phospho jnk Search Results


phospho jnk  (R&D Systems)
99
R&D Systems phospho jnk
Figure 1 Alterations in MAPK activity are associated with IR or HR. Representative immunoblots (a, c, e) and a summary graph (b, d) are shown. (a, b). Three animals undergoing heterotopic heart transplantation were analysed in each group. Treatment conditions were as follows: Co, untreated animals; H, 45 min of ischemia; R1-R4, hearts exposed to 45 min of ischemia and either 10 min (R1), 2 h (R2), 12 h (R3), 24 h (R4) or 48 h (R5), of reperfusion. BALB/c mouse heart lysates display low levels of ERK1,2 activity in the control group (Co). 45 min of ischemia increased stress kinase activity (p38: 4.6-fold increase, *P < 0.05 vs. control; <t>JNK:</t> 9.4-fold increase, *P < 0.05 vs. control) but <t>left</t> <t>ERK</t> 1,2 unaf- fected. 10 min of reperfusion (R1) caused a significant increase in ERK activity (ERK1,2: 8.4-fold increase, **P < 0.01 vs. control), and a further increase in p38 (p38: 9.4-fold increase, **P < 0.01 vs. control) and JNK (JNK1,2: 57.7-fold increase, **P < 0.01 vs. control) activity. After 2 h of reperfusion (R2) JNK (JNK1,2: 2.6-fold increase) and p38 (p38: 0.6-fold) activity had returned to control (Co) levels, while ERK (ERK1,2: 4.8-fold increase) activation still did not return to prereperfusion levels and stayed above levels in control hearts until the end of the observation period (ERK1,2: 2.73-fold increase). Data are expressed as mean ± SEM (of n = 3). (c–e) Changes in MAPK signaling in HL-1 cells and primary BALB/c car- diomyocytes subjected to 45 min of hypoxia (0.5% O2, 37 C, serum-/glucose-free medium) and up to 48 h of reoxygenation. The treatment conditions were as follows: Co, untreated cells; H, 45 min of hypoxia R1-R4: hypoxia (45 min) followed by reoxygenation in growth medium for 10 min (R1), 2 h (R2), 24 h (R3) or 48 h (R4), respectively. 45 min of hypoxia increased activity of all three MAPKs, 10 min of reperfusion lead to a further increase in their activities. After 2 h of reperfusion JNK and p38 activity had ceased while ERK activity still had not returned to control levels. Data are expressed as mean ± SEM (n = 3, all **P < 0.01). In the case of primary cardiomyocytes a single experiment was performed.
Phospho Jnk, supplied by R&D Systems, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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phospho sapk jnk cell signaling technology  (Cell Signaling Technology Inc)
99
Cell Signaling Technology Inc phospho sapk jnk cell signaling technology
Figure 1 Alterations in MAPK activity are associated with IR or HR. Representative immunoblots (a, c, e) and a summary graph (b, d) are shown. (a, b). Three animals undergoing heterotopic heart transplantation were analysed in each group. Treatment conditions were as follows: Co, untreated animals; H, 45 min of ischemia; R1-R4, hearts exposed to 45 min of ischemia and either 10 min (R1), 2 h (R2), 12 h (R3), 24 h (R4) or 48 h (R5), of reperfusion. BALB/c mouse heart lysates display low levels of ERK1,2 activity in the control group (Co). 45 min of ischemia increased stress kinase activity (p38: 4.6-fold increase, *P < 0.05 vs. control; <t>JNK:</t> 9.4-fold increase, *P < 0.05 vs. control) but <t>left</t> <t>ERK</t> 1,2 unaf- fected. 10 min of reperfusion (R1) caused a significant increase in ERK activity (ERK1,2: 8.4-fold increase, **P < 0.01 vs. control), and a further increase in p38 (p38: 9.4-fold increase, **P < 0.01 vs. control) and JNK (JNK1,2: 57.7-fold increase, **P < 0.01 vs. control) activity. After 2 h of reperfusion (R2) JNK (JNK1,2: 2.6-fold increase) and p38 (p38: 0.6-fold) activity had returned to control (Co) levels, while ERK (ERK1,2: 4.8-fold increase) activation still did not return to prereperfusion levels and stayed above levels in control hearts until the end of the observation period (ERK1,2: 2.73-fold increase). Data are expressed as mean ± SEM (of n = 3). (c–e) Changes in MAPK signaling in HL-1 cells and primary BALB/c car- diomyocytes subjected to 45 min of hypoxia (0.5% O2, 37 C, serum-/glucose-free medium) and up to 48 h of reoxygenation. The treatment conditions were as follows: Co, untreated cells; H, 45 min of hypoxia R1-R4: hypoxia (45 min) followed by reoxygenation in growth medium for 10 min (R1), 2 h (R2), 24 h (R3) or 48 h (R4), respectively. 45 min of hypoxia increased activity of all three MAPKs, 10 min of reperfusion lead to a further increase in their activities. After 2 h of reperfusion JNK and p38 activity had ceased while ERK activity still had not returned to control levels. Data are expressed as mean ± SEM (n = 3, all **P < 0.01). In the case of primary cardiomyocytes a single experiment was performed.
