受体 FKBP12 结合来抑制 mTOR。FKBP12-雷帕霉素复合物直接与 mTOR 的 FKBP12-雷帕霉素结合 (FRB) 域结合,从而抑制其活性。

mTOR (mammalian target of Rapamycin) is a protein that in humans is encoded by the mTOR gene. mTOR is a serine/threonine protein kinase that regulates cell growth, cell proliferation, cell motility, cell survival, protein synthesis, and transcription. mTOR belongs to the phosphatidylinositol 3-kinase-related kinase protein family. mTOR integrates the input from upstream pathways, including growth factors and amino acids. mTOR also senses cellular nutrient, oxygen, and energy levels. The mTOR pathway is dysregulated in human diseases, such as diabetes, obesity, depression, and certain cancers. Rapamycin inhibits mTOR by associating with its intracellular receptor FKBP12. The FKBP12-rapamycin complex binds directly to the FKBP12-Rapamycin Binding (FRB) domain of mTOR, inhibiting its activity.

Cat. No. Product Name Effect Purity Chemical Structure
  • HY-107363
    FT-1518 Inhibitor 98.62%
    FT-1518 是一种选择性的,可口服的,有效的新一代 mTORC1mTORC2 抑制剂,具有抗肿瘤的活性。
    FT-1518
  • HY-162382
    KTC1101 Inhibitor 98.09%
    KTC1101 是一种口服活性的泛 PI3K 抑制剂。KTC1101 可抑制 PI3K 信号通路,并减少下游 AKTmTOR 磷酸化,降低 Ki67 的表达量。KTC1101 的抗肿瘤活性有双重作用机制,即直接抑制肿瘤细胞生长和动态增强免疫反应。
    KTC1101
  • HY-12652
    AZD3147 Inhibitor 99.93%
    AZD3147 是一种有效的、具有口服活性的、选择性 mTORC1mTORC2 的双重抑制剂,IC50 值为 1.5 nM。AZD3147 对 PI3K 也具有一定的选择性作用。
    AZD3147
  • HY-N6896
    Isoviolanthin

