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Data set for transcriptional response to depletion of the Shoc2 scaffolding protein

Eric C Rouchka1, Myoungkun Jeoung2, Eun Ryoung Jang2

  • 1Department of Computer Engineering and Computer Science, University of Louisville, Louisville, KY 40292, United States; Kentucky Biomedical Research Infrastructure Network Bioinformatics Core, University of Louisville, Louisville, KY 40292, United States.

Data in Brief
|April 15, 2016
PubMed

Insights

The scaffold protein SHOC2 (Suppressor of Clear, Caenorhabditis elegans Homolog) influences the RAS/ERK1/2 pathway. This study details gene expression changes in SHOC2-depleted cells, revealing insights into ERK1/2 signaling.

Area of Science:

  • Molecular Biology
  • Cell Signaling
  • Genomics

Background:

  • The Suppressor of Clear, Caenorhabditis elegans Homolog (SHOC2) functions as a scaffold protein.
  • SHOC2 positively regulates the RAS/ERK1/2 MAP kinase signaling cascade.

Purpose of the Study:

  • To investigate the transcriptional response of the ERK1/2 pathway mediated by the SHOC2 scaffolding module.
  • To characterize gene expression changes in cells with and without SHOC2 following Epidermal Growth Factor Receptor (EGFR) activation.

Main Methods:

  • Utilized RNA sequencing to analyze gene expression profiles.
  • Compared gene expression in Cos1 cells expressing non-targeting shRNA (Cos-NT) versus SHOC2-depleted Cos1 cells (Cos-LV1).
  • Stimulated the ERK1/2 pathway using Epidermal Growth Factor Receptor (EGFR) activation.

Main Results:

  • Generated raw gene expression data for Cos-NT and Cos-LV1 cell lines.
  • Data includes triplicates for each condition, providing a robust dataset for analysis.
  • The dataset captures the transcriptional landscape of SHOC2-dependent ERK1/2 signaling.

Conclusions:

  • This data article provides a foundational dataset for understanding SHOC2's role in ERK1/2 signaling.
  • The raw gene expression data is publicly available for further research and analysis.
  • Facilitates deeper investigation into SHOC2-mediated transcriptional regulation in cellular signaling pathways.

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