Phospho Sapk Jnk Cell Signaling Technology, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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phospho jnk antibody  (Cell Signaling Technology Inc)
98
Cell Signaling Technology Inc phospho jnk antibody
Figure 1 Alterations in MAPK activity are associated with IR or HR. Representative immunoblots (a, c, e) and a summary graph (b, d) are shown. (a, b). Three animals undergoing heterotopic heart transplantation were analysed in each group. Treatment conditions were as follows: Co, untreated animals; H, 45 min of ischemia; R1-R4, hearts exposed to 45 min of ischemia and either 10 min (R1), 2 h (R2), 12 h (R3), 24 h (R4) or 48 h (R5), of reperfusion. BALB/c mouse heart lysates display low levels of ERK1,2 activity in the control group (Co). 45 min of ischemia increased stress kinase activity (p38: 4.6-fold increase, *P < 0.05 vs. control; <t>JNK:</t> 9.4-fold increase, *P < 0.05 vs. control) but <t>left</t> <t>ERK</t> 1,2 unaf- fected. 10 min of reperfusion (R1) caused a significant increase in ERK activity (ERK1,2: 8.4-fold increase, **P < 0.01 vs. control), and a further increase in p38 (p38: 9.4-fold increase, **P < 0.01 vs. control) and JNK (JNK1,2: 57.7-fold increase, **P < 0.01 vs. control) activity. After 2 h of reperfusion (R2) JNK (JNK1,2: 2.6-fold increase) and p38 (p38: 0.6-fold) activity had returned to control (Co) levels, while ERK (ERK1,2: 4.8-fold increase) activation still did not return to prereperfusion levels and stayed above levels in control hearts until the end of the observation period (ERK1,2: 2.73-fold increase). Data are expressed as mean ± SEM (of n = 3). (c–e) Changes in MAPK signaling in HL-1 cells and primary BALB/c car- diomyocytes subjected to 45 min of hypoxia (0.5% O2, 37 C, serum-/glucose-free medium) and up to 48 h of reoxygenation. The treatment conditions were as follows: Co, untreated cells; H, 45 min of hypoxia R1-R4: hypoxia (45 min) followed by reoxygenation in growth medium for 10 min (R1), 2 h (R2), 24 h (R3) or 48 h (R4), respectively. 45 min of hypoxia increased activity of all three MAPKs, 10 min of reperfusion lead to a further increase in their activities. After 2 h of reperfusion JNK and p38 activity had ceased while ERK activity still had not returned to control levels. Data are expressed as mean ± SEM (n = 3, all **P < 0.01). In the case of primary cardiomyocytes a single experiment was performed.
Phospho Jnk Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti phospho sapk jnk mouse mab  (Cell Signaling Technology Inc)
93
Cell Signaling Technology Inc anti phospho sapk jnk mouse mab
Figure 1 Alterations in MAPK activity are associated with IR or HR. Representative immunoblots (a, c, e) and a summary graph (b, d) are shown. (a, b). Three animals undergoing heterotopic heart transplantation were analysed in each group. Treatment conditions were as follows: Co, untreated animals; H, 45 min of ischemia; R1-R4, hearts exposed to 45 min of ischemia and either 10 min (R1), 2 h (R2), 12 h (R3), 24 h (R4) or 48 h (R5), of reperfusion. BALB/c mouse heart lysates display low levels of ERK1,2 activity in the control group (Co). 45 min of ischemia increased stress kinase activity (p38: 4.6-fold increase, *P < 0.05 vs. control; <t>JNK:</t> 9.4-fold increase, *P < 0.05 vs. control) but <t>left</t> <t>ERK</t> 1,2 unaf- fected. 10 min of reperfusion (R1) caused a significant increase in ERK activity (ERK1,2: 8.4-fold increase, **P < 0.01 vs. control), and a further increase in p38 (p38: 9.4-fold increase, **P < 0.01 vs. control) and JNK (JNK1,2: 57.7-fold increase, **P < 0.01 vs. control) activity. After 2 h of reperfusion (R2) JNK (JNK1,2: 2.6-fold increase) and p38 (p38: 0.6-fold) activity had returned to control (Co) levels, while ERK (ERK1,2: 4.8-fold increase) activation still did not return to prereperfusion levels and stayed above levels in control hearts until the end of the observation period (ERK1,2: 2.73-fold increase). Data are expressed as mean ± SEM (of n = 3). (c–e) Changes in MAPK signaling in HL-1 cells and primary BALB/c car- diomyocytes subjected to 45 min of hypoxia (0.5% O2, 37 C, serum-/glucose-free medium) and up to 48 h of reoxygenation. The treatment conditions were as follows: Co, untreated cells; H, 45 min of hypoxia R1-R4: hypoxia (45 min) followed by reoxygenation in growth medium for 10 min (R1), 2 h (R2), 24 h (R3) or 48 h (R4), respectively. 45 min of hypoxia increased activity of all three MAPKs, 10 min of reperfusion lead to a further increase in their activities. After 2 h of reperfusion JNK and p38 activity had ceased while ERK activity still had not returned to control levels. Data are expressed as mean ± SEM (n = 3, all **P < 0.01). In the case of primary cardiomyocytes a single experiment was performed.
