Pamela Pennington Lockyer
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Also affiliated: University of North Carolina at Chapel Hill (2007–2021); Mayo Clinic (2012); University of North Carolina Health Care (2010–2016); NewYork–Presbyterian Hospital (2017); The University of Texas MD Anderson Cancer Center (2019–2024); North Carolina State University (2010); University of Freiburg (2010–2012); Baylor College of Medicine (2015–2017); Chinese Academy of Medical Sciences & Peking Union Medical College (2011); Mayo Clinic in Florida (2012); UNC Lineberger Comprehensive Cancer Center (2010)
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Biomedical Subjects
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Biography and Research Information
OverviewAI-generated summary
Pamela Pennington Lockyer's research focuses on cellular mechanisms of disease, particularly involving protein degradation pathways and their role in conditions such as aging, cardiac disease, and myelodysplastic syndromes. She investigates the function of ubiquitin-protein ligases, including CHIP and MuRF1, in cellular processes like protein quality control and the response to cellular stress, such as pressure overload in the heart. Her work has explored how deficiencies in these ligases can lead to accelerated aging phenotypes and how their activity can be protective against cardiac ischemia/reperfusion injury.
Furthermore, Lockyer's research extends to the signaling pathways regulated by the LRP1 receptor in endothelial cells. This work has elucidated LRP1's role in angiogenesis, metabolic responses, and its interaction with signaling systems like BMP and PPARγ. More recently, her group has studied stem cell architecture in the context of myelodysplastic syndrome progression and its implications for predicting treatment responses. Lockyer leads a research group at the University of Arkansas for Medical Sciences and has a publication record including work on mouse models and human disease.
Metrics
- h-index: 20
- Publications: 80
- Citations: 1,468
Selected Publications
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Epigenetic dysregulation and therapeutic targeting of RET receptor tyrosine kinase in high‐risk KMT2A ‐rearranged acute myeloid leukaemia (2025)
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Epigenetic Dysregulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in High-Risk KMT2A-Rearranged Pediatric Acute Myeloid Leukemia (2025)
Federal Grants 1 $1 total
Collaboration Network
Top Collaborators
- Epigenetic Dysregulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in High-Risk KMT2A-Rearranged Pediatric Acute Myeloid Leukemia
- Epigenetic dysregulation and therapeutic targeting of RET receptor tyrosine kinase in high‐risk KMT2A ‐rearranged acute myeloid leukaemia
- Epigenetic Dysregulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in High-Risk KMT2A-Rearranged Pediatric Acute Myeloid Leukemia
- Epigenetic dysregulation and therapeutic targeting of RET receptor tyrosine kinase in high‐risk KMT2A ‐rearranged acute myeloid leukaemia
- Epigenetic Dysregulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in High-Risk KMT2A-Rearranged Pediatric Acute Myeloid Leukemia
- Epigenetic dysregulation and therapeutic targeting of RET receptor tyrosine kinase in high‐risk KMT2A ‐rearranged acute myeloid leukaemia
- Epigenetic Dysregulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in High-Risk KMT2A-Rearranged Pediatric Acute Myeloid Leukemia
- Epigenetic dysregulation and therapeutic targeting of RET receptor tyrosine kinase in high‐risk KMT2A ‐rearranged acute myeloid leukaemia
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