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Status |
Public on Oct 05, 2018 |
Title |
TRIM28 protects TRIM24 from SPOP-mediated degradation and promotes prostate cancer progression [ChIP-seq] |
Organism |
Homo sapiens |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
|
Summary |
In this study, proteomic profiling of TRIM24 interactome in conjunction with shRNA screening of TRIM24 top-interactors nominated that TRIM28 is indispensable for TRIM24 protein stability. We showed that TRIM28 stabilizes TRIM24 against SPOP-mediated ubiquitination and degradation. TRIM28 promotes TRIM24 and AR transcription activity, androgen-dependent and -independent PCa growth. In addition, we demonstrated that TRIM28 level in high in advanced PCa, which drives TRIM24/AR transcription activity in a similar manner to SPOP mutation, which implies that TRIM28 potentially dictates the therapeutic outcome of TRIM24-targeted therapy.
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Overall design |
genetic modification design
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Contributor(s) |
Yu J, Fong K |
Citation(s) |
30479348 |
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Submission date |
Dec 15, 2017 |
Last update date |
Feb 04, 2020 |
Contact name |
Jindan Yu |
E-mail(s) |
jindan.yu@emory.edu
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Organization name |
Emory University
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Department |
Urology
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Lab |
Jindan Yu's lab
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Street address |
E330, 1760 Haygood Dr NE
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City |
Atlanta |
State/province |
GA |
ZIP/Postal code |
30322 |
Country |
USA |
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Platforms (1) |
GPL15456 |
Illumina HiScanSQ (Homo sapiens) |
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Samples (7)
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This SubSeries is part of SuperSeries: |
GSE108146 |
TRIM28 protects TRIM24 from SPOP-mediated degradation and promotes prostate cancer progression |
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Relations |
BioProject |
PRJNA422654 |
SRA |
SRP126894 |