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Associate Professor Nathan Palpant
Associate Professor

Nathan Palpant

Email: 
Phone: 
+61 7 334 62054

Overview

Background

Career Summary: 2009: PhD, University of Michigan, USA with training in cardiac physiology, modelling myocardial ischemia in vivo and in vitro, and development of therapeutic approaches for myocardial ischemia; 2009–2015: Postdoctoral Research Fellow, University of Washington, Institute for Stem Cell and Regenerative Medicine, USA with training in stem cell biology, genomics, genome editing, and cell therapeutics for ischemic heart disease; 2015–current: Group Leader, University of Queensland (UQ), Institute for Molecular Bioscience; 2022-current: Associate Professor, UQ; 2018–2021 and 2023-2026: National Heart Foundation Future Leader Fellow. Dr. Palpant’s research team has expertise in human stem cell biology, computational genomics, and cardiac physiology, which enables them to translate outcomes from cell biology and genomics to disease modelling, drug discovery, and preclinical modelling.

Availability

Associate Professor Nathan Palpant is:
Available for supervision
Media expert

Qualifications

  • Doctoral Diploma, University of Michigan

Research interests

  • Developing new drugs for heart disease

    Our work aims to prevent organ damage associated with ischemic injuries of the heart. There are no drugs that prevent organ damage caused by these injuries, which ultimately leads to heart failure, making ischemic heart disease the leading cause of death worldwide. This project aims to identify new molecular targets coupled with development of a novel pharmacological inhibitors as novel therapeutics to promote rapid and more effective recovery following an acute cardiovascular event. Development of new cardiovascular drugs will address a major clinical area of unmet need, thereby decreasing mortality, improving recovery and quality-of-life for survivors, and drastically reducing the burden of these diseases. Conditions caused by obstruction of blood flow to the heart are the most common emergency manifestation of cardiovascular disease. Although acute reperfusion therapies have improved patient outcomes, mortality remains high and heart attacks are one of the largest attributable risks for heart failure (HF). Myocardial sensitivity to ischemia-reperfusion injury (IRI) therefore remains a primary point of vulnerability underlying cardiovascular disease, which is the leading cause of morbidity and mortality worldwide. Despite decades of preclinical therapeutic development, there are no drugs in clinical use that block the acute injury response to cardiac ischemia. My research group has discovered a new therapeutic drug to prevent injuries of the heart, a peptide (Hi1a) isolated from venom of the Fraser Island funnel-web spider. Hi1a is a safe and potent therapeutic that we have shown improves heart recovery after myocardial infarction (MI) and greatly enhances the performance of donor hearts procured for transplantation. These remarkable therapeutic properties stem from Hi1a’s ability to protect heart muscle cells from ischemic injury by inhibiting an ion channel known as acid-sensing ion channel 1a (ASIC1a). More broadly, my research program is advancing studies on Hi1a alongside development of other novel therapeutic drugs that reduce the scope and spread of organ injury to the heart after ischemic injuries. These research projects integrate information from diverse sources to establish rationale and mechanism including population statistical genetics methods (e.g. GWAS), CRISPR genetic perturbation studies in iPSCs, functional studies in cell models, and animal models of disease.

