Ana Clara P. Azevedo‐Pouly
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Also affiliated: United States Food and Drug Administration (2019–2022); University of Utah (2017); University of Florida (2022); Arkansas Children's Research Institute (2021–2026); The Ohio State University (2011–2017); The University of Texas Southwestern Medical Center (2016–2023)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Ana Clara P. Azevedo‐Pouly's research focuses on understanding the molecular mechanisms regulating cell identity and homeostasis, particularly in the context of pancreatic development and cancer. Her work has investigated the roles of key transcription factors, such as PTF1A and MIST1, in maintaining the pancreatic acinar phenotype in adult mice. Azevedo‐Pouly has also explored the involvement of microRNAs in cancer, including their potential as therapeutic agents and their function in regulating tumor suppressor genes in breast cancer. Her research utilizes various model systems, including mice and cell lines, and employs techniques for RNA isolation from challenging tissues. She has a record of 34 publications, with an h-index of 13 and 786 citations. Azevedo‐Pouly collaborates with researchers at the University of Arkansas for Medical Sciences, including Randall R Rainwater, Brian Koss, Lauren Appell, and Melanie Barker.
Metrics
- h-index: 13
- Publications: 35
- Citations: 790
Selected Publications
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DNA-PKcs Controls the Cytotoxic T-Cell Response to Cancer and Transplant Allograft Through Regulating LAT-Dependent Signaling (2025)
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DNA-PKcs governs LAT-dependent signaling in CD4 + and CD8 + T cells (2025)
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The use of DNAPK inhibitors increases the efficacy of Lentiviral vectors and decreases off-target effects. (2024)
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Discovery of the DNA-PKcs inhibitor DA-143 which exhibits enhanced solubility relative to NU7441 (2024)
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Chemical inhibition of DNA‐PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells (2023)
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DNA-PKcs is required for the activation and cytotoxicity of CD8+ effector T cells (2022)
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Potential role of the apelin‐APJ pathway in sex‐related differential cardiotoxicity induced by doxorubicin in mice (2022)
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Pharmacological inhibition and reversal of pancreatic acinar ductal metaplasia (2022)
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Inhibition of DNA-PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells (2022)
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DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells (2021)
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DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells (2021)
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Concerted cell and in vivo screen for pancreatic ductal adenocarcinoma (PDA) chemotherapeutics (2020)
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Knockout of Acinar Enriched microRNAs in Mice Promote Duct Formation But Not Pancreatic Cancer (2019)
Collaboration Network
Top Collaborators
- DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells
- Chemical inhibition of DNA‐PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
- Discovery of the DNA-PKcs inhibitor DA-143 which exhibits enhanced solubility relative to NU7441
- DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells
- Inhibition of DNA-PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
Showing 5 of 9 shared publications
- DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells
- Chemical inhibition of DNA‐PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
- Discovery of the DNA-PKcs inhibitor DA-143 which exhibits enhanced solubility relative to NU7441
- DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells
- Inhibition of DNA-PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
Showing 5 of 9 shared publications
- DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells
- Chemical inhibition of DNA‐PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
- Discovery of the DNA-PKcs inhibitor DA-143 which exhibits enhanced solubility relative to NU7441
- DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells
- Inhibition of DNA-PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
Showing 5 of 8 shared publications
- DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells
- DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells
- DNA-PKcs governs LAT-dependent signaling in CD4 + and CD8 + T cells
- DNA-PKcs Controls the Cytotoxic T-Cell Response to Cancer and Transplant Allograft Through Regulating LAT-Dependent Signaling
- Chemical inhibition of DNA‐PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
- Inhibition of DNA-PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
- DNA-PKcs governs LAT-dependent signaling in CD4 + and CD8 + T cells
- DNA-PKcs Controls the Cytotoxic T-Cell Response to Cancer and Transplant Allograft Through Regulating LAT-Dependent Signaling
- Chemical inhibition of DNA‐PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
- Inhibition of DNA-PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
- DNA-PKcs is required for the activation and cytotoxicity of CD8+ effector T cells
- Chemical inhibition of DNA‐PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
- Inhibition of DNA-PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
- DNA-PKcs is required for the activation and cytotoxicity of CD8+ effector T cells
- Chemical inhibition of DNA‐PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
- Discovery of the DNA-PKcs inhibitor DA-143 which exhibits enhanced solubility relative to NU7441
- DNA-PKcs governs LAT-dependent signaling in CD4 + and CD8 + T cells
- Pharmacological inhibition and reversal of pancreatic acinar ductal metaplasia
- Knockout of Acinar Enriched microRNAs in Mice Promote Duct Formation But Not Pancreatic Cancer
- Pharmacological inhibition and reversal of pancreatic acinar ductal metaplasia
- Knockout of Acinar Enriched microRNAs in Mice Promote Duct Formation But Not Pancreatic Cancer
- DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells
- DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells
- DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells
- DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells
- DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells
- DNA-PKcs kinase activity stabilizes the transcription factor Egr1 in activated immune cells
- Chemical inhibition of DNA‐PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
- Inhibition of DNA-PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
- Chemical inhibition of DNA‐PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
- Inhibition of DNA-PKcs impairs the activation and cytotoxicity of CD4 + helper and CD8 + effector T cells
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