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December 21, 2005Physiological Genomics

Distinct gene expression profiles in adult mouse heart following targeted MAP kinase activation

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Population

Three transgenic adult mouse models with cardiac-specific and temporally regulated expression of activated…

Design

Preclinical

Follow-up

4-7 days (early) and 2-4 weeks (late)

Authors

SMScherise MitchellAOAsuka OtaWFWilliam Foster

Discussion

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Overview

Hypothesis-generating for MAPK pathway targeting in hypertrophy; leaves open clinical translation pending human validation.

Structured PICO

P
Population
Three transgenic adult mouse models with cardiac-specific and temporally regulated expression of activated mutants of Ras, MKK3, and MKK7
I
Intervention
Transgene induction to activate ERK, p38, and JNK MAP kinase cascades
O
Outcome
Gene expression profiles determined using cDNA microarrayssurrogate

The study maps the distinct and shared gene expression profiles driven by ERK, p38, and JNK pathways in the adult heart, providing insights into their roles in cardiac hypertrophy and heart failure.

Cite This Study

Mitchell et al. (2005) studied this question.

synapsesocial.com/papers/6a7029a9f44fa9f079ddb898https://doi.org/10.1152/physiolgenomics.00224.2005
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Temporal activation of c‐Jun N‐terminal kinase in adult transgenic heart via cre‐loxP‐mediated DNA recombination2003 · 83 citations
  2. 2Cardiac Hypertrophy Induced by Mitogen-activated Protein Kinase Kinase 7, a Specific Activator for c-Jun NH2-terminal Kinase in Ventricular Muscle Cells1998 · 338 citations
  3. 3Role of the stress-activated protein kinases in endothelin-induced cardiomyocyte hypertrophy.1998 · 195 citations
  4. 4Sarcoplasmic reticulum calcium defect in Ras-induced hypertrophic cardiomyopathy heart2004 · 91 citations
  5. 5The Molecular Mechanism of Cardiac Hypertrophy and Failure1999 · 52 citations