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-155747
    FDW028 Inhibitor 99.51%
    FDW028 是一种强效、高选择性的 FUT8 抑制剂。FUT8 通过伴侣介导的自噬 (CMA) 途径去聚焦化和促进 B7-H3 的溶酶体降解,显示出强大的抗肿瘤活性。FUT8 可用于转移性结直肠癌 (mCRC) 的研究。
    FDW028
  • HY-13246
    Apitolisib Inhibitor 99.29%
    Apitolisib (GDC-0980; GNE 390; RG 7422) 是一种口服有效的 PI3KmTOR (TORC1/2) 激酶抑制剂,抑制 PI3Kα/PI3Kβ/PI3Kδ/PI3Kγ 的活性,IC50 值为 5 nM/27 nM/7 nM/14 nM。 抑制mTORKi?为 17 nM。
    Apitolisib
  • HY-16962
    CC-115 Inhibitor 99.82%
    CC-115 是一种有效的双重 DNA-PKmTOR 抑制剂,IC50 分别为 13 nM 和 21 nM。CC-115 阻断 mTORC1mTORC2 信号通路。
    CC-115
  • HY-15174
    Dactolisib Tosylate Inhibitor 99.87%
    Dactolisib Tosylate (BEZ235 Tosylate) 是PI3KmTOR的双重激酶抑制剂,对PI3Kα, β, γ, δ 的IC50值分别为4, 75, 7, 5 nM。Dactolisib Tosylate (BEZ235 Tosylate) 抑制 mTORC1mTORC2
    Dactolisib Tosylate
  • HY-15900
    Voxtalisib Inhibitor 99.18%
    Voxtalisib (XL765) 是一种有效的 PI3K 抑制剂,抑制p110αp110βp110γp110δIC50 分别为 39, 113, 9 和 43 nM,也抑制 DNA-PK (IC50=150 nM) 和 mTOR (IC50=157 nM)。Voxtalisib (XL765) 抑制 mTORC1mTORC2IC50s 分别为 160 和 910 nM。
    Voxtalisib
  • HY-134904
    RMC-6272 Inhibitor
    RMC-6272 (RM-006) 是一种双空间的,选择性的 mTORC1 抑制剂,对 mTORC1 的抑制作用比 mTORC2 强且选择性 >10 倍。与雷帕霉素相比,RMC-6272 对 mTORC1 的抑制作用增强,并在 TSC2 阴性肿瘤中诱导更多的细胞死亡。
    RMC-6272
  • HY-13334A
    BGT226 Inhibitor 99.51%
    BGT226 (NVP-BGT226) 是一种 PI3K (针对 PI3KαPI3KβPI3KγIC50分别是4 nM,63 nM,38 nM ) /mTOR 双抑制剂,对人头颈癌细胞具有较强的生长抑制活性。
    BGT226
  • HY-12868
    Bimiralisib Inhibitor 99.80%
    Bimiralisib (PQR309) 是一种有效的,可渗透脑的,PI3K/mTOR 抑制剂,抑制 PI3Kα, PI3Kδ, PI3Kβ, PI3KγmTORIC50 分别为 33 nM,451 nM,661 nM,708 nM 和 89 nM。Bimiralisib 是 mTORC1mTORC2 抑制剂。
    Bimiralisib
  • HY-B0766
    Bicyclol

