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mk2 inhibitor iii  (MedChemExpress)
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MedChemExpress mk2 inhibitor iii
<t>MK2</t> catalyzes RSK1 phosphorylation at Ser-380. A , HeLa cells were treated with 10 μM MK2 inhibitor <t>III</t> (MK2 inh III) for 30 min and then stimulated with 10 ng/ml EGF for 10 min or 50 μM anisomycin for 20 min. B , HeLa cells were transfected with siRNA against MK2 or the negative control. At 48 h post-transfection, cells were stimulated with 10 ng/ml EGF for 10 min or 50 μM anisomycin for 20 min. A and B , Whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, pRSK, phospho-MK2 (pMK2), and α-Tubulin. Red arrow , phosphorylated MK2; blue arrow , non-phosphorylated MK2. C , HEK293 cells were transfected with expression vectors for EGFP-tagged kinase-dead EphA2 (EphA2-KD-EGFP), FLAG-tagged RSK1, FLAG-tagged p38α, MK2 (wild-type (WT) or kinase-dead mutant (KD)), and/or an empty vector. At 24 h post-transfection, whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, pRSK, FLAG, MK2, and β-Actin. D , HeLa cells were treated with 10 μM MK2 inhibitor III and then stimulated with 100 μM CDDP for 3 h or 0.3 M NaCl (Osmo) for 10 min. Whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, pRSK, pMK2, and α-Tubulin. E , immunoprecipitated RSK1 and RSK2 prepared from HeLa cells were incubated with recombinant human active GST-MK2 at 30 °C for 30 min. Reaction mixtures were analyzed by immunoblotting with anti-phospho-RSK (Ser-380 of RSK1; Ser-386 of RSK2), RSK1, RSK2, and pMK2 antibodies. EphA2, ephrin type-A receptor 2; MK2, MAPK-activated protein kinase 2, RSK, p90 ribosomal S6 kinase.
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MK2 catalyzes RSK1 phosphorylation at Ser-380. A , HeLa cells were treated with 10 μM MK2 inhibitor III (MK2 inh III) for 30 min and then stimulated with 10 ng/ml EGF for 10 min or 50 μM anisomycin for 20 min. B , HeLa cells were transfected with siRNA against MK2 or the negative control. At 48 h post-transfection, cells were stimulated with 10 ng/ml EGF for 10 min or 50 μM anisomycin for 20 min. A and B , Whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, pRSK, phospho-MK2 (pMK2), and α-Tubulin. Red arrow , phosphorylated MK2; blue arrow , non-phosphorylated MK2. C , HEK293 cells were transfected with expression vectors for EGFP-tagged kinase-dead EphA2 (EphA2-KD-EGFP), FLAG-tagged RSK1, FLAG-tagged p38α, MK2 (wild-type (WT) or kinase-dead mutant (KD)), and/or an empty vector. At 24 h post-transfection, whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, pRSK, FLAG, MK2, and β-Actin. D , HeLa cells were treated with 10 μM MK2 inhibitor III and then stimulated with 100 μM CDDP for 3 h or 0.3 M NaCl (Osmo) for 10 min. Whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, pRSK, pMK2, and α-Tubulin. E , immunoprecipitated RSK1 and RSK2 prepared from HeLa cells were incubated with recombinant human active GST-MK2 at 30 °C for 30 min. Reaction mixtures were analyzed by immunoblotting with anti-phospho-RSK (Ser-380 of RSK1; Ser-386 of RSK2), RSK1, RSK2, and pMK2 antibodies. EphA2, ephrin type-A receptor 2; MK2, MAPK-activated protein kinase 2, RSK, p90 ribosomal S6 kinase.

