Mark Manzano
Asssistant Professor
Also affiliated: Northwestern University (2013–2020); Georgetown University (2010–2016); Georgetown University Medical Center (2010–2014); Winthrop Rockefeller Foundation (2022–2024)
Faculty Researcher
Microbiology & Immunology, College of Medicine
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Mark Manzano, an Assistant Professor in Microbiology & Immunology at the University of Arkansas for Medical Sciences, investigates host-pathogen interactions and biological processes using functional genomics, particularly CRISPR screens. His laboratory's work focuses on Primary Effusion Lymphoma (PEL), an aggressive B cell cancer associated with the Kaposi’s sarcoma-associated herpesvirus (KSHV/HHV8). PEL cells depend on viral genes that alter host gene expression to promote tumor cell proliferation and survival. Manzano's research has identified over 200 host genes essential for PEL cell growth and survival, aiming to elucidate their specific functions within B cell lymphoma.
Utilizing CRISPR/Cas9, CRISPRi, and CRISPRa technologies, his lab conducts genome-wide screens to uncover functional genetic interactions and identify synthetic lethality and rescue pathways. This unbiased approach seeks to reveal novel therapeutic targets and understand the molecular mechanisms underlying KSHV latency and KSHV-transformed cell line dependence on specific host genes, such as MCL1. Manzano has secured significant federal funding for his research, including multiple NIH grants totaling over $1.3 million, focusing on KSHV pathogenesis, oncogenic roles of viral genes, and epigenetic regulation of viral latency.
Metrics
- h-index: 15
- Publications: 32
- Citations: 1,340
Selected Publications
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Cytotoxicity of activator expression in CRISPR-based transcriptional activation systems (2025)
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Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment (2025)
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The Mitochondrial Ubiquitin Ligase MARCHF5 Cooperates with MCL1 to Inhibit Apoptosis in KSHV-Transformed Primary Effusion Lymphoma Cell Lines (2024)
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Cytotoxicity of Activator Expression in CRISPR-based Transcriptional Activation Systems (2024)
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Molecular Mechanisms of KSHV Latency Establishment and Maintenance (2024)
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Suppression of TRIP13 Induces Metabolic Changes and Potentiates Ferroptosis in Multiple Myeloma (2023)
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Intrinsic p53 Activation Restricts Gammaherpesvirus-Driven Germinal Center B Cell Expansion during Latency Establishment (2023)
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CRISPR screens identify novel regulators of cFLIP dependency and ligand-independent, TRAIL-R1-mediated cell death (2023)
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Expression Ratios of the Antiapoptotic BCL2 Family Members Dictate the Selective Addiction of Kaposi’s Sarcoma-Associated Herpesvirus-Transformed Primary Effusion Lymphoma Cell Lines to MCL1 (2022)
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Expression Ratios of the Anti-Apoptotic BCL2 Family Members Dictate the Selective Addiction of KSHV-Transformed Primary Effusion Lymphoma Cell Lines to MCL1 (2022)
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CRISPR Screens Identify Novel Regulators of cFLIP Dependency and Ligand-Independent, TRAIL-R1-Mediated Cell Death (2022)
Federal Grants 4 $1,371,020 total
Lytic viral genes in the pathogenesis of oncogenic gammaherpesviruses
Role of a latent OriLyt RNA in KSHV latency in primary effusion lymphoma
Oncogenic Roles and Therapeutic Potential of MCL1 Addiction in Primary Effusion Lymphoma
Collaboration Network
Top Collaborators
- CRISPR screens identify novel regulators of cFLIP dependency and ligand-independent, TRAIL-R1-mediated cell death
