S6 Kinase

信号通路图

研究领域

抑制剂选择性比较

特异性亚型抑制剂

S6 Kinase产品

所有产品 S6 Kinase抑制剂(10)

产品目录	产品描述	文献引用	实验数据
S2843	BI-D1870 BI-D1870是一种ATP-竞争性S6 ribosome抑制剂，在无细胞试验中作用于RSK1/2/3/K4，IC50分别为31 nM/24 nM/18 nM/15 nM，作用于RSK比作用于MST2，GSK-3β，MARK3，CK1和Aurora B选择性高10到100倍。	Nat Cell Biol, 2019, 21(6):778-790 Cell Rep, 2019, 26(12):3391-3399 Antiviral Res, 2019, 170:104572	Expressions of active forms of all p90RSK isoforms were assessed by immunoblotting in Control vs. GR cells following treatment with increasing concentrations of BI-D1870 for 24 hours. Actin was included as a loading control.
S1558	AT7867 AT7867是一种有效的，ATP竞争性的Akt1/2/3和p70S6K/PKA抑制剂，无细胞试验中IC50分别为32 nM/17 n/47 nM和85 nM/20 nM，对AGC激酶家族以外几乎没有抑制活性。	FEBS Lett, 2019, 593(2):175-186 PLoS One, 2019, 14(6):e0218537 Oncogenesis, 2018, 7(2):23	UMUC-6 cells were treated with the indicated concentrations of AT7867 for 72 hours. Relative cytotoxicity compared to untreated control cells was assessed by alamarBlue. Each data points represents the mean of three independent experiments and the error bars represent the standard error of the mean.
S2163	PF-4708671 PF-4708671是一种细胞渗透性p70 ribosomal S6 kinase(S6K1亚型)抑制剂，在无细胞试验中K_i/IC50为20 nM/160 nM，作用于S6K1比作用于S6K2选择性高400倍，作用于S6K1比作用于MSK1和RSK1/2选择性分别高4和20倍以上，是第一个报道的S6K1特异性抑制剂。	Nat Cell Biol, 2019, 21(6):778-790 Oncogene, 2019, 38(35):6270-6282 Platelets, 2019, 30(2):241-250	After treated with PF-4708671 (PF, 10 uM) and 4EGI-1 (50 uM) for 48 h, GRP78 and ATF4 in QBC939, RBE and HCCC-9810 cells were analyzed using western blot.
S1582	H 89 2HCl H 89 2HCl是一种有效的PKA抑制剂，无细胞试验中K_i为48 nM，作用于PKA比作用于PKG选择性高10倍，比作用于PKC，MLCK，钙调蛋白激酶II和酪蛋白激I/II选择性高500倍。	Nat Cell Biol, 2019, 21(6):778-790 Proc Natl Acad Sci U S A, 2019, 116(27):13374-13383 J Clin Endocrinol Metab, 2019, 104(5):1697-1711	The effects of H89 on bTSH-induced FASN downregulation in 3T3-L1 adipocytes. Differentiated 3T3-L1 adipocytes were pretreated with either 20 µmol/L H89 or vehicle for 1 h, then treated with 0.2 µM bTSH for 8 h. Levels of FASN, pCREB, pERK1/2 and pJNK were determined by Western blotting.