Journal: The Journal of Biological Chemistry

Article Title: Cellular stress induces non-canonical activation of the receptor tyrosine kinase EphA2 through the p38-MK2-RSK signaling pathway

doi: 10.1016/j.jbc.2023.104699

Figure Lengend Snippet: MK2 catalyzes RSK1 phosphorylation at Ser-380. A , HeLa cells were treated with 10 μM MK2 inhibitor III (MK2 inh III) for 30 min and then stimulated with 10 ng/ml EGF for 10 min or 50 μM anisomycin for 20 min. B , HeLa cells were transfected with siRNA against MK2 or the negative control. At 48 h post-transfection, cells were stimulated with 10 ng/ml EGF for 10 min or 50 μM anisomycin for 20 min. A and B , Whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, pRSK, phospho-MK2 (pMK2), and α-Tubulin. Red arrow , phosphorylated MK2; blue arrow , non-phosphorylated MK2. C , HEK293 cells were transfected with expression vectors for EGFP-tagged kinase-dead EphA2 (EphA2-KD-EGFP), FLAG-tagged RSK1, FLAG-tagged p38α, MK2 (wild-type (WT) or kinase-dead mutant (KD)), and/or an empty vector. At 24 h post-transfection, whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, pRSK, FLAG, MK2, and β-Actin. D , HeLa cells were treated with 10 μM MK2 inhibitor III and then stimulated with 100 μM CDDP for 3 h or 0.3 M NaCl (Osmo) for 10 min. Whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, pRSK, pMK2, and α-Tubulin. E , immunoprecipitated RSK1 and RSK2 prepared from HeLa cells were incubated with recombinant human active GST-MK2 at 30 °C for 30 min. Reaction mixtures were analyzed by immunoblotting with anti-phospho-RSK (Ser-380 of RSK1; Ser-386 of RSK2), RSK1, RSK2, and pMK2 antibodies. EphA2, ephrin type-A receptor 2; MK2, MAPK-activated protein kinase 2, RSK, p90 ribosomal S6 kinase.

Article Snippet: Recombinant human EGF was obtained from R&D Systems; recombinant human active GST-MK2 protein was from Carna Biosciences; a phos-tag ligand, anisomycin, NaCl, and CDDP were from Wako Pure Chemical Industries; SB203580 and TMZ were from Merck KGaA; MK2 inhibitor III and GSK2334470 were from MedChemExpress; BI-D1870 was from BioVision; BIRB796, Skepinone-L, and BX-702 were from Selleck Chemicals.

Techniques: Transfection, Negative Control, Expressing, Mutagenesis, Plasmid Preparation, Immunoprecipitation, Incubation, Recombinant, Western Blot

MK2 induced the atypical activation of RSK. A and B , HeLa cells were stimulated with 10 ng/ml EGF for 10 min or 50 μM anisomycin for 20 min. C and D , HeLa cells were treated with 10 μM MK2 inhibitor III for 30 min and then stimulated with 10 ng/ml EGF for 10 min ( C ) or 50 μM anisomycin for 20 min ( D ). Whole-cell lysates were separated by Zn 2+ Phos-tag SDS-PAGE, followed by immunoblotting with an anti-phospho-RSK (Ser-380 and Thr-573), RSK1, or RSK2 antibody. The images of RSK1 in A ( dark ) and B ( right ) are from the same blot.

Journal: The Journal of Biological Chemistry

Article Title: Cellular stress induces non-canonical activation of the receptor tyrosine kinase EphA2 through the p38-MK2-RSK signaling pathway

doi: 10.1016/j.jbc.2023.104699

Figure Lengend Snippet: MK2 induced the atypical activation of RSK. A and B , HeLa cells were stimulated with 10 ng/ml EGF for 10 min or 50 μM anisomycin for 20 min. C and D , HeLa cells were treated with 10 μM MK2 inhibitor III for 30 min and then stimulated with 10 ng/ml EGF for 10 min ( C ) or 50 μM anisomycin for 20 min ( D ). Whole-cell lysates were separated by Zn 2+ Phos-tag SDS-PAGE, followed by immunoblotting with an anti-phospho-RSK (Ser-380 and Thr-573), RSK1, or RSK2 antibody. The images of RSK1 in A ( dark ) and B ( right ) are from the same blot.

Article Snippet: Recombinant human EGF was obtained from R&D Systems; recombinant human active GST-MK2 protein was from Carna Biosciences; a phos-tag ligand, anisomycin, NaCl, and CDDP were from Wako Pure Chemical Industries; SB203580 and TMZ were from Merck KGaA; MK2 inhibitor III and GSK2334470 were from MedChemExpress; BI-D1870 was from BioVision; BIRB796, Skepinone-L, and BX-702 were from Selleck Chemicals.