    异佛来心苷

    Inhibitor 99.66%
    Isoviolanthin 是一种黄酮类糖苷。Isoviolanthin 可从 Dendrobium officinale 中提取。Isoviolanthin 对 KDM6BCHAC2ESCO2IPO4 具有强的结合亲和力。Isoviolanthin 可降低 MMP-2MMP-9。Isoviolanthin 可抑制 TGF-β/SmadPI3K/Akt/mTOR 信号通路。Isoviolanthin 可增加 Fhl3 的表达。Isoviolanthin 具有细胞保护作用。Isoviolanthin 对肝细胞癌具有抗癌活性。
    Isoviolanthin
  • HY-124582
    NEO214 Activator ≥98.0%
    NEO214 是一种自噬 (Autophagy) 抑制剂,是 PDE4 抑制剂 Rolipram (HY-16900) 与紫苏醇 (HY-N7000) 的共价偶联物,具有抗癌活性和血脑屏障 (BBB) 透过性。NEO214 可以阻止自噬-溶酶体融合,从而阻止自噬流并引发神经胶质瘤细胞死亡。该过程涉及 mTOR 激活,和 TFEB (转录因子 EB) 聚集。NEO214 抑制胶质母细胞瘤细胞的巨自噬/自噬,有克服胶质母细胞瘤的化疗耐药性的潜力。
    NEO214
  • HY-122665
    HTH-01-091 Inhibitor 98.64%
    HTH-01-091 是一种强效且选择性的 maternal embryonic leucine zipper kinase (MELK) 抑制剂,其 IC50 为 10.5 nM。HTH-01-091 还能抑制 PIM1/2/3RIPK2DYRK3smMLCKCLK2。HTH-01-091 可用于乳腺癌研究。
    HTH-01-091
  • HY-P1823
    C-Reactive Protein (CRP) (174-185) Modulator 99.88%
    C-Reactive Protein (CRP) 是一种抗肺炎球菌血浆蛋白,可作为炎症标志物。C-Reactive Protein 可以通过激活补体保护小鼠免受肺炎球菌感染。C-Reactive Protein 可以通过 CD64/AKT/mTOR 通路抑制 caspase-3/9 的激活从而促进舌鳞状细胞癌小鼠的化疗耐药性。
    C-Reactive Protein (CRP) (174-185)
  • HY-15271
    WYE-687 Inhibitor 98.05%
    WYE-687 是一种 ATP 竞争性的 mTOR 抑制剂,IC50为 7 nM。WYE-687 抑制 mTORC1mTORC2 活化。WYE-687 也抑制 PI3KαPI3KγIC50 分别为 81 nM 和 3.11 μM。
    WYE-687
  • HY-101776A
    Desmethyl-VS-5584 hydrochloride Inhibitor 98.63%
    Desmethyl-VS-5584 hydrochloride 是VS-5584的二甲基类似物,是一种具有吡啶[2,3-d]嘧啶结构的强效选择性 mTOR/PI3K 双重抑制剂。
    Desmethyl-VS-5584 hydrochloride
  • HY-139142
    Simufilam Inhibitor 98.08%
    Simufilam (PTI-125) 是一种口服活性 FLNA 调节剂。Simufilam 恢复 NMDAR 信号传导和 Arc 表达。Simufilam 通过恢复 FLNA 的正常构象抑制过度活跃的 mTOR 信号传导,改善胰岛素敏感性,减少 Aβ42 引发的神经炎症和 tau 蛋白过度磷酸化。Simufilam 可用于阿尔茨海默症的研究。
    Simufilam
  • HY-101955
    (2S,6S)-Hydroxynorketamine hydrochloride Activator 99.30%
    (2S,6S)-Hydroxynorketamine hydrochloride 是具有神经松弛作用的活性分子,具有潜在的抗抑郁和镇痛作用。(2S,6S)-Hydroxynorketamine hydrochloride 能够激活 mTOR 通路、提高下游靶点磷酸化水平,还能够拮抗 α7-烟碱乙酰胆碱受体 (nAChR),发挥神经活性。
    (2S,6S)-Hydroxynorketamine hydrochloride
  • HY-114267
    Cbz-B3A Inhibitor 98.63%
    Cbz-B3A 是 mTORC1 转导的有效选择性抑制剂,与泛素1、2、4 结合,Cbz-B3A 还能抑制 eIF4E 结合蛋白的磷酸化。
    Cbz-B3A
  • HY-145931
    CC214-2 Inhibitor 98.41%
    CC214-2 是一种口服有效的 mTOR 激酶抑制剂。CC214-2 靶向 mTORC1 (pS6) 和 mTORC2 (pAktS473)。CC214-2 诱导自噬,自噬即是结核病宿主定向治疗 (HDT) 的潜在靶点。CC214-2 对结核病 (TB) 表现出协同抑菌和杀菌活性,并能够缩短产生效力的时间。CC214-2 还抑制雷帕霉素 (HY-10219) 耐药信号,并在体外和体内抑制胶质母细胞瘤的生长。
    CC214-2
  • HY-17471AR
    Metformin hydrochloride (Standard)

    盐酸二甲双胍 (标准品)

