A5024746090- PARP inhibition in cancer therapy
- Prostate Cancer Treatment and Research
- DNA Repair Mechanisms
- Cell death mechanisms and regulation
- Estrogen and related hormone effects
- Signaling Pathways in Disease
- Nuclear Structure and Function
- Cancer, Lipids, and Metabolism
- Metal-Catalyzed Oxygenation Mechanisms
- Nanoparticles: synthesis and applications
- Calcium signaling and nucleotide metabolism
- Cancer-related Molecular Pathways
- Pesticide Exposure and Toxicity
- Cellular transport and secretion
- Click Chemistry and Applications
- Toxin Mechanisms and Immunotoxins
- Carcinogens and Genotoxicity Assessment
- RNA Research and Splicing
- Biotin and Related Studies
University of Virginia
2017-2024
Rzeszów University
2013
Abstract Androgen signaling through the androgen receptor (AR) directs gene expression in both normal and prostate cancer cells. regulates multiple aspects of AR life cycle, including its localization post-translational modification, but understanding how modifications are read integrated with activity has been difficult. Here, we show that ADP-ribosylation a nuclear pathway mediated by Parp7. We Parp7 mono-ADP-ribosylates agonist-bound AR, ADP-ribosyl-cysteines within N-terminal domain...
Abstract The Ran GTPase regulates nuclear import and export by controlling the assembly state of transport complexes. This involves direct action RanGTP, which is generated in nucleus chromatin‐associated nucleotide exchange factor, RCC1. interactions with RCC1 contribute to formation a nuclear:cytoplasmic (N:C) protein gradient interphase cells. In previous work, we showed that disrupted fibroblasts from Hutchinson–Gilford progeria syndrome (HGPS) patients. disruption these cells caused...
The ADP-ribosyltransferase PARP7 modulates protein function by conjugating ADP-ribose to the side chains of acceptor amino acids. has been shown affect gene expression in prostate cancer cells and certain other cell types mechanisms that include transcription factor ADP-ribosylation. Here, we use a recently developed catalytic inhibitor PARP7, RBN2397, study effects inhibition androgen receptor (AR)-positive AR-negative cells. We find RBN2397 nanomolar potency for inhibiting androgen-induced...
We have previously demonstrated that checkpoint kinase 2 (CHK2) is a critical negative regulator of androgen receptor (AR) transcriptional activity, prostate cancer (PCa) cell growth, and sensitivity. now uncovered the AR directly interacts with CHK2 ionizing radiation (IR) increases this interaction. This IR-induced increase in AR-CHK2 interactions requires phosphorylation activity. PCa associated mutants impaired activity reduced interactions. The destabilization - induced by variants...
The androgen receptor (AR) tranduces the effects of circulating and tumor-derived androgens to nucleus through ligand-induced changes in protein conformation, localization, engagement with chromatin binding sites. Understanding these events their integration signal transduction is critical for defining how AR drives prostate cancer unveiling pathway features that are amenable therapeutic intervention. Here, we describe a novel post-transcriptional mechanism controls levels on associated gene...
Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | 1479-6848 (online)
<div>Abstract<p>The ADP-ribosyltransferase PARP7 modulates protein function by conjugating ADP-ribose to the side chains of acceptor amino acids. has been shown affect gene expression in prostate cancer cells and certain other cell types mechanisms that include transcription factor ADP-ribosylation. Here, we use a recently developed catalytic inhibitor PARP7, RBN2397, study effects inhibition androgen receptor-positive receptor-negative cells. We find RBN2397 nanomolar potency...
<p>BBQ and FICZ treatment activates AHR signaling in prostate cancer cells</p>
<p>The growth inhibitory effect of RBN2397 in prostate cells is not dependent on TBK1 and JAK1/2 kinase activity</p>
<div><p>The ADP-ribosyltransferase PARP7 modulates protein function by conjugating ADP-ribose to the side chains of acceptor amino acids. has been shown affect gene expression in prostate cancer cells and certain other cell types mechanisms that include transcription factor ADP-ribosylation. Here, we use a recently developed catalytic inhibitor PARP7, RBN2397, study effects inhibition androgen receptor (AR)-positive AR-negative cells. We find RBN2397 nanomolar potency for...
<p>RBN2397 inhibition of prostate cancer cell growth requires PARP7 over-expression</p>
<p>Cell cycle distributions of cell lines treated with RBN2397 plus androgen or AHR agonist</p>
<p>FACS analysis of NCI-H660 cells for detection necrosis and apoptosis</p>
<p>Extendend analysis of PARP7 expression in prostate cancer</p>
<p>The growth inhibitory effect of RBN2397 in prostate cells is not dependent on TBK1 and JAK1/2 kinase activity</p>
<p>FACS analysis of NCI-H660 cells for detection necrosis and apoptosis</p>
<p>Extendend analysis of PARP7 expression in prostate cancer</p>
<p>RBN2397 inhibition of prostate cancer cell growth requires PARP7 over-expression</p>
<p>BBQ and FICZ treatment activates AHR signaling in prostate cancer cells</p>
<p>Cell cycle distributions of cell lines treated with RBN2397 plus androgen or AHR agonist</p>