Sean T. Wickers

ORCID: 0000-0003-2672-2899
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About
Contact & Profiles
Research Areas
  • Protein Degradation and Inhibitors
  • Supramolecular Self-Assembly in Materials
  • RNA Interference and Gene Delivery
  • Heart Failure Treatment and Management
  • Blood Pressure and Hypertension Studies
  • Phosphodiesterase function and regulation
  • Genomics and Chromatin Dynamics
  • Polydiacetylene-based materials and applications
  • Ubiquitin and proteasome pathways

University of Colorado Denver
2015-2016

Denver School of Nursing
2016

University of Colorado System
2016

University of Denver
2016

BRD4 governs pathological cardiac gene expression by binding acetylated chromatin, resulting in enhanced RNA polymerase II (Pol II) phosphorylation and transcription elongation. Here, we describe a signal-dependent mechanism for the regulation of cardiomyocytes. is suppressed microRNA-9 (miR-9), which targets 3′ UTR Brd4 transcript. In response to stress stimuli, miR-9 downregulated, leading derepression enrichment at long-range super-enhancers (SEs) associated with genes. A mimic represses...

10.1016/j.celrep.2016.06.074 article EN cc-by-nc-nd Cell Reports 2016-07-16

Self-assembling peptides serve as a versatile tool in stem cell and tissue engineering for advancing next-generation medical therapies.

10.1039/c5bm00550g article EN Biomaterials Science 2016-01-01

BRD4 is a member of the BET family proteins, which contain tandem reader domains (bromodomains) that bind to acetylated histone tails within chromatin. We recently demonstrated JQ1, small molecule prevents BRD4-chromatin interaction, potently blocks pathological cardiac hypertrophy and improves function in pre-clinical models. functions as nodal regulator transcriptional program for by recruiting P-TEFb gene regulatory elements, resulting phosphorylation RNA polymerase II (Pol II),...

10.1161/res.117.suppl_1.131 article EN Circulation Research 2015-07-17
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