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Hepatic SILAC proteomic data from PANDER transgenic model.

Mark G Athanason1, Stanley M Stevens1, Brant R Burkhardt1

  • 1University of South Florida, Department of Cell Biology, Microbiology and Molecular Biology, USA.

Data in Brief
|September 20, 2016
PubMed
Summary
This summary is machine-generated.

This study used proteomic analysis to investigate the PANDER transgenic mouse model, revealing significant alterations in hepatic lipogenesis and Liver X Receptor activation. These findings offer insights into metabolic dysregulation in this PANDER transgenic model.

Keywords:
FAM3BLipogenesisLiverPANDERProteomicsTransgenic

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Area of Science:

  • Proteomics
  • Metabolomics
  • Molecular Biology

Background:

  • The PANcreatic-Derived factor (PANDER) transgenic mouse (PANTG) model exhibits altered metabolic states.
  • Understanding hepatic lipogenesis and Liver X Receptor (LXR) activation is crucial for metabolic research.

Purpose of the Study:

  • To quantitatively profile the proteome of PANTG mouse livers.
  • To identify changes in hepatic lipogenesis and LXR activation in PANTG mice under various metabolic conditions.

Main Methods:

  • "Spike-in" SILAC-based proteomic analysis of liver tissues from PANTG and wild-type mice.
  • Mass spectrometry data processed using MaxQuant with the Andromeda search algorithm against the Mus musculus UniprotKB database.
  • Statistical significance determined using the Significance A outlier test in Perseus software.

Main Results:

  • Quantitative proteomic profiling revealed significant alterations in hepatic lipogenesis pathways.
  • Evidence of Liver X Receptor (LXR) pathway activation was identified in PANTG mice.
  • Ingenuity Pathway Analysis identified altered pathways and upstream regulators in PANTG mice.

Conclusions:

  • Proteomic data provides a comprehensive view of metabolic changes in the PANDER transgenic mouse model.
  • The study highlights the role of PANDER in regulating hepatic lipogenesis and LXR activation.
  • These findings contribute to understanding the molecular mechanisms underlying metabolic dysregulation in PANTG mice.