    双环醇

    99.91%
    Bicyclol (SY801) 是一种具有口服活性的传统中药五味子的衍生物,具有多种生物活性,包括抗病毒、抗炎、免疫调节、抗氧化、抗脂肪变性、抗纤维化和抗肿瘤作用。Bicyclol 通过调节热休克蛋白的表达,发挥抗肝细胞凋亡 (apoptosis) 的作用,并抑制 ROS-MAPK-NF-κB 通路的激活,降低丙型肝炎病毒感染肝细胞中 NF-κB 的活化和炎症因子水平,从而预防急性肝损伤中的铁死亡 (Ferroptosis)。此外,Bicyclol 能够改变 Mdr-1、GSH/GSTBcl-2 的表达,提高细胞内抗癌药物浓度,使耐药细胞对抗癌药物增敏,同时调控 PI3K/AKTRas/Raf/MEK/ERK 通路,以抑制人恶性肝癌细胞的增殖。Bicyclol 适用于慢性肝炎、急性肝损伤、非酒精性脂肪性肝病、肝纤维化和肝细胞癌的研究。
    Bicyclol
  • HY-16956
    Onatasertib Inhibitor 99.13%
    Onatasertib (CC-223) 是一种口服有效的 mTOR 激酶抑制剂,抑制 mTOR 激酶,IC50 为 16 nM。Onatasertib 抑制 mTORC1mTORC2
    Onatasertib
  • HY-50908
    Ridaforolimus Inhibitor 99.75%
    Ridaforolimus (MK-8669) 是一种有效和选择性的 mTOR 抑制剂,在 HT-1080 细胞中抑制 S6 磷酸化的 IC50 值为 0.2 nM。
    Ridaforolimus
  • HY-12036
    GSK1059615 Inhibitor ≥99.0%
    GSK1059615 是 PI3Kα/β/δ/γ 可逆的抑制剂,同时也抑制 mTORIC50 值分别为 0.4 nM/0.6 nM/2 nM/5 nM 和 12 nM。
    GSK1059615
  • HY-N0486S1
    L-Leucine-13C

    L-亮氨酸 13C

    Activator 99.4%
    L-Leucine-13C 是一种 13C 标记的 L-Leucine。L-Leucine 是一种必需的支链氨基酸 (BCAA),可激活 mTOR 信号通路。
    L-Leucine-<sup>13</sup>C
  • HY-10044
    WYE-132 Inhibitor 99.90%
    WYE-132 (WYE-125132) 是一种高度有效的 ATP 竞争性和特异性 mTOR 激酶抑制剂 (IC50 为 0.19±0.07 nM)。WYE-132 (WYE-125132) 抑制 mTORC1mTORC2
    WYE-132
  • HY-13431
    KU-0060648 Inhibitor 99.62%
    KU-0060648 是 PI3KDNA-PK 的双重抑制剂,抑制 PI3Kα, PI3Kβ, PI3Kγ, PI3KδDNA-PKIC50 值分别为 4 nM,0.5 nM,0.1 nM,0.594 nM 和 8.6 nM 。
    KU-0060648
  • HY-115449
    Chromeceptin p53 Inhibitor 99.80%
    Chromeceptin (94G6) 是一种IGF 信号通路 抑制剂。Chromeceptin 抑制肝细胞和 HCC 细胞中 IGF2 的 mRNA 和蛋白质水平。Chromeceptin 抑制 AKTmTOR 的磷酸化水平。
    Chromeceptin
  • HY-N6626
    Pyraclostrobin

    吡唑醚菌酯

    99.91%
    Pyraclostrobin 是一种高效广谱的杀菌剂,Pyraclostrobin 可通过激活 AMPK/mTOR 信号通路诱导 DNA 氧化损伤、线粒体功能障碍和自噬 (autophagy)。Pyraclostrobin 可用于控制农作物病害。
    Pyraclostrobin
  • HY-N0486S9
    L-Leucine-d3

    L-亮氨酸-d3

    Activator 99.93%
    L-Leucine-d3 是 L-Leucine 的氘代物。L-Leucine 是一种必需的支链氨基酸 (BCAA),可激活 mTOR 信号通路。
    L-Leucine-d<sub>3</sub>
  • HY-10372
    PP121 Inhibitor 98.67%
    PP121是多靶点激酶抑制剂,抑制 mTORDNK-PKVEGFR2/KDR/Flk-1SrcPDGFRIC50 值分别为10,60,12,14,2 nM。
    PP121
  • HY-10683
    PKI-402 Inhibitor 98.43%
    PKI-402 是一种有效的 PI3KmTOR 抑制剂,抑制 PI3Kα, mTOR, PI3Kβ, PI3KδPI3KγIC50 分别为 2, 3, 7, 14 和 16 nM。
    PKI-402
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.

Your Search Returned No Results.

Sorry. There is currently no product that acts on isoform together.

Please try each isoform separately.