S7704	LY2584702 Tosylate LY2584702 Tosylate是一种选择性的，ATP竞争性p70S6K抑制剂，IC50为 4 nM。Phase 1。	Nat Cell Biol, 2019, 21(6):778-790 PLoS One, 2017, 12(1):e0169804 Cell Rep, 2017, 18(9):2088-2095	Samples were processed and analyzed for S6 and phospho-S6 content as described in methods.
S8518	AD80 AD80，一种多激酶抑制剂，对人源RET、BRAF、S6K和SRC活性较强，但对mTOR的活性比AD57或AD58弱。其对RET的IC50值为4 nM。
S7871	LJI308 LJI308是一种有效的，泛-RSK (p90核糖体S6激酶)抑制剂，对RSK1，RSK2，和 RSK3的 IC50 分别为 6 nM，4 nM 和 13 nM。	Cancer Discov, 2019, 9(2):264-281 Int J Mol Sci, 2018, 19(8)
S7870	LJH685 LJH685是一种高效的RSK抑制剂，其对RSK1, RSK2和RSK3的IC50分别为6 nM, 5 nM和4 nM。	Oncotarget, 2017, 8(22):35761-35775	In (E), single (left panel) and double resistant (right panel) SKMel28 cells were treated with vemurafenib, the RSK inhibitor LJH-685 or the combination.
S7563	AT13148 AT13148是一种口服的，ATP竞争性的，多AGC kinase抑制剂，对Akt1/2/3，p70S6K，PKA，和ROCKI/II的IC50分别为38 nM/402 nM/50 nM，8 nM，3 nM，和6 nM/4 nM。Phase 1。	Nat Cell Biol, 2019, 21(6):778-790 Cancer Sci, 2016, 107(11):1563-1571 Biochem Biophys Res Commun, 2016, 478(1):330-6	AT13148 exerts cytotoxic and anti-proliferative activity against human gastric cancer cells. Human gastric cancer cells (HGC-27, AGS, SNU-601, N87 and MKN-28 lines) or GEC-1 gastric epithelial cells were treated with applied concentration of AT13148 for indicated time, cell survival (A and E), cell proliferation (B and F), cell cycle distribution (C, for HGC-27 cells) and cell death (D, for HGC-27 cells) were tested by the described assays, separately. Data were presented as mean ± SD. “Ctrl” stands for untreated control cells (For all figures). “hr/hrs” stands for hour/hours (For all figures). Experiments in this figure were repeated for five times. *p < 0.05 vs. “Ctrl” group.
S7698	LY2584702 LY2584702是一种选择性的，ATP竞争性的p70S6K抑制剂，IC50为4 nM。Phase 1。	Cell Rep, 2019, 26(12):3391-3399 J Immunol, 2019, 203(1):137-147 Antiviral Res, 2018, 158:13-24	Murine DCs were pretreated with PBS or kinase inhibitors (10 μmol/l) wortmanni LY2584702 2 h prior to nicotine (10−7 mol/l) 12~15 h stimulation. MR expression was determined via western blot analyses (C, F). β-actin was used as an internal control.