  • Building tools to predict how the genome controls cells

    This work focuses on development of disease-agnostic, high throughput and scalable functional genomics methods that integrate computational predictions and disease modelling to study mechanisms controlling cell differentiation and genetic causes of disease. Genome sequencing is a powerful tool for studying the biological basis of disease, yet out of millions of data points, finding the underlying cause of disease can be difficult. Current protocols for classifying variants from patient DNA data largely rely on prior knowledge about normal and abnormal gene variation contained in large public databases, known disease-causing gene panels, or identifying variants causing amino acid changes in proteins (which only comprise 2% of the genome). Despite these powerful approaches, studies indicate that classifying variants as pathogenic occurs in only a minority of cases and among variants reported in ClinVar, a public archive of relationships between human variation and phenotype, wherein a large proportion (37%) are classified as variants of unknown significance (VUS). New approaches are needed to improve variant prioritisation and classification from genetic data. My research group is developing unsupervised, genome-wide computational analysis methods to reveal genetic mechanisms of development and disease. For example, our recent work developed TRIAGE which uses epigenetic modification of DNA-binding histone proteins to identify regions of the genome that are critical determinants of cell decisions and functions. Using data from >800 cell types, we identified genomic “hot-spots” that, when mutated, are associated with diseases, including neurological and cardiovascular diseases, multi-organ syndromes, and cancer. Our data show that TRIAGE regions of the genome are enriched for pathological variants (especially those causing congenital diseases), intolerant to mutations, have significantly increased effects on complex trait phenotypes, and encode genes that are key determinants of cell differentiation and morphogenesis. This area of my program focuses four design criteria in developing and implementing computational tools to facilitate novel discovery in cells. Simplicity: We are building methods that help organise genomic information in an unsupervised manner across the human genome. These methods can be used to analyse orthogonal data (e.g. patient genetic data) to identify genetic causes of disease or development and/or reveal relationships between gene groups that inform programs controlling cell decisions and functions. Versatility: We aim to develop methods that can be used with any genomic data that maps to genes or a chromosomal address including analysis of patient genetic data or any genomic data type (GWAS, SNPs, RNAseq etc). Furthermore, these methods are ideal models to weight regions of the genome in genetic analysis tools such as polygenic risk scores or machine learning algorithms. Disease-agnostic: Using a systems level approach, these methods enable broad implementation in data analysis pipelines for any data sample from any cell, tissue, disease, or individual. Efficient functional screening: These prediction methods provide robust rationale for wet lab cell biology to functionally test novel hypotheses derived from computational prediction methods in functional genomics studies.

  • Harnessing control of stem cell decisions and functions

    Cell differentiation is a process involving the continuous coordination of gene expression programs that guide undifferentiated cells into specific, functional cell types. The mechanisms controlling cell differentiation are not well understood. Recent advances in stem cell biology and tissue engineering have highlighted this fundamental knowledge gap. For example, cells derived from pluripotent stem cells (iPSCs) are often heterogeneous, display physiological properties reminiscent of fetal cells and fail to fully mature towards an adult functional state. Our inability to accurately guide cell differentiation pathways currently limits the utility of iPSC-derived cell products in research, tissue engineering, and drug discovery. Despite these profound limitations, the stem cell market is forecasted to grow to nearly $6B USD by 2025. The anticipated impact of the stem cell sector is dependent on precision control of cell differentiation into cell types that model human physiology. Efforts to dissect cell differentiation mechanisms and recapitulate human development using iPSCs have encountered the following major challenges: 1) we lack fundamental understanding of human developmental biology, 2) we lack sufficient scale of data mapping gene expression changes controlling cell processes over time, 3) among the thousands of genes expressed in cells, we lack the ability to efficiently identify genes (especially non-transcription factors) responsible for guiding specific cell differentiation processes, and 4) we do not understand how and when to effectively perturb these specialised gene programs to customise cell differentiation decisions or functions. My group is developing the data, tools, and cell biology perturbation and phenotyping strategies to address these limitations, positioning us to establish new insights into cell biology of differentiation. Using our expertise in stem cell and cardiovascular developmental biology, we are studying how gene programs change as cells move across the cell developmental lineages and identifying genetic on/off switches that control cell choices and functions during differentiation.

Research impacts

Advancing stem cells toward clinical testing: Work by Dr Palpant on iPSC genome engineering and differentiation protocols led to him receiving the 2015 Young Investigator Award from the International Society for Heart Research. This work resulted in a licensed patent (US Patent 10,612,002; 2020) on derivation of hPSCs-endothelial cells. This patent and seminal studies on regenerating the mammalian heart with iPSC-derived heart muscle (Nature x2) formed the basis for Sana Biotechnology (USA; USD $700M series A VC investment in 2019). Dr Palpant has an ongoing collaboration with Sana CSO Professor Charles Murry (including publications and a 2017 UQ Global Strategy and Partnership Award) to advance discoveries for commercialisation by Sana.

