rabbit anti p mk2 Search Results


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MMI-0100 prevented DSS-induced colon colitis by activating <t>MK2</t> signaling pathway. ( A , B ) The production of p-MK2, MK2 was investigated by WB and quantified with statistical significances. Data are presented as mean ± SD. ** p < 0.01 for between DSS group and control group; ### p < 0.001 for between MMI-0100 and DSS group.
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Cell Signaling Technology Inc anti jnk
MMI-0100 prevented DSS-induced colon colitis by activating <t>MK2</t> signaling pathway. ( A , B ) The production of p-MK2, MK2 was investigated by WB and quantified with statistical significances. Data are presented as mean ± SD. ** p < 0.01 for between DSS group and control group; ### p < 0.001 for between MMI-0100 and DSS group.
Anti Jnk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MMI-0100 prevented DSS-induced colon colitis by activating <t>MK2</t> signaling pathway. ( A , B ) The production of p-MK2, MK2 was investigated by WB and quantified with statistical significances. Data are presented as mean ± SD. ** p < 0.01 for between DSS group and control group; ### p < 0.001 for between MMI-0100 and DSS group.
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MMI-0100 prevented DSS-induced colon colitis by activating <t>MK2</t> signaling pathway. ( A , B ) The production of p-MK2, MK2 was investigated by WB and quantified with statistical significances. Data are presented as mean ± SD. ** p < 0.01 for between DSS group and control group; ### p < 0.001 for between MMI-0100 and DSS group.
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Cell Signaling Technology Inc anti p mek1 2
MMI-0100 prevented DSS-induced colon colitis by activating <t>MK2</t> signaling pathway. ( A , B ) The production of p-MK2, MK2 was investigated by WB and quantified with statistical significances. Data are presented as mean ± SD. ** p < 0.01 for between DSS group and control group; ### p < 0.001 for between MMI-0100 and DSS group.
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Cell Signaling Technology Inc anti p38β
Figure 6. p38α−/− mice have improved post-myocardial infarction (MI) cardiac function. A, Representative M-mode ECGs for p38αf/f and p38α−/− mice in the sham group and LAD coronary ligation group on day 7 after surgery. B, Echocardiography quantification of left ventricular ejection fraction (LVEF), fractional shortening (FS), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular internal diameter end diastole (LVIDd), and left ventricular internal diameter end systole (LVIDs) for p38αf/f and p38α−/− mice in the sham group and LAD coronary ligation group on day 7 after surgery (n=5; ***P<0.001, and **P<0.01). C, Masson trichrome staining of heart sections from p38αf/f and p38α−/− mice and quantification of infarct size (mean % of left ventricle [LV] area, n=5; ***P<0.001). D, The representative images of immunostaining CD45 and relative white blood cell (WBC) counts per high power field (HPF) in heart sections from p38αf/f and p38α−/− mice on day 3 post-MI (n=5; **P<0.01). E, Representative images of immunostaining of CD42c and relative platelet counts per HPF in heart sections from p38αf/f and p38α−/− mice on day 3 post-MI (n=5; ***P<0.001). F, The phosphor- ylation and total levels of p38, MK2, cPLA2, ERK1/2, ERK5, and JNKs in p38αf/f and p38α−/− platelets obtained from the corresponding mice on day 3 and 7 post-MI. G, A diagram of proposed <t>p38</t> signaling pathway in platelet activation and MI deterioration. IVS indicates interventricular septal; LVEIDd, left ventricular internal diameter end diastole; LVEIDs, left ventricular internal diameter end systole; and PW, posterior wall.
Anti P38β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


MMI-0100 prevented DSS-induced colon colitis by activating MK2 signaling pathway. ( A , B ) The production of p-MK2, MK2 was investigated by WB and quantified with statistical significances. Data are presented as mean ± SD. ** p < 0.01 for between DSS group and control group; ### p < 0.001 for between MMI-0100 and DSS group.

Journal: Molecules

Article Title: MMI-0100 Ameliorates Dextran Sulfate Sodium-Induced Colitis in Mice through Targeting MK2 Pathway

doi: 10.3390/molecules24152832

Figure Lengend Snippet: MMI-0100 prevented DSS-induced colon colitis by activating MK2 signaling pathway. ( A , B ) The production of p-MK2, MK2 was investigated by WB and quantified with statistical significances. Data are presented as mean ± SD. ** p < 0.01 for between DSS group and control group; ### p < 0.001 for between MMI-0100 and DSS group.

Article Snippet: Anti-p-MK2 Rabbit mAb , 1:1000 , 3007S , CST, USA.

Techniques: Control

Antibody information used in this experiment.

