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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
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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.
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Overall design |
Primary Human Hepatocytes were transduced with either DNAJB1::PRKACA, ATP1B1::PRKACA, PRKACA or kinase inactive DNAJB1::PRKACA or dsRED.
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Contributor(s) |
Requena D, Shirani M, deJong YP, Simon SM |
Citation(s) |
38888469 |
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Submission date |
Jul 18, 2023 |
Last update date |
Sep 12, 2024 |
Contact name |
David Requena |
E-mail(s) |
drequena@rockefeller.edu
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Phone |
(917) 293-6642
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Organization name |
Rockefeller University
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Lab |
Laboratory of Cellular Biophysics
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Street address |
1230 York Avenue
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City |
New York |
State/province |
NY |
ZIP/Postal code |
10065 |
Country |
USA |
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Platforms (1) |
GPL24676 |
Illumina NovaSeq 6000 (Homo sapiens) |
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Samples (15)
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GSM7643721 |
Transduced with ATP1B1::PRKACA sample 1 |
GSM7643722 |
Transduced with ATP1B1::PRKACA sample 2 |
GSM7643723 |
Transduced with ATP1B1::PRKACA sample 3 |
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Relations |
BioProject |
PRJNA996178 |