Techniques: Activation Assay, SDS Page, Western Blot

MK2-induced EphA2 phosphorylation is independent of the CTK activity of RSK. A and B , HEK293 cells were transfected with the expression vectors for FLAG-tagged RSK1 (wild-type (WT) or CTK-dead mutant (CTKm)), FLAG-tagged constitutively activated MEK1 (MEK1-CA-FLAG), MK2, FLAG-tagged constitutively activated p38α (p38α-CA-FLAG), and/or an empty vector. At 24 h post-transfection, whole-cell lysates were immunoblotted with primary antibodies against phospho-RSK at Ser-380 (pRSK), FLAG, pMK2, MK2, and β-Actin. C – E , HEK293 cells were transfected with the expression vectors for EphA2-KD-EGFP, RSK1-CTKm-FLAG (Ser-380 WT, Ala-substitute mutation (SA) or Ser-221 SA), MK2, p38α-CA-FLAG, and/or an empty vector. At 24 h post-transfection, whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, pRSK, FLAG, pMK2, and β-Actin. F , HeLa cells were treated with 10 μM GSK2334470 for 30 min and then stimulated with 10 ng/ml EGF for 10 min or 50 μM anisomycin for 20 min. Whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2 and α-Tubulin. G , a schematic diagram of RSK phosphorylation induced by MK2 or ERK. CTK, carboxyl-terminal kinase; EphA2, ephrin type-A receptor 2; MK2, MAPK-activated protein kinase 2; NTK, amino-terminal kinase, RSK, p90 ribosomal S6 kinase.

Journal: The Journal of Biological Chemistry

Article Title: Cellular stress induces non-canonical activation of the receptor tyrosine kinase EphA2 through the p38-MK2-RSK signaling pathway

doi: 10.1016/j.jbc.2023.104699

Figure Lengend Snippet: MK2-induced EphA2 phosphorylation is independent of the CTK activity of RSK. A and B , HEK293 cells were transfected with the expression vectors for FLAG-tagged RSK1 (wild-type (WT) or CTK-dead mutant (CTKm)), FLAG-tagged constitutively activated MEK1 (MEK1-CA-FLAG), MK2, FLAG-tagged constitutively activated p38α (p38α-CA-FLAG), and/or an empty vector. At 24 h post-transfection, whole-cell lysates were immunoblotted with primary antibodies against phospho-RSK at Ser-380 (pRSK), FLAG, pMK2, MK2, and β-Actin. C – E , HEK293 cells were transfected with the expression vectors for EphA2-KD-EGFP, RSK1-CTKm-FLAG (Ser-380 WT, Ala-substitute mutation (SA) or Ser-221 SA), MK2, p38α-CA-FLAG, and/or an empty vector. At 24 h post-transfection, whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, pRSK, FLAG, pMK2, and β-Actin. F , HeLa cells were treated with 10 μM GSK2334470 for 30 min and then stimulated with 10 ng/ml EGF for 10 min or 50 μM anisomycin for 20 min. Whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2 and α-Tubulin. G , a schematic diagram of RSK phosphorylation induced by MK2 or ERK. CTK, carboxyl-terminal kinase; EphA2, ephrin type-A receptor 2; MK2, MAPK-activated protein kinase 2; NTK, amino-terminal kinase, RSK, p90 ribosomal S6 kinase.

Article Snippet: Recombinant human EGF was obtained from R&D Systems; recombinant human active GST-MK2 protein was from Carna Biosciences; a phos-tag ligand, anisomycin, NaCl, and CDDP were from Wako Pure Chemical Industries; SB203580 and TMZ were from Merck KGaA; MK2 inhibitor III and GSK2334470 were from MedChemExpress; BI-D1870 was from BioVision; BIRB796, Skepinone-L, and BX-702 were from Selleck Chemicals.