Anti Phospho Sapk Jnk Mouse Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1 rr  (Proteintech)
96
Proteintech 1 rr
Figure 1 Alterations in MAPK activity are associated with IR or HR. Representative immunoblots (a, c, e) and a summary graph (b, d) are shown. (a, b). Three animals undergoing heterotopic heart transplantation were analysed in each group. Treatment conditions were as follows: Co, untreated animals; H, 45 min of ischemia; R1-R4, hearts exposed to 45 min of ischemia and either 10 min (R1), 2 h (R2), 12 h (R3), 24 h (R4) or 48 h (R5), of reperfusion. BALB/c mouse heart lysates display low levels of ERK1,2 activity in the control group (Co). 45 min of ischemia increased stress kinase activity (p38: 4.6-fold increase, *P < 0.05 vs. control; <t>JNK:</t> 9.4-fold increase, *P < 0.05 vs. control) but <t>left</t> <t>ERK</t> 1,2 unaf- fected. 10 min of reperfusion (R1) caused a significant increase in ERK activity (ERK1,2: 8.4-fold increase, **P < 0.01 vs. control), and a further increase in p38 (p38: 9.4-fold increase, **P < 0.01 vs. control) and JNK (JNK1,2: 57.7-fold increase, **P < 0.01 vs. control) activity. After 2 h of reperfusion (R2) JNK (JNK1,2: 2.6-fold increase) and p38 (p38: 0.6-fold) activity had returned to control (Co) levels, while ERK (ERK1,2: 4.8-fold increase) activation still did not return to prereperfusion levels and stayed above levels in control hearts until the end of the observation period (ERK1,2: 2.73-fold increase). Data are expressed as mean ± SEM (of n = 3). (c–e) Changes in MAPK signaling in HL-1 cells and primary BALB/c car- diomyocytes subjected to 45 min of hypoxia (0.5% O2, 37 C, serum-/glucose-free medium) and up to 48 h of reoxygenation. The treatment conditions were as follows: Co, untreated cells; H, 45 min of hypoxia R1-R4: hypoxia (45 min) followed by reoxygenation in growth medium for 10 min (R1), 2 h (R2), 24 h (R3) or 48 h (R4), respectively. 45 min of hypoxia increased activity of all three MAPKs, 10 min of reperfusion lead to a further increase in their activities. After 2 h of reperfusion JNK and p38 activity had ceased while ERK activity still had not returned to control levels. Data are expressed as mean ± SEM (n = 3, all **P < 0.01). In the case of primary cardiomyocytes a single experiment was performed.
