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We are analyzing https://link.springer.com/article/10.1186/1471-213x-3-11.

Title:
Knockout of ERK5 causes multiple defects in placental and embryonic development | BMC Developmental Biology
Description:
Backgroud ERK5 is a member of the mitogen activated protein kinase family activated by certain mitogenic or stressful stimuli in cells, but whose physiological role is largely unclear. Results To help determine the function of ERK5 we have used gene targeting to inactivate this gene in mice. Here we report that ERK5 knockout mice die at approximately E10.5. In situ hybridisation for ERK5, and its upstream activator MKK5, showed strong expression in the head and trunk of the embryo at this stage of development. Between E9.5 and E10.5, multiple developmental problems are seen in the ERK5-/- embryos, including an increase in apoptosis in the cephalic mesenchyme tissue, abnormalities in the hind gut, as well as problems in vascular remodelling, cardiac development and placental defects. Conclusion Erk5 is essential for early embryonic development, and is required for normal development of the vascular system and cell survival.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Science
  • Health & Fitness

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

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Traffic Estimate {πŸ“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? {πŸ’Έ}

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Keywords {πŸ”}

erk, embryos, pubmed, type, wild, development, article, google, scholar, cas, expression, knockout, cephalic, mesenchyme, blood, mice, fig, embryonic, kinase, heart, vessels, sections, placental, protein, cells, cell, figure, head, mkk, showed, problems, region, placentas, analysis, cardiac, biol, authors, embryo, apoptosis, reported, knockouts, compared, central, defects, full, role, gene, situ, angiogenesis, size,

Topics {βœ’οΈ}

mitogen-activated protein kinase adapter protein lad/ribp article download pdf thr-xaa-tyr motif protein kinase erk5/bmk1 open access license mapk kinase kinase normal post-natal growth epidermal growth factor strain-independent postnatal neurodegeneration intraplacental yolk sac/sinus oxidative stress-mediated activation mek1-deficient mice reveals kinase inhibitors pd184352 full size image thymidine kinase cassette p38alpha map kinase mek5-bmk1/erk5 pathway ventricular muscle-restricted targeting authors’ original file redox-sensitive kinase yolk sacs separated cell proliferation induced privacy choices/manage cookies chorionic plate erk5-/- yolk sacs map kinase p38 full access related subjects receptor tyrosine kinases developmental biology mekk2 activate mkk5 erk1/2 kinase activation metastatic prostate cancer stress-induced phosphorylation upstream kinase mkk5 article yan transcription factor mef2c rxralpha gene reveals smooth muscle cells general growth retardation large blood vessels early embryonic development neuregulin signal transduction positive cell lines temporally specific pattern trophoblast-specific cdna negative selection marker dominant negative effect erk5-/- mutant yolk

Schema {πŸ—ΊοΈ}

WebPage:
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         headline:Knockout of ERK5 causes multiple defects in placental and embryonic development
         description:ERK5 is a member of the mitogen activated protein kinase family activated by certain mitogenic or stressful stimuli in cells, but whose physiological role is largely unclear. To help determine the function of ERK5 we have used gene targeting to inactivate this gene in mice. Here we report that ERK5 knockout mice die at approximately E10.5. In situ hybridisation for ERK5, and its upstream activator MKK5, showed strong expression in the head and trunk of the embryo at this stage of development. Between E9.5 and E10.5, multiple developmental problems are seen in the ERK5-/- embryos, including an increase in apoptosis in the cephalic mesenchyme tissue, abnormalities in the hind gut, as well as problems in vascular remodelling, cardiac development and placental defects. Erk5 is essential for early embryonic development, and is required for normal development of the vascular system and cell survival.
         datePublished:2003-12-16T00:00:00Z
         dateModified:2003-12-16T00:00:00Z
         pageStart:1
         pageEnd:21
         sameAs:https://doi.org/10.1186/1471-213X-3-11
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            Placental Development
            ERK5 Protein
            Chorionic Plate
            Mitogen Activate Protein Kinase Kinase Kinase
            Developmental Biology
            Animal Models
            Life Sciences
            general
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      headline:Knockout of ERK5 causes multiple defects in placental and embryonic development
      description:ERK5 is a member of the mitogen activated protein kinase family activated by certain mitogenic or stressful stimuli in cells, but whose physiological role is largely unclear. To help determine the function of ERK5 we have used gene targeting to inactivate this gene in mice. Here we report that ERK5 knockout mice die at approximately E10.5. In situ hybridisation for ERK5, and its upstream activator MKK5, showed strong expression in the head and trunk of the embryo at this stage of development. Between E9.5 and E10.5, multiple developmental problems are seen in the ERK5-/- embryos, including an increase in apoptosis in the cephalic mesenchyme tissue, abnormalities in the hind gut, as well as problems in vascular remodelling, cardiac development and placental defects. Erk5 is essential for early embryonic development, and is required for normal development of the vascular system and cell survival.
      datePublished:2003-12-16T00:00:00Z
      dateModified:2003-12-16T00:00:00Z
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      pageEnd:21
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         Wild Type Embryo
         Placental Development
         ERK5 Protein
         Chorionic Plate
         Mitogen Activate Protein Kinase Kinase Kinase
         Developmental Biology
         Animal Models
         Life Sciences
         general
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                  address:
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            affiliation:
                  name:University of Dundee
                  address:
                     name:Faculty of Life Sciences, University of Dundee, Dundee, UK
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Calum Thompson
            affiliation:
                  name:University of Dundee
                  address:
                     name:CHIPS, University of Dundee, Dundee, UK
                     type:PostalAddress
                  type:Organization
            type:Person
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                  address:
                     name:MRC Protein Phosphorylation Unit, University of Dundee, Dundee, UK
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      affiliation:
            name:University of Dundee
            address:
               name:MRC Protein Phosphorylation Unit, University of Dundee, Dundee, UK
               type:PostalAddress
            type:Organization
      name:Julia Carr
      affiliation:
            name:University of Dundee
            address:
               name:MRC Protein Phosphorylation Unit, University of Dundee, Dundee, UK
               type:PostalAddress
            type:Organization
      name:Peter R Ashby
      affiliation:
            name:University of Dundee
            address:
               name:Division of Cell and Developmental Biology, University of Dundee, Dundee, UK
               type:PostalAddress
            type:Organization
      name:Victoria Murry-Tait
      affiliation:
            name:University of Dundee
            address:
               name:Faculty of Life Sciences, University of Dundee, Dundee, UK
               type:PostalAddress
            type:Organization
      name:Calum Thompson
      affiliation:
            name:University of Dundee
            address:
               name:CHIPS, University of Dundee, Dundee, UK
               type:PostalAddress
            type:Organization
      name:J Simon C Arthur
      affiliation:
            name:University of Dundee
            address:
               name:MRC Protein Phosphorylation Unit, University of Dundee, Dundee, UK
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:MRC Protein Phosphorylation Unit, University of Dundee, Dundee, UK
      name:MRC Protein Phosphorylation Unit, University of Dundee, Dundee, UK
      name:Division of Cell and Developmental Biology, University of Dundee, Dundee, UK
      name:Faculty of Life Sciences, University of Dundee, Dundee, UK
      name:CHIPS, University of Dundee, Dundee, UK
      name:MRC Protein Phosphorylation Unit, University of Dundee, Dundee, UK

External Links {πŸ”—}(198)

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