    Inhibitor 99.97%
    Metformin hydrochloride (Standard) 是 Metformin (hydrochloride) 的分析标准品。本产品用于研究及分析应用。 Metformin hydrochloride (1,1-Dimethylbiguanide) 抑制肝脏中的线粒体呼吸链,导致 AMPK 活化,增强胰岛素敏感性,可用于 2 型糖尿病的研究。Metformin hydrochloride 也抑制肝脏缺血/再灌注损伤引起的肝脏氧化应激、亚硝化应激、炎症和细胞凋亡 (apoptosis)。此外,Metformin hydrochloride 还通过激活 AMPK 和抑制 mTOR 信号通路,调节自噬相关蛋白的表达,从而诱导肿瘤细胞自噬 (autophagy) 并抑制体外和体内肾细胞癌生长。
    Metformin hydrochloride (Standard)
  • HY-N2303
    Eriocalyxin B Inhibitor 99.93%
    Eriocalyxin B 是一种可以从中草药毛萼香茶菜中分离得到的二萜类化合物。Eriocalyxin B 具有抗癌、抗炎和抑制脂肪生成等多种活性。Eriocalyxin B 能够诱导肿瘤细胞凋亡 (apoptosis) 和自噬 (autophagy)。Eriocalyxin B 可用于癌症和自身免疫性疾病等的研究。
    Eriocalyxin B
  • HY-143510
    RMC-4627 99.20%
    RMC-4627是一种选择性的 mTORC1 抑制剂,可激活4EBP1并抑制肿瘤生长。
    RMC-4627
  • HY-11080A
    PKI-179 hydrochloride Inhibitor 99.66%
    PKI-179 hydrochloride 是一种有效的和具有口服活性的双重 PI3K/mTOR 抑制剂,对 PI3K-αPI3K-βPI3K-γPI3K-δmTORIC50 值分别为 8 nM,24 nM,74 nM,77 nM 和 0.42 nM。PKI-179 hydrochloride 还表现出对 E545KH1047R 的活性,IC50 值分别为 14 nM 和 11 nM。PKI-179 hydrochloride 在体内显示出抗肿瘤活性。
    PKI-179 hydrochloride
  • HY-N9942
    Physalin A Inhibitor 99.22%
    Physalin A 是一种具有生物活性的醉茄内酯。Physalin A 在椎间盘退变模型中表现出抗炎、抗纤维化和改善自噬 (autophagy) 的作用。Physalin A 具有抗肿瘤活性,可诱导细胞凋亡 (apoptosis),ROS 产生和 G2/M 期细胞周期阻滞。此外。Physalin A 可显著提高醌还原酶活性,来提高解毒酶的表达。
    Physalin A
  • HY-N6996R
    Methyl Eugenol (Standard)

    甲基丁香酚 (Standard)

    Inhibitor
    Methyl Eugenol (Standard) 是 Methyl Eugenol 的分析标准品。本产品用于研究及分析应用。Methyl Eugenol 是一种具有口服活性的东方果类小实蝇 (Hendel) 的诱捕剂。Methyl Eugenol 具有抗癌和抗炎活性。Methyl Eugenol 能诱导细胞自噬。Methyl Eugenol 可以用于肠缺血/再灌注损伤的研究。
    Methyl Eugenol (Standard)
  • HY-N2911
    Auriculasin Inhibitor 98.58%
    Auriculasin 是一种抗癌剂,可靶向 VEGFR2PI3K/AKT/mTORMAPK 等信号通路。Auriculasin 可抑制细胞增殖、诱导细胞凋亡 (apoptosis)、抑制血管生成;并能够促进线粒体氧化应激和铁死亡 (ferroptosis)。Auriculasin 还对大麻素受体 CB1 具有活性,IC50 为 8.92 μM。Auriculasin 可用于癌症研究,尤其是前列腺癌、非小细胞肺癌等相关疾病,以及抗血管生成药物开发的研究。
    Auriculasin
目录号 产品名 / 同用名 应用 反应物种

