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  2. Matching Content Categories
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  4. Monthly Traffic Estimate
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We are analyzing https://link.springer.com/article/10.1007/s00395-005-0566-z.

Title:
Localizing extracellular signal–regulated kinase (ERK) in pharmacological preconditioning's trigger pathway | Basic Research in Cardiology
Description:
Acetylcholine (ACh) and opioid receptor agonists trigger the preconditioned phenotype through sequential activation of the epidermal growth factor (EGF) receptor, phosphatidylinositol 3-kinase (PI3-K), Akt, and nitric oxide synthase (NOS), and opening of mitochondrial (mito) KATP channels with the generation of reactive oxygen species (ROS). Although extracellular signal–regulated kinase (ERK) has recently been reported to be part of this pathway, its location has not been determined. To address this issue, we administered a 5–min pulse of ACh (550 µM) prior to 30 min of ischemia in isolated rabbit hearts. It reduced infarction from 30.4 ± 2.2% of the risk zone in control hearts to 12.3 ± 2.8% and co–administration of the MEK, and, therefore, downstream ERK inhibitor U0126 abolished protection (29.1 ± 4.6% infarction) con.rming ERK
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Education
  • Science
  • Telecommunications

Content Management System {šŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {šŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {šŸ’ø}

We're unsure if the website is profiting.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {šŸ”}

google, scholar, cas, article, downey, cohen, pubmed, erk, ros, kinase, res, critz, mitochondrial, production, preconditioning, philipp, opening, physiol, research, acetylcholine, receptor, activation, akt, nos, katp, channels, signalling, privacy, cookies, content, basic, extracellular, trigger, pathway, cui, ach, rabbit, bradykinin, access, cardiovasc, cardiol, qin, alabama, data, publish, search, signalregulated, egf, generation, hearts,

Topics {āœ’ļø}

met5-enkephalin-induced cardioprotection occurs extracellular signal–regulated kinase month download article/chapter Ī“1-opioid receptor-induced cardioprotection Ī“-opioid agonist dadle article basic research adenosine activate pi3-kinase nitric oxide synthase full article pdf privacy choices/manage cookies mitokatp channel opening u0126 blocked phosphorylation preconditioning- induced protection adult rabbit cardiomyocytes mek inhibitors u0126 related subjects bradykinin-induced preconditioning placing erk downstream measuring ros production generating mitochondrial ros mitochondrial katp channels increased ros production mitochondrial ros generation tyrosine kinase-dependent european economic area scope submit manuscript epidermal growth factor reactive oxygen species atpsensitive potassium channels bradykinin trigger preconditioning 4-dihydroxybenzoate protect myocardium receptor tyrosine kinases conditions privacy policy isolated rabbit cardiomyocytes adenosine antagonist spt generating free radicals inhibitor wortmannin blocked src-kinase activation egfr tyrosine kinase protein–coupled agonists placing erk upstream myocardial infarction van winkle dm pro-survival kinases activating prosurvival kinases accepting optional cookies protein kinase akt acetylcholineinduced production gi proteins isolated rabbit hearts