- Cytotoxicity of Activator Expression in CRISPR-based Transcriptional Activation Systems
- CRISPR Screens Identify Novel Regulators of cFLIP Dependency and Ligand-Independent, TRAIL-R1-Mediated Cell Death
- Cytotoxicity of activator expression in CRISPR-based transcriptional activation systems
- Expression Ratios of the Antiapoptotic BCL2 Family Members Dictate the Selective Addiction of Kaposi’s Sarcoma-Associated Herpesvirus-Transformed Primary Effusion Lymphoma Cell Lines to MCL1
- Expression Ratios of the Anti-Apoptotic BCL2 Family Members Dictate the Selective Addiction of KSHV-Transformed Primary Effusion Lymphoma Cell Lines to MCL1
- Suppression of TRIP13 Induces Metabolic Changes and Potentiates Ferroptosis in Multiple Myeloma
- The Mitochondrial Ubiquitin Ligase MARCHF5 Cooperates with MCL1 to Inhibit Apoptosis in KSHV-Transformed Primary Effusion Lymphoma Cell Lines
- Expression Ratios of the Antiapoptotic BCL2 Family Members Dictate the Selective Addiction of Kaposi’s Sarcoma-Associated Herpesvirus-Transformed Primary Effusion Lymphoma Cell Lines to MCL1
- Expression Ratios of the Anti-Apoptotic BCL2 Family Members Dictate the Selective Addiction of KSHV-Transformed Primary Effusion Lymphoma Cell Lines to MCL1
- The Mitochondrial Ubiquitin Ligase MARCHF5 Cooperates with MCL1 to Inhibit Apoptosis in KSHV-Transformed Primary Effusion Lymphoma Cell Lines
- Expression Ratios of the Antiapoptotic BCL2 Family Members Dictate the Selective Addiction of Kaposi’s Sarcoma-Associated Herpesvirus-Transformed Primary Effusion Lymphoma Cell Lines to MCL1
- Expression Ratios of the Anti-Apoptotic BCL2 Family Members Dictate the Selective Addiction of KSHV-Transformed Primary Effusion Lymphoma Cell Lines to MCL1
- The Mitochondrial Ubiquitin Ligase MARCHF5 Cooperates with MCL1 to Inhibit Apoptosis in KSHV-Transformed Primary Effusion Lymphoma Cell Lines
- Molecular Mechanisms of KSHV Latency Establishment and Maintenance
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 Activation Restricts Gammaherpesvirus-Driven Germinal Center B Cell Expansion during Latency Establishment
- Molecular Mechanisms of KSHV Latency Establishment and Maintenance
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 Activation Restricts Gammaherpesvirus-Driven Germinal Center B Cell Expansion during Latency Establishment
- CRISPR screens identify novel regulators of cFLIP dependency and ligand-independent, TRAIL-R1-mediated cell death
- CRISPR Screens Identify Novel Regulators of cFLIP Dependency and Ligand-Independent, TRAIL-R1-Mediated Cell Death
- CRISPR screens identify novel regulators of cFLIP dependency and ligand-independent, TRAIL-R1-mediated cell death
- CRISPR Screens Identify Novel Regulators of cFLIP Dependency and Ligand-Independent, TRAIL-R1-Mediated Cell Death
- CRISPR screens identify novel regulators of cFLIP dependency and ligand-independent, TRAIL-R1-mediated cell death
- CRISPR Screens Identify Novel Regulators of cFLIP Dependency and Ligand-Independent, TRAIL-R1-Mediated Cell Death
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 Activation Restricts Gammaherpesvirus-Driven Germinal Center B Cell Expansion during Latency Establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 Activation Restricts Gammaherpesvirus-Driven Germinal Center B Cell Expansion during Latency Establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 Activation Restricts Gammaherpesvirus-Driven Germinal Center B Cell Expansion during Latency Establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 Activation Restricts Gammaherpesvirus-Driven Germinal Center B Cell Expansion during Latency Establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 Activation Restricts Gammaherpesvirus-Driven Germinal Center B Cell Expansion during Latency Establishment
- Cytotoxicity of Activator Expression in CRISPR-based Transcriptional Activation Systems
- Cytotoxicity of activator expression in CRISPR-based transcriptional activation systems
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