1 Rr, supplied by Proteintech, 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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anti p jnk  (Cell Signaling Technology Inc)
97
Cell Signaling Technology Inc anti p jnk
Figure 1 Alterations in MAPK activity are associated with IR or HR. Representative immunoblots (a, c, e) and a summary graph (b, d) are shown. (a, b). Three animals undergoing heterotopic heart transplantation were analysed in each group. Treatment conditions were as follows: Co, untreated animals; H, 45 min of ischemia; R1-R4, hearts exposed to 45 min of ischemia and either 10 min (R1), 2 h (R2), 12 h (R3), 24 h (R4) or 48 h (R5), of reperfusion. BALB/c mouse heart lysates display low levels of ERK1,2 activity in the control group (Co). 45 min of ischemia increased stress kinase activity (p38: 4.6-fold increase, *P < 0.05 vs. control; <t>JNK:</t> 9.4-fold increase, *P < 0.05 vs. control) but <t>left</t> <t>ERK</t> 1,2 unaf- fected. 10 min of reperfusion (R1) caused a significant increase in ERK activity (ERK1,2: 8.4-fold increase, **P < 0.01 vs. control), and a further increase in p38 (p38: 9.4-fold increase, **P < 0.01 vs. control) and JNK (JNK1,2: 57.7-fold increase, **P < 0.01 vs. control) activity. After 2 h of reperfusion (R2) JNK (JNK1,2: 2.6-fold increase) and p38 (p38: 0.6-fold) activity had returned to control (Co) levels, while ERK (ERK1,2: 4.8-fold increase) activation still did not return to prereperfusion levels and stayed above levels in control hearts until the end of the observation period (ERK1,2: 2.73-fold increase). Data are expressed as mean ± SEM (of n = 3). (c–e) Changes in MAPK signaling in HL-1 cells and primary BALB/c car- diomyocytes subjected to 45 min of hypoxia (0.5% O2, 37 C, serum-/glucose-free medium) and up to 48 h of reoxygenation. The treatment conditions were as follows: Co, untreated cells; H, 45 min of hypoxia R1-R4: hypoxia (45 min) followed by reoxygenation in growth medium for 10 min (R1), 2 h (R2), 24 h (R3) or 48 h (R4), respectively. 45 min of hypoxia increased activity of all three MAPKs, 10 min of reperfusion lead to a further increase in their activities. After 2 h of reperfusion JNK and p38 activity had ceased while ERK activity still had not returned to control levels. Data are expressed as mean ± SEM (n = 3, all **P < 0.01). In the case of primary cardiomyocytes a single experiment was performed.
Anti P Jnk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti phosphojnk  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc anti phosphojnk
Figure 1 Alterations in MAPK activity are associated with IR or HR. Representative immunoblots (a, c, e) and a summary graph (b, d) are shown. (a, b). Three animals undergoing heterotopic heart transplantation were analysed in each group. Treatment conditions were as follows: Co, untreated animals; H, 45 min of ischemia; R1-R4, hearts exposed to 45 min of ischemia and either 10 min (R1), 2 h (R2), 12 h (R3), 24 h (R4) or 48 h (R5), of reperfusion. BALB/c mouse heart lysates display low levels of ERK1,2 activity in the control group (Co). 45 min of ischemia increased stress kinase activity (p38: 4.6-fold increase, *P < 0.05 vs. control; <t>JNK:</t> 9.4-fold increase, *P < 0.05 vs. control) but <t>left</t> <t>ERK</t> 1,2 unaf- fected. 10 min of reperfusion (R1) caused a significant increase in ERK activity (ERK1,2: 8.4-fold increase, **P < 0.01 vs. control), and a further increase in p38 (p38: 9.4-fold increase, **P < 0.01 vs. control) and JNK (JNK1,2: 57.7-fold increase, **P < 0.01 vs. control) activity. After 2 h of reperfusion (R2) JNK (JNK1,2: 2.6-fold increase) and p38 (p38: 0.6-fold) activity had returned to control (Co) levels, while ERK (ERK1,2: 4.8-fold increase) activation still did not return to prereperfusion levels and stayed above levels in control hearts until the end of the observation period (ERK1,2: 2.73-fold increase). Data are expressed as mean ± SEM (of n = 3). (c–e) Changes in MAPK signaling in HL-1 cells and primary BALB/c car- diomyocytes subjected to 45 min of hypoxia (0.5% O2, 37 C, serum-/glucose-free medium) and up to 48 h of reoxygenation. The treatment conditions were as follows: Co, untreated cells; H, 45 min of hypoxia R1-R4: hypoxia (45 min) followed by reoxygenation in growth medium for 10 min (R1), 2 h (R2), 24 h (R3) or 48 h (R4), respectively. 45 min of hypoxia increased activity of all three MAPKs, 10 min of reperfusion lead to a further increase in their activities. After 2 h of reperfusion JNK and p38 activity had ceased while ERK activity still had not returned to control levels. Data are expressed as mean ± SEM (n = 3, all **P < 0.01). In the case of primary cardiomyocytes a single experiment was performed.