Schema {šŸ—ŗļø}

WebPage:
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         headline:Localizing extracellular signal–regulated kinase (ERK) in pharmacological preconditioning's trigger pathway
         description:Acetylcholine (ACh) and opioid receptor agonists trigger the preconditioned phenotype through sequential activation of the epidermal growth factor (EGF) receptor, phosphatidylinositol 3-kinase (PI3-K), Akt, and nitric oxide synthase (NOS), and opening of mitochondrial (mito) KATP channels with the generation of reactive oxygen species (ROS). Although extracellular signal–regulated kinase (ERK) has recently been reported to be part of this pathway, its location has not been determined. To address this issue, we administered a 5–min pulse of ACh (550 µM) prior to 30 min of ischemia in isolated rabbit hearts. It reduced infarction from 30.4 ± 2.2% of the risk zone in control hearts to 12.3 ± 2.8% and co–administration of the MEK, and, therefore, downstream ERK inhibitor U0126 abolished protection (29.1 ± 4.6% infarction) con.rming ERK's involvement. MitoKATP opening was monitored in adult rabbit cardiomyocytes by measuring ROS production with MitoTracker Red. ROS production was increased by each of three G protein–coupled agonists: ACh (250 µM), bradykinin (BK) (500 nM), and the Ī“-opioid agonist DADLE (20 nM). Co–incubation with the MEK inhibitors U0126 (500 nM) or PD 98059 (10 µM) blocked the increased ROS production seen with all three agonists. Direct activation of its receptor by EGF increased ROS production and PD 98059 blocked that increase, thus placing ERK downstream of the EGF receptor. Desferoxamine (DFO) which opens mitoKATP through direct activation of NOS also increased ROS. PD 98059 could not block DFO–induced ROS production, placing ERK upstream of NOS. In isolated hearts, ACh caused phosphorylation of both Akt and ERK. U0126 blocked phosphorylation of ERK but not of Akt. The PI3–K inhibitor wortmannin blocked both. Together these data indicate that ERK is located between Akt and NOS.
         datePublished:2005-11-11T00:00:00Z
         dateModified:2005-11-11T00:00:00Z
         pageStart:159
         pageEnd:167
         sameAs:https://doi.org/10.1007/s00395-005-0566-z
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ScholarlyArticle:
      headline:Localizing extracellular signal–regulated kinase (ERK) in pharmacological preconditioning's trigger pathway
      description:Acetylcholine (ACh) and opioid receptor agonists trigger the preconditioned phenotype through sequential activation of the epidermal growth factor (EGF) receptor, phosphatidylinositol 3-kinase (PI3-K), Akt, and nitric oxide synthase (NOS), and opening of mitochondrial (mito) KATP channels with the generation of reactive oxygen species (ROS). Although extracellular signal–regulated kinase (ERK) has recently been reported to be part of this pathway, its location has not been determined. To address this issue, we administered a 5–min pulse of ACh (550 µM) prior to 30 min of ischemia in isolated rabbit hearts. It reduced infarction from 30.4 ± 2.2% of the risk zone in control hearts to 12.3 ± 2.8% and co–administration of the MEK, and, therefore, downstream ERK inhibitor U0126 abolished protection (29.1 ± 4.6% infarction) con.rming ERK's involvement. MitoKATP opening was monitored in adult rabbit cardiomyocytes by measuring ROS production with MitoTracker Red. ROS production was increased by each of three G protein–coupled agonists: ACh (250 µM), bradykinin (BK) (500 nM), and the Ī“-opioid agonist DADLE (20 nM). Co–incubation with the MEK inhibitors U0126 (500 nM) or PD 98059 (10 µM) blocked the increased ROS production seen with all three agonists. Direct activation of its receptor by EGF increased ROS production and PD 98059 blocked that increase, thus placing ERK downstream of the EGF receptor. Desferoxamine (DFO) which opens mitoKATP through direct activation of NOS also increased ROS. PD 98059 could not block DFO–induced ROS production, placing ERK upstream of NOS. In isolated hearts, ACh caused phosphorylation of both Akt and ERK. U0126 blocked phosphorylation of ERK but not of Akt. The PI3–K inhibitor wortmannin blocked both. Together these data indicate that ERK is located between Akt and NOS.
      datePublished:2005-11-11T00:00:00Z
      dateModified:2005-11-11T00:00:00Z
      pageStart:159
      pageEnd:167
      sameAs:https://doi.org/10.1007/s00395-005-0566-z
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         acetylcholine
         bradykinin
         DADLE
         ERK
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         Cardiology
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                  name:University of South Alabama College of Medicine
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                  name:West German Heart Center Essen, University of Duisberg-Essen
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                     name:Department of Cardiology, West German Heart Center Essen, University of Duisberg-Essen, Essen, Germany
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                  name:University of South Alabama College of Medicine
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                     name:Department of Physiology MSB 3074, University of South Alabama College of Medicine, Mobile, USA
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         name:Department of Cell Biology and Neuroscience, University of South Alabama, Mobile, USA
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         name:Department of Physiology MSB 3074, University of South Alabama College of Medicine, Mobile, USA
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               name:Department of Physiology MSB 3074, University of South Alabama College of Medicine, Mobile, USA
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            name:West German Heart Center Essen, University of Duisberg-Essen
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            address:
               name:Department of Cell Biology and Neuroscience, University of South Alabama, Mobile, USA
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            name:University of South Alabama College of Medicine
            address:
               name:Department of Physiology MSB 3074, University of South Alabama College of Medicine, Mobile, USA
               type:PostalAddress
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      name:V. Solodushko
      affiliation:
            name:University of South Alabama College of Medicine
            address:
               name:Department of Physiology MSB 3074, University of South Alabama College of Medicine, Mobile, USA
               type:PostalAddress
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      name:M. V. Cohen
      affiliation:
            name:University of South Alabama College of Medicine
            address:
               name:Department of Physiology MSB 3074, University of South Alabama College of Medicine, Mobile, USA
               type:PostalAddress
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            address:
               name:Departments of Physiology and Medicine, College of Medicine, University of South Alabama, Mobile, USA
               type:PostalAddress
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      name:J. M. Downey
      affiliation:
            name:University of South Alabama College of Medicine
            address:
               name:Department of Physiology MSB 3074, University of South Alabama College of Medicine, Mobile, USA
               type:PostalAddress
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      email:[email protected]
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      name:Department of Physiology MSB 3074, University of South Alabama College of Medicine, Mobile, USA
      name:Department of Cardiology, West German Heart Center Essen, University of Duisberg-Essen, Essen, Germany
      name:Department of Cell Biology and Neuroscience, University of South Alabama, Mobile, USA
      name:Department of Physiology MSB 3074, University of South Alabama College of Medicine, Mobile, USA
      name:Department of Physiology MSB 3074, University of South Alabama College of Medicine, Mobile, USA
      name:Department of Physiology MSB 3074, University of South Alabama College of Medicine, Mobile, USA
      name:Departments of Physiology and Medicine, College of Medicine, University of South Alabama, Mobile, USA
      name:Department of Physiology MSB 3074, University of South Alabama College of Medicine, Mobile, USA
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