Journal: Molecules

Article Title: MMI-0100 Ameliorates Dextran Sulfate Sodium-Induced Colitis in Mice through Targeting MK2 Pathway

doi: 10.3390/molecules24152832

Figure Lengend Snippet: Antibody information used in this experiment.

Article Snippet: Anti-p-MK2 Rabbit mAb , 1:1000 , 3007S , CST, USA.

Techniques: Concentration Assay

Figure 6. p38α−/− mice have improved post-myocardial infarction (MI) cardiac function. A, Representative M-mode ECGs for p38αf/f and p38α−/− mice in the sham group and LAD coronary ligation group on day 7 after surgery. B, Echocardiography quantification of left ventricular ejection fraction (LVEF), fractional shortening (FS), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular internal diameter end diastole (LVIDd), and left ventricular internal diameter end systole (LVIDs) for p38αf/f and p38α−/− mice in the sham group and LAD coronary ligation group on day 7 after surgery (n=5; ***P<0.001, and **P<0.01). C, Masson trichrome staining of heart sections from p38αf/f and p38α−/− mice and quantification of infarct size (mean % of left ventricle [LV] area, n=5; ***P<0.001). D, The representative images of immunostaining CD45 and relative white blood cell (WBC) counts per high power field (HPF) in heart sections from p38αf/f and p38α−/− mice on day 3 post-MI (n=5; **P<0.01). E, Representative images of immunostaining of CD42c and relative platelet counts per HPF in heart sections from p38αf/f and p38α−/− mice on day 3 post-MI (n=5; ***P<0.001). F, The phosphor- ylation and total levels of p38, MK2, cPLA2, ERK1/2, ERK5, and JNKs in p38αf/f and p38α−/− platelets obtained from the corresponding mice on day 3 and 7 post-MI. G, A diagram of proposed p38 signaling pathway in platelet activation and MI deterioration. IVS indicates interventricular septal; LVEIDd, left ventricular internal diameter end diastole; LVEIDs, left ventricular internal diameter end systole; and PW, posterior wall.

Journal: Arteriosclerosis, Thrombosis, and Vascular Biology

Article Title: Platelet-Specific p38α Deficiency Improved Cardiac Function After Myocardial Infarction in Mice

doi: 10.1161/atvbaha.117.309856

Figure Lengend Snippet: Figure 6. p38α−/− mice have improved post-myocardial infarction (MI) cardiac function. A, Representative M-mode ECGs for p38αf/f and p38α−/− mice in the sham group and LAD coronary ligation group on day 7 after surgery. B, Echocardiography quantification of left ventricular ejection fraction (LVEF), fractional shortening (FS), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular internal diameter end diastole (LVIDd), and left ventricular internal diameter end systole (LVIDs) for p38αf/f and p38α−/− mice in the sham group and LAD coronary ligation group on day 7 after surgery (n=5; ***P<0.001, and **P<0.01). C, Masson trichrome staining of heart sections from p38αf/f and p38α−/− mice and quantification of infarct size (mean % of left ventricle [LV] area, n=5; ***P<0.001). D, The representative images of immunostaining CD45 and relative white blood cell (WBC) counts per high power field (HPF) in heart sections from p38αf/f and p38α−/− mice on day 3 post-MI (n=5; **P<0.01). E, Representative images of immunostaining of CD42c and relative platelet counts per HPF in heart sections from p38αf/f and p38α−/− mice on day 3 post-MI (n=5; ***P<0.001). F, The phosphor- ylation and total levels of p38, MK2, cPLA2, ERK1/2, ERK5, and JNKs in p38αf/f and p38α−/− platelets obtained from the corresponding mice on day 3 and 7 post-MI. G, A diagram of proposed p38 signaling pathway in platelet activation and MI deterioration. IVS indicates interventricular septal; LVEIDd, left ventricular internal diameter end diastole; LVEIDs, left ventricular internal diameter end systole; and PW, posterior wall.

Article Snippet: Anti-p38 (#9212), anti-ERK1/2 (#4696), anti-JNK (#9258), anti-ERK5 (#3552), anti-p38α (#2371), anti-p38β (#2339), anti-p38γ (#2307), anti-p38δ (#9214), anti-phosphospecific (P)-p38 (#9211), anti-P-ERK1/2 (#4370), anti-P-JNK (#4668), anti-P-ERK5 (#3371), anti-MAPKAPK2 (MK2) (#12155), anti-P-MK2 (Thr222) (#3316), anti-P-cPLA2 (Ser505) (#2831), anti-P-MEK1/2 (#9154) and anti-GAPDH (#5174) were from Cell Signaling Technology (Danvers, MA).

Techniques: Ligation, Staining, Immunostaining, Activation Assay