JNK
シグナル伝達経路
研究分野
阻害剤の選択性比較
| カタログ番号 | 製品カタログ | 溶解度(25°C) | ||
|---|---|---|---|---|
| 水 | DMSO | アルコール | ||
| S1460 | SP600125 | <1 mg/mL | 44 mg/mL | <1 mg/mL |
| S4901 | JNK-IN-8 | <1 mg/mL | 100 mg/mL | <1 mg/mL |
| S7508 | JNK Inhibitor IX | <1 mg/mL | 20 mg/mL | <1 mg/mL |
| S8490 | Tanzisertib(CC-930) | 4 mg/mL | 89 mg/mL | 89 mg/mL |
| S8201 | BI-78D3 | <1 mg/mL | 100 mg/mL | <1 mg/mL |
| S7409 | Anisomycin | <1 mg/mL | 41 mg/mL | 17 mg/mL |
| S7637 | DTP3 | 100 mg/mL | 100 mg/mL | 100 mg/mL |
JNK製品
| 製品コード | 製品説明 | 文献中Selleckの製品使用例 | お客様のフィードバック |
|---|---|---|---|
| S1460 |
SP600125SP600125 is a broad-spectrum JNK inhibitor for JNK1, JNK2 and JNK3 with IC50 of 40 nM, 40 nM and 90 nM in cell-free assays, respectively; 10-fold greater selectivity against MKK4, 25-fold greater selectivity against MKK3, MKK6, PKB, and PKCα, and 100-fold selectivity against ERK2, p38, Chk1, EGFR etc. |
Loss of DUSP4 function upregulates IL-6 and IL-8 and enhances mammosphere growth. Immunoblot analysis of MDA-231 cells after treatment of 24 hours with 1 umol/L selumetinib (MEKi) or 10 umol/L SP600125 (JNKi). I, MDA-231 mammosphere formation quantitated by GelCount software 7 days after siRNA transfection. Where indicated, selumetinib (MEKi) or SP600125 (JNK1) or the combination was added to the mammosphere cultures.
|
|
| S4901 |
JNK-IN-8JNK-IN-8 is the first irreversible JNK inhibitor for JNK1, JNK2 and JNK3 with IC50 of 4.7 nM, 18.7 nM and 1 nM, >10-fold selectivity against MNK2, Fms and no inhibition to c-Kit, Met, PDGFRβin A375 cell line. |
SCC-9 cells were pre-treated with JNK inhibitor SP 600125 (1 umol/L) or JNK-IN-8 (1 umol/L) for 1 h, cells were also stimulated with indicated AZD8055 and cultured for 72 h, cell survival was analyzed. Scramble RNAi or JNK1/2 RNAi (JNK RNAi-1 or JNK RNAi-2, see methods) transfected HEK-293 cells were stimulated with AZD8055, cells were further cultured for 72 h before cell survival was tested. |
|
| S7508 |
JNK Inhibitor IXJNK inhibitor IX is a selective and potent JNK inhibitor with pIC50 of 6.5 and 6.7 for JNK2 and JNK3, respectively. |
ICT induces JNK activation, mediating mPTP opening and CRC cell necrosis. JNK expression (p- and regular) in HT-29 or the primary CRC cells stimulated with applied ICT was tested by Western blots (a).
HT-29 cells were pre-treated with JNK inhibitors SP600125 (SP), JNK inhibitor IX (JNK-IX), and JNK-IN-8 (JNKi-8) (5 μM each) for 1 h, followed by ICT (25 μM) stimulation, MMP decrease was tested by
JC-10 dye assay (b, after 12 h), and cell necrosis was tested by LDH release assay (c, after 72 h).
|
|
| S8490 |
Tanzisertib(CC-930)CC-930 is kinetically competitive with ATP in the JNK-dependent phosphorylation of the protein substrate c-Jun and potent against all isoforms of JNK (Ki(JNK1) = 44 ± 3 nM, IC50(JNK1) = 61 nM, Ki(JNK2) = 6.2 ± 0.6 nM, IC50(JNK2) = 5 nM, IC50(JNK3) = 5 nM) and selective against MAP kinases ERK1 and p38a with IC50 of 0.48 and 3.4 μM respectively. |
||
| S8201 |
BI-78D3BI-78D3 is a competitive JNK inhibitor with IC50 of 280nM that displays > 100 fold selectivity over p38α and no activity at mTOR and PI-3K. |
||
| S7409 |
AnisomycinAnisomycin is an antibiotic, which inhibits protein synthesis, and also act as a JNK activator. |
Effect of TMZ (100 μmol/l for U87 cells, 50 μmol/l for U251 cells), anisomycin (4 μmol/l), SB203580 (10 μmol/l), TMZ+SB203580 (10 μmol/l) treatment on thephosphorylation of p38 and AQP4 for 24 h in U87 cells and U251 cells, detected by Western blotting. (A) Protein expression of p-p38, p38 and AQP4 in U87 cells with differenttreatments. (B) The ration of p-p38/p38 in U87 cells. (C) The proportion of AQP4 in GAPDH in U87 cells. (D) Protein expression of p-p38, p38 and AQP4 in U251 cells withdifferent treatments. (E) The ration of p-p38/p38 in U251 cells. (F) The proportion of AQP4 in GAPDH in U251 cells. *P< 0.05 versus the control group |
|
| S7637 |
DTP3DTP3 is a selective GADD45β/MKK7 inhibitor, which inhibits cancer-selective NF-κB survival pathway. |
| 製品コード | 製品説明 | 文献中Selleckの製品使用例 | お客様のフィードバック |
|---|---|---|---|
| S1460 |
SP600125SP600125 is a broad-spectrum JNK inhibitor for JNK1, JNK2 and JNK3 with IC50 of 40 nM, 40 nM and 90 nM in cell-free assays, respectively; 10-fold greater selectivity against MKK4, 25-fold greater selectivity against MKK3, MKK6, PKB, and PKCα, and 100-fold selectivity against ERK2, p38, Chk1, EGFR etc. |
Loss of DUSP4 function upregulates IL-6 and IL-8 and enhances mammosphere growth. Immunoblot analysis of MDA-231 cells after treatment of 24 hours with 1 umol/L selumetinib (MEKi) or 10 umol/L SP600125 (JNKi). I, MDA-231 mammosphere formation quantitated by GelCount software 7 days after siRNA transfection. Where indicated, selumetinib (MEKi) or SP600125 (JNK1) or the combination was added to the mammosphere cultures.
