PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12487375-6 2002 Furthermore, exposure to acrolein results in activation of members of the mitogen-activated protein kinase (MAPK) family and protein tyrosine kinases. Acrolein 25-33 mitogen activated protein kinase 3 Rattus norvegicus 108-112 12487375-7 2002 The extracellular signal-regulated kinases 1 and 2 (ERK1/2), stress-activated protein kinases/c-jun NH2-terminal kinases (SAPK/JNK) and p38MAPK are effectively and transiently activated by acrolein in a concentration and time-dependent fashion. Acrolein 189-197 mitogen activated protein kinase 3 Rattus norvegicus 4-50 12487375-7 2002 The extracellular signal-regulated kinases 1 and 2 (ERK1/2), stress-activated protein kinases/c-jun NH2-terminal kinases (SAPK/JNK) and p38MAPK are effectively and transiently activated by acrolein in a concentration and time-dependent fashion. Acrolein 189-197 mitogen activated protein kinase 3 Rattus norvegicus 52-58 12487375-8 2002 While all three MAPKs exhibit significant activation within 5 min of exposure to acrolein, maximum activation (ERK1/2 and p38MAPK) or close to maximum activation (SAPK/JNK) occurs on exposure to 5 microg/ml acrolein for 2 h. Acrolein-induced activation of MAPKs is further substantiated by the activation of transcription factors, c-jun and activator transcription factor-2 (ATF-2), by acrolein-activated SAPK/JNK and p38MAPK, respectively. Acrolein 207-215 mitogen activated protein kinase 3 Rattus norvegicus 111-117 12487375-16 2002 These results provide the first evidence that the activation of both growth-regulated (ERK1/2) and stress-regulated (SAPK/JNK and p38MAPK) MAPKs as well as tyrosine kinases are involved in the mediation of acrolein-induced effects on VSMC, which may play a crucial role in vascular pathogenesis due to environmentally and endogenously produced acrolein. Acrolein 206-214 mitogen activated protein kinase 3 Rattus norvegicus 87-93 12487375-16 2002 These results provide the first evidence that the activation of both growth-regulated (ERK1/2) and stress-regulated (SAPK/JNK and p38MAPK) MAPKs as well as tyrosine kinases are involved in the mediation of acrolein-induced effects on VSMC, which may play a crucial role in vascular pathogenesis due to environmentally and endogenously produced acrolein. Acrolein 344-352 mitogen activated protein kinase 3 Rattus norvegicus 87-93 21422526-10 2011 Acrolein also induced the phosphorylation of p66shc and of ERK1/2 after 30 min of treatment. Acrolein 0-8 mitogen activated protein kinase 3 Rattus norvegicus 59-65