Anti Phosphojnk, 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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pathscan phosoho sapk jnk thr183 tyr185 sandwich elisa kit  (Cell Signaling Technology Inc)
93
Cell Signaling Technology Inc pathscan phosoho sapk jnk thr183 tyr185 sandwich elisa kit
Figure 1 Alterations in MAPK activity are associated with IR or HR. Representative immunoblots (a, c, e) and a summary graph (b, d) are shown. (a, b). Three animals undergoing heterotopic heart transplantation were analysed in each group. Treatment conditions were as follows: Co, untreated animals; H, 45 min of ischemia; R1-R4, hearts exposed to 45 min of ischemia and either 10 min (R1), 2 h (R2), 12 h (R3), 24 h (R4) or 48 h (R5), of reperfusion. BALB/c mouse heart lysates display low levels of ERK1,2 activity in the control group (Co). 45 min of ischemia increased stress kinase activity (p38: 4.6-fold increase, *P < 0.05 vs. control; <t>JNK:</t> 9.4-fold increase, *P < 0.05 vs. control) but <t>left</t> <t>ERK</t> 1,2 unaf- fected. 10 min of reperfusion (R1) caused a significant increase in ERK activity (ERK1,2: 8.4-fold increase, **P < 0.01 vs. control), and a further increase in p38 (p38: 9.4-fold increase, **P < 0.01 vs. control) and JNK (JNK1,2: 57.7-fold increase, **P < 0.01 vs. control) activity. After 2 h of reperfusion (R2) JNK (JNK1,2: 2.6-fold increase) and p38 (p38: 0.6-fold) activity had returned to control (Co) levels, while ERK (ERK1,2: 4.8-fold increase) activation still did not return to prereperfusion levels and stayed above levels in control hearts until the end of the observation period (ERK1,2: 2.73-fold increase). Data are expressed as mean ± SEM (of n = 3). (c–e) Changes in MAPK signaling in HL-1 cells and primary BALB/c car- diomyocytes subjected to 45 min of hypoxia (0.5% O2, 37 C, serum-/glucose-free medium) and up to 48 h of reoxygenation. The treatment conditions were as follows: Co, untreated cells; H, 45 min of hypoxia R1-R4: hypoxia (45 min) followed by reoxygenation in growth medium for 10 min (R1), 2 h (R2), 24 h (R3) or 48 h (R4), respectively. 45 min of hypoxia increased activity of all three MAPKs, 10 min of reperfusion lead to a further increase in their activities. After 2 h of reperfusion JNK and p38 activity had ceased while ERK activity still had not returned to control levels. Data are expressed as mean ± SEM (n = 3, all **P < 0.01). In the case of primary cardiomyocytes a single experiment was performed.
Pathscan Phosoho Sapk Jnk Thr183 Tyr185 Sandwich Elisa Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti phospho sapk jnk  (Cell Signaling Technology Inc)
93
Cell Signaling Technology Inc anti phospho sapk jnk
Figure 1 Alterations in MAPK activity are associated with IR or HR. Representative immunoblots (a, c, e) and a summary graph (b, d) are shown. (a, b). Three animals undergoing heterotopic heart transplantation were analysed in each group. Treatment conditions were as follows: Co, untreated animals; H, 45 min of ischemia; R1-R4, hearts exposed to 45 min of ischemia and either 10 min (R1), 2 h (R2), 12 h (R3), 24 h (R4) or 48 h (R5), of reperfusion. BALB/c mouse heart lysates display low levels of ERK1,2 activity in the control group (Co). 45 min of ischemia increased stress kinase activity (p38: 4.6-fold increase, *P < 0.05 vs. control; <t>JNK:</t> 9.4-fold increase, *P < 0.05 vs. control) but <t>left</t> <t>ERK</t> 1,2 unaf- fected. 10 min of reperfusion (R1) caused a significant increase in ERK activity (ERK1,2: 8.4-fold increase, **P < 0.01 vs. control), and a further increase in p38 (p38: 9.4-fold increase, **P < 0.01 vs. control) and JNK (JNK1,2: 57.7-fold increase, **P < 0.01 vs. control) activity. After 2 h of reperfusion (R2) JNK (JNK1,2: 2.6-fold increase) and p38 (p38: 0.6-fold) activity had returned to control (Co) levels, while ERK (ERK1,2: 4.8-fold increase) activation still did not return to prereperfusion levels and stayed above levels in control hearts until the end of the observation period (ERK1,2: 2.73-fold increase). Data are expressed as mean ± SEM (of n = 3). (c–e) Changes in MAPK signaling in HL-1 cells and primary BALB/c car- diomyocytes subjected to 45 min of hypoxia (0.5% O2, 37 C, serum-/glucose-free medium) and up to 48 h of reoxygenation. The treatment conditions were as follows: Co, untreated cells; H, 45 min of hypoxia R1-R4: hypoxia (45 min) followed by reoxygenation in growth medium for 10 min (R1), 2 h (R2), 24 h (R3) or 48 h (R4), respectively. 45 min of hypoxia increased activity of all three MAPKs, 10 min of reperfusion lead to a further increase in their activities. After 2 h of reperfusion JNK and p38 activity had ceased while ERK activity still had not returned to control levels. Data are expressed as mean ± SEM (n = 3, all **P < 0.01). In the case of primary cardiomyocytes a single experiment was performed.
