Seongok Lee
Post Doctoral Fellow
postdoc
Radiation Oncology, College of Medicine
Research Areas
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Biography and Research Information
OverviewAI-generated summary
Seongok Lee's research focuses on cellular mechanisms related to DNA repair, protein homeostasis, and organ transplantation. Lee has investigated the role of ZMYM2 in restricting 53BP1 at DNA double-strand breaks to facilitate BRCA1 loading and homologous recombination, and the regulation of 53BP1 recruitment at damaged chromatin by evolved histone tails. Further work examines how UBA80 and UBA52 influence RNF168-dependent histone ubiquitination and DNA repair. In the context of transplantation, Lee's work includes studying the immunoproteasome in rat kidney allografts and its impact on function after cold storage and transplantation. Research also explores the role of Complement 5 in mitochondria during kidney ischemia-reperfusion injury in rats and the mitigation of post-ischemia and reperfusion kidney injury in complement 5 knockout rats. Lee's scholarship includes 13 publications with 123 citations and an h-index of 3.
Metrics
- h-index: 3
- Publications: 14
- Citations: 124
Selected Publications
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Complement 5's Role in Mitochondria During Kidney Ischemia-Reperfusion Injury in Rats (2025)
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Post‐ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat (2025)
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Mechanism of Impaired Protein Homeostasis in Kidney Grafts Following Cold Storage and Transplantation (Abstract ID: 162640) (2025)
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Ischemia and Reperfusion (IRI)-Induced Kidney Injury Is Attenuated by Complement 5 Gene Deletion (Abstract ID: 161749) (2025)
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Mechanism of Impaired Protein Homeostasis in Kidney Grafts following Cold Storage and Transplant (2024)
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Evolved histone tail regulates 53BP1 recruitment at damaged chromatin (2024)
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Normal Proteasome Function Is Needed to Prevent Kidney Graft Injury during Cold Storage Followed by Transplantation (2024)
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Cold Storage Followed by Transplantation Induces Immunoproteasome in Rat Kidney Allografts: Inhibition of Immunoproteasome Does Not Improve Function (2024)
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Ischemia-Reperfusion-Mediated Kidney Injury Is Attenuated in a New Complement 5 Knockout Model (2023)
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Cold Storage-Mediated p38MAPK Activation: A Potential Contributor of Proteasome Dysfunction and Kidney Damage After Transplantation (2023)
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Mechanism of Cold Storage-Mediated Regulation of Heat Shock Proteins in Renal Grafts After Transplantation (2023)
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UBA80 and UBA52 fine-tune RNF168-dependent histone ubiquitination and DNA repair (2023)
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ZMYM2 restricts 53BP1 at DNA double-strand breaks to favor BRCA1 loading and homologous recombination (2022)
Collaboration Network
Top Collaborators
- Mechanism of Cold Storage-Mediated Regulation of Heat Shock Proteins in Renal Grafts After Transplantation
- Cold Storage-Mediated p38MAPK Activation: A Potential Contributor of Proteasome Dysfunction and Kidney Damage After Transplantation
- Ischemia-Reperfusion-Mediated Kidney Injury Is Attenuated in a New Complement 5 Knockout Model
- Mechanism of Impaired Protein Homeostasis in Kidney Grafts following Cold Storage and Transplant
- Ischemia and Reperfusion (IRI)-Induced Kidney Injury Is Attenuated by Complement 5 Gene Deletion (Abstract ID: 161749)
Showing 5 of 8 shared publications
- Cold Storage-Mediated p38MAPK Activation: A Potential Contributor of Proteasome Dysfunction and Kidney Damage After Transplantation
- Ischemia-Reperfusion-Mediated Kidney Injury Is Attenuated in a New Complement 5 Knockout Model
- Ischemia and Reperfusion (IRI)-Induced Kidney Injury Is Attenuated by Complement 5 Gene Deletion (Abstract ID: 161749)
- Post‐ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat
- Complement 5's Role in Mitochondria During Kidney Ischemia-Reperfusion Injury in Rats
- Ischemia-Reperfusion-Mediated Kidney Injury Is Attenuated in a New Complement 5 Knockout Model
- Ischemia and Reperfusion (IRI)-Induced Kidney Injury Is Attenuated by Complement 5 Gene Deletion (Abstract ID: 161749)
- Post‐ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat
- Complement 5's Role in Mitochondria During Kidney Ischemia-Reperfusion Injury in Rats
- 725-P: Low Fasting Glucose and Insulin Deficiency Were Related with Superiority of Insulin Degludec/Aspart Compared with Basal Insulin in Patients with Type 2 Diabetes
- 834-P: A Prospective Study on Switching from Basal Insulin to Insulin Degludec/Insulin Aspart, in Patients with Type 2 Diabetes Whose FPG Levels Are Lower Than Those Predicted by Their HbA1c
- 725-P: Low Fasting Glucose and Insulin Deficiency Were Related with Superiority of Insulin Degludec/Aspart Compared with Basal Insulin in Patients with Type 2 Diabetes
- 834-P: A Prospective Study on Switching from Basal Insulin to Insulin Degludec/Insulin Aspart, in Patients with Type 2 Diabetes Whose FPG Levels Are Lower Than Those Predicted by Their HbA1c
- Mechanism of Impaired Protein Homeostasis in Kidney Grafts Following Cold Storage and Transplantation (Abstract ID: 162640)
- Post‐ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat
- Post‐ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat
- Complement 5's Role in Mitochondria During Kidney Ischemia-Reperfusion Injury in Rats
- Post‐ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat
- Complement 5's Role in Mitochondria During Kidney Ischemia-Reperfusion Injury in Rats
- 725-P: Low Fasting Glucose and Insulin Deficiency Were Related with Superiority of Insulin Degludec/Aspart Compared with Basal Insulin in Patients with Type 2 Diabetes
- 725-P: Low Fasting Glucose and Insulin Deficiency Were Related with Superiority of Insulin Degludec/Aspart Compared with Basal Insulin in Patients with Type 2 Diabetes
- 725-P: Low Fasting Glucose and Insulin Deficiency Were Related with Superiority of Insulin Degludec/Aspart Compared with Basal Insulin in Patients with Type 2 Diabetes
- 834-P: A Prospective Study on Switching from Basal Insulin to Insulin Degludec/Insulin Aspart, in Patients with Type 2 Diabetes Whose FPG Levels Are Lower Than Those Predicted by Their HbA1c
- 834-P: A Prospective Study on Switching from Basal Insulin to Insulin Degludec/Insulin Aspart, in Patients with Type 2 Diabetes Whose FPG Levels Are Lower Than Those Predicted by Their HbA1c
- 834-P: A Prospective Study on Switching from Basal Insulin to Insulin Degludec/Insulin Aspart, in Patients with Type 2 Diabetes Whose FPG Levels Are Lower Than Those Predicted by Their HbA1c
- 834-P: A Prospective Study on Switching from Basal Insulin to Insulin Degludec/Insulin Aspart, in Patients with Type 2 Diabetes Whose FPG Levels Are Lower Than Those Predicted by Their HbA1c
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