产品目录	产品描述	文献引用	实验数据
S2843	BI-D1870 BI-D1870是一种ATP-竞争性S6 ribosome抑制剂，在无细胞试验中作用于RSK1/2/3/K4，IC50分别为31 nM/24 nM/18 nM/15 nM，作用于RSK比作用于MST2，GSK-3β，MARK3，CK1和Aurora B选择性高10到100倍。	Nat Cell Biol,2019, 21(6):778-790 Cell Rep,2019, 26(12):3391-3399 Antiviral Res,2019, 170:104572	Expressions of active forms of all p90RSK isoforms were assessed by immunoblotting in Control vs. GR cells following treatment with increasing concentrations of BI-D1870 for 24 hours. Actin was included as a loading control.
S1558	AT7867 AT7867是一种有效的，ATP竞争性的Akt1/2/3和p70S6K/PKA抑制剂，无细胞试验中IC50分别为32 nM/17 n/47 nM和85 nM/20 nM，对AGC激酶家族以外几乎没有抑制活性。	FEBS Lett,2019, 593(2):175-186 PLoS One,2019, 14(6):e0218537 Oncogenesis,2018, 7(2):23	UMUC-6 cells were treated with the indicated concentrations of AT7867 for 72 hours. Relative cytotoxicity compared to untreated control cells was assessed by alamarBlue. Each data points represents the mean of three independent experiments and the error bars represent the standard error of the mean.
S2163	PF-4708671 PF-4708671是一种细胞渗透性p70 ribosomal S6 kinase(S6K1亚型)抑制剂，在无细胞试验中K_i/IC50为20 nM/160 nM，作用于S6K1比作用于S6K2选择性高400倍，作用于S6K1比作用于MSK1和RSK1/2选择性分别高4和20倍以上，是第一个报道的S6K1特异性抑制剂。	Nat Cell Biol,2019, 21(6):778-790 Oncogene,2019, 38(35):6270-6282 Platelets,2019, 30(2):241-250	After treated with PF-4708671 (PF, 10 uM) and 4EGI-1 (50 uM) for 48 h, GRP78 and ATF4 in QBC939, RBE and HCCC-9810 cells were analyzed using western blot.
S1582	H 89 2HCl H 89 2HCl是一种有效的PKA抑制剂，无细胞试验中K_i为48 nM，作用于PKA比作用于PKG选择性高10倍，比作用于PKC，MLCK，钙调蛋白激酶II和酪蛋白激I/II选择性高500倍。	Nat Cell Biol,2019, 21(6):778-790 Proc Natl Acad Sci U S A,2019, 116(27):13374-13383 J Clin Endocrinol Metab,2019, 104(5):1697-1711	The effects of H89 on bTSH-induced FASN downregulation in 3T3-L1 adipocytes. Differentiated 3T3-L1 adipocytes were pretreated with either 20 µmol/L H89 or vehicle for 1 h, then treated with 0.2 µM bTSH for 8 h. Levels of FASN, pCREB, pERK1/2 and pJNK were determined by Western blotting.
S7704	LY2584702 Tosylate LY2584702 Tosylate是一种选择性的，ATP竞争性p70S6K抑制剂，IC50为 4 nM。Phase 1。	Nat Cell Biol,2019, 21(6):778-790 PLoS One,2017, 12(1):e0169804 Cell Rep,2017, 18(9):2088-2095	Samples were processed and analyzed for S6 and phospho-S6 content as described in methods.
S8518	AD80 AD80，一种多激酶抑制剂，对人源RET、BRAF、S6K和SRC活性较强，但对mTOR的活性比AD57或AD58弱。其对RET的IC50值为4 nM。
S7871	LJI308 LJI308是一种有效的，泛-RSK (p90核糖体S6激酶)抑制剂，对RSK1，RSK2，和 RSK3的 IC50 分别为 6 nM，4 nM 和 13 nM。	Cancer Discov,2019, 9(2):264-281 Int J Mol Sci,2018, 19(8)
S7870	LJH685 LJH685是一种高效的RSK抑制剂，其对RSK1, RSK2和RSK3的IC50分别为6 nM, 5 nM和4 nM。	Oncotarget,2017, 8(22):35761-35775	In (E), single (left panel) and double resistant (right panel) SKMel28 cells were treated with vemurafenib, the RSK inhibitor LJH-685 or the combination.
S7563	AT13148 AT13148是一种口服的，ATP竞争性的，多AGC kinase抑制剂，对Akt1/2/3，p70S6K，PKA，和ROCKI/II的IC50分别为38 nM/402 nM/50 nM，8 nM，3 nM，和6 nM/4 nM。Phase 1。	Nat Cell Biol,2019, 21(6):778-790 Cancer Sci,2016, 107(11):1563-1571 Biochem Biophys Res Commun,2016, 478(1):330-6	AT13148 exerts cytotoxic and anti-proliferative activity against human gastric cancer cells. Human gastric cancer cells (HGC-27, AGS, SNU-601, N87 and MKN-28 lines) or GEC-1 gastric epithelial cells were treated with applied concentration of AT13148 for indicated time, cell survival (A and E), cell proliferation (B and F), cell cycle distribution (C, for HGC-27 cells) and cell death (D, for HGC-27 cells) were tested by the described assays, separately. Data were presented as mean ± SD. “Ctrl” stands for untreated control cells (For all figures). “hr/hrs” stands for hour/hours (For all figures). Experiments in this figure were repeated for five times. *p < 0.05 vs. “Ctrl” group.
S7698	LY2584702 LY2584702是一种选择性的，ATP竞争性的p70S6K抑制剂，IC50为4 nM。Phase 1。	Cell Rep,2019, 26(12):3391-3399 J Immunol,2019, 203(1):137-147 Antiviral Res,2018, 158:13-24	Murine DCs were pretreated with PBS or kinase inhibitors (10 μmol/l) wortmanni LY2584702 2 h prior to nicotine (10−7 mol/l) 12~15 h stimulation. MR expression was determined via western blot analyses (C, F). β-actin was used as an internal control.