Anti Phospho Sapk Jnk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti phospho sapk jnk/product/Cell Signaling Technology Inc
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mab1205  (R&D Systems)
93
R&D Systems mab1205
Figure 1 Alterations in MAPK activity are associated with IR or HR. Representative immunoblots (a, c, e) and a summary graph (b, d) are shown. (a, b). Three animals undergoing heterotopic heart transplantation were analysed in each group. Treatment conditions were as follows: Co, untreated animals; H, 45 min of ischemia; R1-R4, hearts exposed to 45 min of ischemia and either 10 min (R1), 2 h (R2), 12 h (R3), 24 h (R4) or 48 h (R5), of reperfusion. BALB/c mouse heart lysates display low levels of ERK1,2 activity in the control group (Co). 45 min of ischemia increased stress kinase activity (p38: 4.6-fold increase, *P < 0.05 vs. control; <t>JNK:</t> 9.4-fold increase, *P < 0.05 vs. control) but <t>left</t> <t>ERK</t> 1,2 unaf- fected. 10 min of reperfusion (R1) caused a significant increase in ERK activity (ERK1,2: 8.4-fold increase, **P < 0.01 vs. control), and a further increase in p38 (p38: 9.4-fold increase, **P < 0.01 vs. control) and JNK (JNK1,2: 57.7-fold increase, **P < 0.01 vs. control) activity. After 2 h of reperfusion (R2) JNK (JNK1,2: 2.6-fold increase) and p38 (p38: 0.6-fold) activity had returned to control (Co) levels, while ERK (ERK1,2: 4.8-fold increase) activation still did not return to prereperfusion levels and stayed above levels in control hearts until the end of the observation period (ERK1,2: 2.73-fold increase). Data are expressed as mean ± SEM (of n = 3). (c–e) Changes in MAPK signaling in HL-1 cells and primary BALB/c car- diomyocytes subjected to 45 min of hypoxia (0.5% O2, 37 C, serum-/glucose-free medium) and up to 48 h of reoxygenation. The treatment conditions were as follows: Co, untreated cells; H, 45 min of hypoxia R1-R4: hypoxia (45 min) followed by reoxygenation in growth medium for 10 min (R1), 2 h (R2), 24 h (R3) or 48 h (R4), respectively. 45 min of hypoxia increased activity of all three MAPKs, 10 min of reperfusion lead to a further increase in their activities. After 2 h of reperfusion JNK and p38 activity had ceased while ERK activity still had not returned to control levels. Data are expressed as mean ± SEM (n = 3, all **P < 0.01). In the case of primary cardiomyocytes a single experiment was performed.
Mab1205, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sapk jnk pt183 y185  (Cell Signaling Technology Inc)
93
Cell Signaling Technology Inc sapk jnk pt183 y185
Figure 1 Alterations in MAPK activity are associated with IR or HR. Representative immunoblots (a, c, e) and a summary graph (b, d) are shown. (a, b). Three animals undergoing heterotopic heart transplantation were analysed in each group. Treatment conditions were as follows: Co, untreated animals; H, 45 min of ischemia; R1-R4, hearts exposed to 45 min of ischemia and either 10 min (R1), 2 h (R2), 12 h (R3), 24 h (R4) or 48 h (R5), of reperfusion. BALB/c mouse heart lysates display low levels of ERK1,2 activity in the control group (Co). 45 min of ischemia increased stress kinase activity (p38: 4.6-fold increase, *P < 0.05 vs. control; <t>JNK:</t> 9.4-fold increase, *P < 0.05 vs. control) but <t>left</t> <t>ERK</t> 1,2 unaf- fected. 10 min of reperfusion (R1) caused a significant increase in ERK activity (ERK1,2: 8.4-fold increase, **P < 0.01 vs. control), and a further increase in p38 (p38: 9.4-fold increase, **P < 0.01 vs. control) and JNK (JNK1,2: 57.7-fold increase, **P < 0.01 vs. control) activity. After 2 h of reperfusion (R2) JNK (JNK1,2: 2.6-fold increase) and p38 (p38: 0.6-fold) activity had returned to control (Co) levels, while ERK (ERK1,2: 4.8-fold increase) activation still did not return to prereperfusion levels and stayed above levels in control hearts until the end of the observation period (ERK1,2: 2.73-fold increase). Data are expressed as mean ± SEM (of n = 3). (c–e) Changes in MAPK signaling in HL-1 cells and primary BALB/c car- diomyocytes subjected to 45 min of hypoxia (0.5% O2, 37 C, serum-/glucose-free medium) and up to 48 h of reoxygenation. The treatment conditions were as follows: Co, untreated cells; H, 45 min of hypoxia R1-R4: hypoxia (45 min) followed by reoxygenation in growth medium for 10 min (R1), 2 h (R2), 24 h (R3) or 48 h (R4), respectively. 45 min of hypoxia increased activity of all three MAPKs, 10 min of reperfusion lead to a further increase in their activities. After 2 h of reperfusion JNK and p38 activity had ceased while ERK activity still had not returned to control levels. Data are expressed as mean ± SEM (n = 3, all **P < 0.01). In the case of primary cardiomyocytes a single experiment was performed.