Techniques: Activity Assay, Transfection, Expressing, Mutagenesis, Plasmid Preparation

The p38-MK2-RSK-EphA2 pathway regulates cell migration. HEK293 cells were transfected with the expression vectors for EphA2-KD-EGFP (Ser-897 WT or SA), RSK1-CTKm-FLAG, p38α-CA-FLAG, MK2, and/or an empty vector. At 24 h post-transfection, cells were treated with DMSO or 10 μM BI-D1870 for 2 h ( C and D ). Whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, FLAG, pMK2, and β-Actin ( A and C ). Cell migration was observed using a time-lapse imaging system for 120 min ( B and D ). The accumulated distance of cell migration (μm) was calculated and shown in box and whisker plots. ∗ p < 0.05 by the Tukey–Kramer HSD test. EphA2, ephrin type-A receptor 2; MK2, MAPK-activated protein kinase 2; RSK, p90 ribosomal S6 kinase.

Journal: The Journal of Biological Chemistry

Article Title: Cellular stress induces non-canonical activation of the receptor tyrosine kinase EphA2 through the p38-MK2-RSK signaling pathway

doi: 10.1016/j.jbc.2023.104699

Figure Lengend Snippet: The p38-MK2-RSK-EphA2 pathway regulates cell migration. HEK293 cells were transfected with the expression vectors for EphA2-KD-EGFP (Ser-897 WT or SA), RSK1-CTKm-FLAG, p38α-CA-FLAG, MK2, and/or an empty vector. At 24 h post-transfection, cells were treated with DMSO or 10 μM BI-D1870 for 2 h ( C and D ). Whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, FLAG, pMK2, and β-Actin ( A and C ). Cell migration was observed using a time-lapse imaging system for 120 min ( B and D ). The accumulated distance of cell migration (μm) was calculated and shown in box and whisker plots. ∗ p < 0.05 by the Tukey–Kramer HSD test. EphA2, ephrin type-A receptor 2; MK2, MAPK-activated protein kinase 2; RSK, p90 ribosomal S6 kinase.

Article Snippet: Recombinant human EGF was obtained from R&D Systems; recombinant human active GST-MK2 protein was from Carna Biosciences; a phos-tag ligand, anisomycin, NaCl, and CDDP were from Wako Pure Chemical Industries; SB203580 and TMZ were from Merck KGaA; MK2 inhibitor III and GSK2334470 were from MedChemExpress; BI-D1870 was from BioVision; BIRB796, Skepinone-L, and BX-702 were from Selleck Chemicals.

Techniques: Migration, Transfection, Expressing, Plasmid Preparation, Imaging, Whisker Assay

The p38-MK2-RSK-EphA2 pathway promotes U87-MG cell migration induced by TMZ. A , U87-MG cells were treated with DMSO or 100 μM temozolomide (TMZ) for 48 h. Whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, pRSK, RSK1, RSK2, pp38, p38, pHSP27, HSP27 and β-Actin. B , U87-MG cells were transfected with siRNA against EphA2 (#1 or #2) or the negative control. After 5 h of transfection, cells were treated with DMSO or 100 μM TMZ for 72 h. Cell migration was observed using a time-lapse imaging system for 120 min. The accumulated distance of cell migration (μm) was calculated and shown in box and whisker plots. ∗ p < 0.05 by the Tukey–Kramer HSD test. Whole-cell lysates were immunoblotted with primary antibodies against EphA2 and β-Actin. C – F , U87-MG cells were treated with DMSO or 100 μM TMZ for 72 h, then treated with DMSO, 10 μM BI-D1870 ( C and E ) or 10 μM MK2 inhibitor III ( D and F ) for 2 h. Whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, pRSK, RSK1, RSK2, pHSP27, HSP27, and β-Actin ( C and D ). Cell migration was observed using a time-lapse imaging system for 120 min and the accumulated distance of cell migration (μm) was calculated and shown in box and whisker plots ( E and F ). ∗ p < 0.05 by the Tukey–Kramer HSD test. DMSO, dimethyl sulfoxide; EphA2, ephrin type-A receptor 2; HSP27, heat shock protein 27; RSK, p90 ribosomal S6 kinase.