|
|
| S4901 |
JNK-IN-8JNK-IN-8 is the first irreversible JNK inhibitor for JNK1, JNK2 and JNK3 with IC50 of 4.7 nM, 18.7 nM and 1 nM, >10-fold selectivity against MNK2, Fms and no inhibition to c-Kit, Met, PDGFRβin A375 cell line. |
SCC-9 cells were pre-treated with JNK inhibitor SP 600125 (1 umol/L) or JNK-IN-8 (1 umol/L) for 1 h, cells were also stimulated with indicated AZD8055 and cultured for 72 h, cell survival was analyzed. Scramble RNAi or JNK1/2 RNAi (JNK RNAi-1 or JNK RNAi-2, see methods) transfected HEK-293 cells were stimulated with AZD8055, cells were further cultured for 72 h before cell survival was tested. |
|
| S7508 |
JNK Inhibitor IXJNK inhibitor IX is a selective and potent JNK inhibitor with pIC50 of 6.5 and 6.7 for JNK2 and JNK3, respectively. |
ICT induces JNK activation, mediating mPTP opening and CRC cell necrosis. JNK expression (p- and regular) in HT-29 or the primary CRC cells stimulated with applied ICT was tested by Western blots (a).
HT-29 cells were pre-treated with JNK inhibitors SP600125 (SP), JNK inhibitor IX (JNK-IX), and JNK-IN-8 (JNKi-8) (5 μM each) for 1 h, followed by ICT (25 μM) stimulation, MMP decrease was tested by
JC-10 dye assay (b, after 12 h), and cell necrosis was tested by LDH release assay (c, after 72 h).
|
|
| S8490 |
Tanzisertib(CC-930)CC-930 is kinetically competitive with ATP in the JNK-dependent phosphorylation of the protein substrate c-Jun and potent against all isoforms of JNK (Ki(JNK1) = 44 ± 3 nM, IC50(JNK1) = 61 nM, Ki(JNK2) = 6.2 ± 0.6 nM, IC50(JNK2) = 5 nM, IC50(JNK3) = 5 nM) and selective against MAP kinases ERK1 and p38a with IC50 of 0.48 and 3.4 μM respectively. |
||
| S8201 |
BI-78D3BI-78D3 is a competitive JNK inhibitor with IC50 of 280nM that displays > 100 fold selectivity over p38α and no activity at mTOR and PI-3K. |
| 製品コード | 製品説明 | 文献中Selleckの製品使用例 | お客様のフィードバック |
|---|---|---|---|
| S7409 |
AnisomycinAnisomycin is an antibiotic, which inhibits protein synthesis, and also act as a JNK activator. |
2019, 69(3):489-502 2019, 18(4):379-394 2019, 44(1):89-102 |
Effect of TMZ (100 μmol/l for U87 cells, 50 μmol/l for U251 cells), anisomycin (4 μmol/l), SB203580 (10 μmol/l), TMZ+SB203580 (10 μmol/l) treatment on thephosphorylation of p38 and AQP4 for 24 h in U87 cells and U251 cells, detected by Western blotting. (A) Protein expression of p-p38, p38 and AQP4 in U87 cells with differenttreatments. (B) The ration of p-p38/p38 in U87 cells. (C) The proportion of AQP4 in GAPDH in U87 cells. (D) Protein expression of p-p38, p38 and AQP4 in U251 cells withdifferent treatments. (E) The ration of p-p38/p38 in U251 cells. (F) The proportion of AQP4 in GAPDH in U251 cells. *P< 0.05 versus the control group |
| S7637 |
DTP3DTP3 is a selective GADD45β/MKK7 inhibitor, which inhibits cancer-selective NF-κB survival pathway. |