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phospho c jun n terminal kinase jnk  (R&D Systems)
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R&D Systems phospho c jun n terminal kinase jnk
Figure 1 Alterations in MAPK activity are associated with IR or HR. Representative immunoblots (a, c, e) and a summary graph (b, d) are shown. (a, b). Three animals undergoing heterotopic heart transplantation were analysed in each group. Treatment conditions were as follows: Co, untreated animals; H, 45 min of ischemia; R1-R4, hearts exposed to 45 min of ischemia and either 10 min (R1), 2 h (R2), 12 h (R3), 24 h (R4) or 48 h (R5), of reperfusion. BALB/c mouse heart lysates display low levels of ERK1,2 activity in the control group (Co). 45 min of ischemia increased stress kinase activity (p38: 4.6-fold increase, *P < 0.05 vs. control; <t>JNK:</t> 9.4-fold increase, *P < 0.05 vs. control) but <t>left</t> <t>ERK</t> 1,2 unaf- fected. 10 min of reperfusion (R1) caused a significant increase in ERK activity (ERK1,2: 8.4-fold increase, **P < 0.01 vs. control), and a further increase in p38 (p38: 9.4-fold increase, **P < 0.01 vs. control) and JNK (JNK1,2: 57.7-fold increase, **P < 0.01 vs. control) activity. After 2 h of reperfusion (R2) JNK (JNK1,2: 2.6-fold increase) and p38 (p38: 0.6-fold) activity had returned to control (Co) levels, while ERK (ERK1,2: 4.8-fold increase) activation still did not return to prereperfusion levels and stayed above levels in control hearts until the end of the observation period (ERK1,2: 2.73-fold increase). Data are expressed as mean ± SEM (of n = 3). (c–e) Changes in MAPK signaling in HL-1 cells and primary BALB/c car- diomyocytes subjected to 45 min of hypoxia (0.5% O2, 37 C, serum-/glucose-free medium) and up to 48 h of reoxygenation. The treatment conditions were as follows: Co, untreated cells; H, 45 min of hypoxia R1-R4: hypoxia (45 min) followed by reoxygenation in growth medium for 10 min (R1), 2 h (R2), 24 h (R3) or 48 h (R4), respectively. 45 min of hypoxia increased activity of all three MAPKs, 10 min of reperfusion lead to a further increase in their activities. After 2 h of reperfusion JNK and p38 activity had ceased while ERK activity still had not returned to control levels. Data are expressed as mean ± SEM (n = 3, all **P < 0.01). In the case of primary cardiomyocytes a single experiment was performed.