Journal: The Journal of Biological Chemistry

Article Title: Cellular stress induces non-canonical activation of the receptor tyrosine kinase EphA2 through the p38-MK2-RSK signaling pathway

doi: 10.1016/j.jbc.2023.104699

Figure Lengend Snippet: The p38-MK2-RSK-EphA2 pathway promotes U87-MG cell migration induced by TMZ. A , U87-MG cells were treated with DMSO or 100 μM temozolomide (TMZ) for 48 h. Whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, pRSK, RSK1, RSK2, pp38, p38, pHSP27, HSP27 and β-Actin. B , U87-MG cells were transfected with siRNA against EphA2 (#1 or #2) or the negative control. After 5 h of transfection, cells were treated with DMSO or 100 μM TMZ for 72 h. Cell migration was observed using a time-lapse imaging system for 120 min. The accumulated distance of cell migration (μm) was calculated and shown in box and whisker plots. ∗ p < 0.05 by the Tukey–Kramer HSD test. Whole-cell lysates were immunoblotted with primary antibodies against EphA2 and β-Actin. C – F , U87-MG cells were treated with DMSO or 100 μM TMZ for 72 h, then treated with DMSO, 10 μM BI-D1870 ( C and E ) or 10 μM MK2 inhibitor III ( D and F ) for 2 h. Whole-cell lysates were immunoblotted with primary antibodies against pS-EphA2, EphA2, pRSK, RSK1, RSK2, pHSP27, HSP27, and β-Actin ( C and D ). Cell migration was observed using a time-lapse imaging system for 120 min and the accumulated distance of cell migration (μm) was calculated and shown in box and whisker plots ( E and F ). ∗ p < 0.05 by the Tukey–Kramer HSD test. DMSO, dimethyl sulfoxide; EphA2, ephrin type-A receptor 2; HSP27, heat shock protein 27; RSK, p90 ribosomal S6 kinase.

Article Snippet: Recombinant human EGF was obtained from R&D Systems; recombinant human active GST-MK2 protein was from Carna Biosciences; a phos-tag ligand, anisomycin, NaCl, and CDDP were from Wako Pure Chemical Industries; SB203580 and TMZ were from Merck KGaA; MK2 inhibitor III and GSK2334470 were from MedChemExpress; BI-D1870 was from BioVision; BIRB796, Skepinone-L, and BX-702 were from Selleck Chemicals.

Techniques: Migration, Transfection, Negative Control, Imaging, Whisker Assay

Model of the non-canonical activation of EphA2 by typically or atypically activated RSK. Upon the stimulation of growth factors, ERK typically activates CTK to induce the activation of NTK, resulting in the non-canonical activation of EphA2. On the other hand, cellular stress-activated MK2 catalyzes the phosphorylation of RSK1 at Ser-380 to induce NTK activation in a CTK-independent manner. This atypically activated RSK also induces the non-canonical activation of EphA2 to promote cancer malignancy. CTK, carboxyl-terminal kinase; EphA2, ephrin type-A receptor 2; ERK, extracellular signal-regulated kinase; MK2, MAPK-activated protein kinase 2; NTK, amino-terminal kinase; RSK, p90 ribosomal S6 kinase.

Journal: The Journal of Biological Chemistry

Article Title: Cellular stress induces non-canonical activation of the receptor tyrosine kinase EphA2 through the p38-MK2-RSK signaling pathway

doi: 10.1016/j.jbc.2023.104699

Figure Lengend Snippet: Model of the non-canonical activation of EphA2 by typically or atypically activated RSK. Upon the stimulation of growth factors, ERK typically activates CTK to induce the activation of NTK, resulting in the non-canonical activation of EphA2. On the other hand, cellular stress-activated MK2 catalyzes the phosphorylation of RSK1 at Ser-380 to induce NTK activation in a CTK-independent manner. This atypically activated RSK also induces the non-canonical activation of EphA2 to promote cancer malignancy. CTK, carboxyl-terminal kinase; EphA2, ephrin type-A receptor 2; ERK, extracellular signal-regulated kinase; MK2, MAPK-activated protein kinase 2; NTK, amino-terminal kinase; RSK, p90 ribosomal S6 kinase.

Article Snippet: Recombinant human EGF was obtained from R&D Systems; recombinant human active GST-MK2 protein was from Carna Biosciences; a phos-tag ligand, anisomycin, NaCl, and CDDP were from Wako Pure Chemical Industries; SB203580 and TMZ were from Merck KGaA; MK2 inhibitor III and GSK2334470 were from MedChemExpress; BI-D1870 was from BioVision; BIRB796, Skepinone-L, and BX-702 were from Selleck Chemicals.

Techniques: Activation Assay