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Series GSE237697 Query DataSets for GSE237697
Status Public on May 17, 2024
Title Increased activity of protein kinase A, even without DNAJB1, is sufficient to cause Fibrolamellar hepatocellular carcinoma
Organism Homo sapiens
Experiment type Expression profiling by high throughput sequencing
Summary Most fibrolamellar carcinoma (FLC) is driven by a fusion of DNAJB1 and PRKACA, the catalytic subunit of protein kinase A (PKA). Overexpression of DNAJB1::PRKACA, ATP1B1::PRKACA or PRKACA, but not catalytically inactive kinase, caused similar transcriptomic changes of primary human hepatocytes; these recapitulated most changes observed in FLC. This is consistent with the observation that FLC is found in patients missing a regulatory subunit or with a ATP1B1::PRKACA fusion. Thus, the DNAJB1 domain is not required for FLC.
Overall design Primary Human Hepatocytes were transduced with either DNAJB1::PRKACA, ATP1B1::PRKACA, PRKACA or kinase inactive DNAJB1::PRKACA or dsRED.
Contributor(s) Requena D, Shirani M, deJong YP, Simon SM
Citation missing Has this study been published? Please login to update or notify GEO.
Submission date Jul 18, 2023
Last update date May 17, 2024
Contact name David Requena
Phone (917) 293-6642
Organization name Rockefeller University
Lab Laboratory of Cellular Biophysics
Street address 1230 York Avenue
City New York
State/province NY
ZIP/Postal code 10065
Country USA
Platforms (1)
GPL24676 Illumina NovaSeq 6000 (Homo sapiens)
Samples (15)
GSM7643721 Transduced with ATP1B1::PRKACA sample 1
GSM7643722 Transduced with ATP1B1::PRKACA sample 2
GSM7643723 Transduced with ATP1B1::PRKACA sample 3
BioProject PRJNA996178

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Supplementary file Size Download File type/resource
GSE237697_Normalized_Gene_Counts_Annotated.xlsx 10.9 Mb (ftp)(http) XLSX
GSE237697_Raw_Gene_Counts_Annotated.xlsx 6.1 Mb (ftp)(http) XLSX
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Processed data are available on Series record

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