Phospho C Jun N Terminal Kinase Jnk, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Figure 1 Alterations in MAPK activity are associated with IR or HR. Representative immunoblots (a, c, e) and a summary graph (b, d) are shown. (a, b). Three animals undergoing heterotopic heart transplantation were analysed in each group. Treatment conditions were as follows: Co, untreated animals; H, 45 min of ischemia; R1-R4, hearts exposed to 45 min of ischemia and either 10 min (R1), 2 h (R2), 12 h (R3), 24 h (R4) or 48 h (R5), of reperfusion. BALB/c mouse heart lysates display low levels of ERK1,2 activity in the control group (Co). 45 min of ischemia increased stress kinase activity (p38: 4.6-fold increase, *P < 0.05 vs. control; JNK: 9.4-fold increase, *P < 0.05 vs. control) but left ERK 1,2 unaf- fected. 10 min of reperfusion (R1) caused a significant increase in ERK activity (ERK1,2: 8.4-fold increase, **P < 0.01 vs. control), and a further increase in p38 (p38: 9.4-fold increase, **P < 0.01 vs. control) and JNK (JNK1,2: 57.7-fold increase, **P < 0.01 vs. control) activity. After 2 h of reperfusion (R2) JNK (JNK1,2: 2.6-fold increase) and p38 (p38: 0.6-fold) activity had returned to control (Co) levels, while ERK (ERK1,2: 4.8-fold increase) activation still did not return to prereperfusion levels and stayed above levels in control hearts until the end of the observation period (ERK1,2: 2.73-fold increase). Data are expressed as mean ± SEM (of n = 3). (c–e) Changes in MAPK signaling in HL-1 cells and primary BALB/c car- diomyocytes subjected to 45 min of hypoxia (0.5% O2, 37 C, serum-/glucose-free medium) and up to 48 h of reoxygenation. The treatment conditions were as follows: Co, untreated cells; H, 45 min of hypoxia R1-R4: hypoxia (45 min) followed by reoxygenation in growth medium for 10 min (R1), 2 h (R2), 24 h (R3) or 48 h (R4), respectively. 45 min of hypoxia increased activity of all three MAPKs, 10 min of reperfusion lead to a further increase in their activities. After 2 h of reperfusion JNK and p38 activity had ceased while ERK activity still had not returned to control levels. Data are expressed as mean ± SEM (n = 3, all **P < 0.01). In the case of primary cardiomyocytes a single experiment was performed.

Journal: Transplant international : official journal of the European Society for Organ Transplantation

Article Title: Intracellular signaling pathways control mitochondrial events associated with the development of ischemia/ reperfusion-associated damage.

doi: 10.1111/j.1432-2277.2009.00883.x

Figure Lengend Snippet: Figure 1 Alterations in MAPK activity are associated with IR or HR. Representative immunoblots (a, c, e) and a summary graph (b, d) are shown. (a, b). Three animals undergoing heterotopic heart transplantation were analysed in each group. Treatment conditions were as follows: Co, untreated animals; H, 45 min of ischemia; R1-R4, hearts exposed to 45 min of ischemia and either 10 min (R1), 2 h (R2), 12 h (R3), 24 h (R4) or 48 h (R5), of reperfusion. BALB/c mouse heart lysates display low levels of ERK1,2 activity in the control group (Co). 45 min of ischemia increased stress kinase activity (p38: 4.6-fold increase, *P < 0.05 vs. control; JNK: 9.4-fold increase, *P < 0.05 vs. control) but left ERK 1,2 unaf- fected. 10 min of reperfusion (R1) caused a significant increase in ERK activity (ERK1,2: 8.4-fold increase, **P < 0.01 vs. control), and a further increase in p38 (p38: 9.4-fold increase, **P < 0.01 vs. control) and JNK (JNK1,2: 57.7-fold increase, **P < 0.01 vs. control) activity. After 2 h of reperfusion (R2) JNK (JNK1,2: 2.6-fold increase) and p38 (p38: 0.6-fold) activity had returned to control (Co) levels, while ERK (ERK1,2: 4.8-fold increase) activation still did not return to prereperfusion levels and stayed above levels in control hearts until the end of the observation period (ERK1,2: 2.73-fold increase). Data are expressed as mean ± SEM (of n = 3). (c–e) Changes in MAPK signaling in HL-1 cells and primary BALB/c car- diomyocytes subjected to 45 min of hypoxia (0.5% O2, 37 C, serum-/glucose-free medium) and up to 48 h of reoxygenation. The treatment conditions were as follows: Co, untreated cells; H, 45 min of hypoxia R1-R4: hypoxia (45 min) followed by reoxygenation in growth medium for 10 min (R1), 2 h (R2), 24 h (R3) or 48 h (R4), respectively. 45 min of hypoxia increased activity of all three MAPKs, 10 min of reperfusion lead to a further increase in their activities. After 2 h of reperfusion JNK and p38 activity had ceased while ERK activity still had not returned to control levels. Data are expressed as mean ± SEM (n = 3, all **P < 0.01). In the case of primary cardiomyocytes a single experiment was performed.

Article Snippet: Immunoblots were probed with the following antibodies: phospho-ERK (sc-7383; Santa Cruz Biotechnology, Santa Cruz, CA, USA), phospho JNK (AF-1205; R&D Systems, Minneapolis, MN, USA) or phospho-p38 (9211S, Cell Signaling, Danvers, MA, USA).

Techniques: Activity Assay, Western Blot, Transplantation Assay, Control, Activation Assay