@article{TEXTUAL,
      recid = {9567},
      author = {Johnson, Keven R. and Nicodemus-Johnson, Jessie and  Spindler, Mathew J. and Carnegie, Graeme K.},
      title = {Genome-Wide Gene Expression Analysis Shows AKAP13-Mediated  PKD1 Signaling Regulates the Transcriptional Response to  Cardiac Hypertrophy},
      journal = {PLOS ONE},
      address = {2015-07-20},
      number = {TEXTUAL},
      abstract = {In the heart, scaffolding proteins such as A-Kinase  Anchoring Proteins (AKAPs) play a crucial role in normal  cellular function by serving as a signaling hub for  multiple protein kinases including protein kinase D1  (PKD1). Under cardiac hypertrophic conditions AKAP13  anchored PKD1 activates the transcription factor MEF2  leading to subsequent fetal gene activation and  hypertrophic response. We used an expression microarray to  identify the global transcriptional response in the hearts  of wild-type mice expressing the native form of AKAP13  compared to a gene-trap mouse model expressing a truncated  form of AKAP13 that is unable to bind PKD1 (AKAP13-ΔPKD1).  Microarray analysis showed that AKAP13-ΔPKD1 mice broadly  failed to exhibit the transcriptional profile normally  associated with compensatory cardiac hypertrophy following  trans-aortic constriction (TAC). The identified  differentially expressed genes in WT and AKAP13-ΔPKD1  hearts are vital for the compensatory hypertrophic response  to pressure-overload and include myofilament, apoptotic,  and cell growth/differentiation genes in addition to genes  not previously identified as affected by AKAP13-anchored  PKD1. Our results show that AKAP13-PKD1 signaling is  critical for transcriptional regulation of key contractile,  cell death, and metabolic pathways during the development  of compensatory hypertrophy in vivo.},
      url = {http://knowledge.uchicago.edu/record/9567},
}