The mammalian target of rapamycin (mTOR) signaling pathway integrates both intracellular and extracellular signals and serves as a central regulator of cell metabolism, growth, proliferation and survival[1]. mTOR is the catalytic subunit of two distinct complexes called mTORC1 and mTORC2. mTORC1 comprises DEPTOR, PRAS40, RAPTOR, mLST8, mTOR, whereas mTORC2 comprises DEPTOR, mLST8, PROTOR, RICTOR, mSIN1, mTOR[2]. Rapamycin binds to FKBP12 and inhibits mTORC1 by disrupting the interaction between mTOR and RAPTOR. mTORC1 negatively regulates autophagy through multiple inputs, including inhibitory phosphorylation of ULK1 and TFEB. mTORC1 promotes protein synthesis through activation of the translation initiation promoter S6K and through inhibition of the inhibitory mRNA cap binding 4E-BP1, and regulates glycolysis through HIF-1α. It promotes de novo lipid synthesis through the SREBP transcription factors. mTORC2 inhibits FOXO1,3 through SGK and Akt, which can lead to increased longevity. The complex also regulates actin cytoskeleton assembly through PKC and Rho kinase[3]

 

Growth factors: Growth factors can signal to mTORC1 through both PI3K-Akt and Ras-Raf-MEK-ERK axis. For example, ERK and RSK phosphorylate TSC2, and inhibit it.

 

Insulin Receptor: The activated insulin receptor recruits intracellular adaptor protein IRS1. Phosphorylation of these proteins on tyrosine residues by the insulin receptor initiates the recruitment and activation of PI3K. PIP3 acts as a second messenger which promotes the phosphorylation of Akt and triggers the Akt-dependent multisite phosphorylation of TSC2. TSC is a heterotrimeric complex comprised of TSC1, TSC2, and TBC1D7, and functions as a GTPase activating protein (GAP) for the small GTPase Rheb, which directly binds and activates mTORC1. mTORC2 primarily functions as an effector of insulin/PI3K signaling. 

 

Wnt: The Wnt pathway activates mTORC1. Glycogen synthase kinase 3β (GSK-3β) acts as a negative regulator of mTORC1 by phosphorylating TSC2. mTORC2 is activated by Wnt in a manner dependent on the small GTPase RAC1[4].

 

Amino acids: mTORC1 senses both lysosomal and cytosolic amino acids through distinct mechanisms. Amino acids induce the movement of mTORC1 to lysosomal membranes, where the Rag proteins reside. A complex named Ragulator, interact with the Rag GTPases, recruits them to lysosomes through a mechanism dependent on the lysosomal v-ATPase, and is essential for mTORC1 activation. In turn, lysosomal recruitment enables mTORC1 to interact with GTP-bound RHEB, the end point of growth factor. Cytosolic leucine and arginine signal to mTORC1 through a distinct pathway comprised of the GATOR1 and GATOR2 complexes.    

 

Stresses: mTORC1 responds to intracellular and environmental stresses that are incompatible with growth such as low ATP levels, hypoxia, or DNA damage. A reduction in cellular energy charge, for example during glucose deprivation, activates the stress responsive metabolic regulator AMPK, which inhibits mTORC1 both indirectly, through phosphorylation and activation of TSC2, as well as directly through the phosphorylation of RAPTOR. Sestrin1/2 are two transcriptional targets of p53 that are implicated in the DNA damage response, and they potently activate AMPK, thus mediating the p53-dependent suppression of mTOR activity upon DNA damage. During hypoxia, mitochondrial respiration is impaired, leading to low ATP levels and activation of AMPK. Hypoxia also affects mTORC1 in AMPK-independent ways by inducing the expression of REDD1, the protein products of which then suppress mTORC1 by promoting the assembly of TSC1-TSC2[2].

 

Reference:

[1]. Laplante M, et al.mTOR signaling at a glance.J Cell Sci. 2009 Oct 15;122(Pt 20):3589-94. 
[2]. Zoncu R, et al. mTOR: from growth signal integration to cancer, diabetes and ageing.Nat Rev Mol Cell Biol. 2011 Jan;12(1):21-35. 
[3]. Johnson SC, et al. mTOR is a key modulator of ageing and age-related disease.Nature. 2013 Jan 17;493(7432):338-45.
[4]. Shimobayashi M, et al. Making new contacts: the mTOR network in metabolism and signalling crosstalk.Nat Rev Mol Cell Biol. 2014 Mar;15(3):155-62.

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