Genomic innovation for drug discovery: Dr Palpant has been at the forefront of research into innovative genomics algorithms and sequencing methods. His work developing a computational method to identify genetic features controlling cells resulted in the Lorne Genome Millennium Science Award (2019) and led to current funded collaborations with HAYA Therapeutics (Switzerland; USD $16M series A VC investment, 2020), Merck (Germany), and ConcR (UK) resulting in >$600K in industry funding for early access to these discovery platforms.

New drug therapeutics for cardiovascular disease: Dr Palpant has led development of Hi1a as a novel cardiovascular drug. These discoveries stemmed from his expertise in using human pluripotent stem cell biology and disease modelling of acquired heart disease. This work was recognised by the Cardiac Society for Australia and New Zealand Ralph Reader Prize and resulted in a provisional patent on ASIC1a-knockout iPSCs (PAT-02408-US-01). The clinical impact of this work has resulted in a UQ spinout company, Infensa Bioscience to commercialise Hi1a for clinical testing. He is scientific co-founder and on the scientific advisory board of Infensa Bioscience.

Publication Impact Metrics: Dr Palpant's expertise in pluripotent stem cell biology, cardiac muscle cells, and genomics has resulted in publications cited 7-fold higher than the field average (Topic E 4031 FWCI of 7.37, SciVal). His research has been featured on the ABC, Newsweek, The Guardian, and The Washington Post.

Professional Standing: Since 2019, Dr Palpant has been involved in national initiatives including as co-chair of the Queensland Cardiovascular Research Network and advisory member of the Precision Medicine Flagship for the Australian Cardiovascular Alliance. His expertise is reflected in his role on the steering committee for the Australian Functional Genomics Network. Dr Palpant has given seminars and presentations throughout Australia, USA, Europe, Singapore, China, and Japan. He reviews for journals including Science, Nature Methods, Cell Stem Cell, and JCI Insights.

Works

Search Professor Nathan Palpant’s works on UQ eSpace

84 works between 2007 and 2024

61 - 80 of 84 works

2015

Journal Article

Inhibition of β-catenin signaling respecifies anterior-like endothelium into beating human cardiomyocytes

Palpant, Nathan J., Pabon, Lil, Roberts, Meredith, Hadland, Brandon, Jones, Daniel, Jones, Christina, Moon, Randall T., Ruzzo, Walter L., Bernstein, Irwin, Zheng, Ying and Murry, Charles E. (2015). Inhibition of β-catenin signaling respecifies anterior-like endothelium into beating human cardiomyocytes. Development (Cambridge), 142 (18), 3198-3209. doi: 10.1242/dev.117010

Inhibition of β-catenin signaling respecifies anterior-like endothelium into beating human cardiomyocytes

2014

Journal Article

Proliferation at the heart of preadolescence

Palpant, Nathan J. and Murry, Charles E. (2014). Proliferation at the heart of preadolescence. Cell, 157 (4), 765-767. doi: 10.1016/j.cell.2014.04.025

Proliferation at the heart of preadolescence

2014

Book Chapter

Methods for assessing the electromechanical integration of human pluripotent stem cell-derived cardiomyocyte grafts

Zhu, Wei-Zhong, Filice, Dominic, Palpant, Nathan J. and Laflamme, Michael A. (2014). Methods for assessing the electromechanical integration of human pluripotent stem cell-derived cardiomyocyte grafts. Cardiac tissue engineering: methods and protocols. (pp. 229-247) edited by Radisci, Milica and Black III, Lauren D.. New York, NY United States: Springer New York. doi: 10.1007/978-1-4939-1047-2_20

Methods for assessing the electromechanical integration of human pluripotent stem cell-derived cardiomyocyte grafts

2014

Journal Article

Human embryonic-stem-cell-derived cardiomyocytes regenerate non-human primate hearts

Chong, James J. H., Yang, Xiulan, Don, Creighton W., Minami, Elina, Liu, Yen-Wen, Weyers, Jill J., Mahoney, William M., Van Biber, Benjamin, Cook, Savannah M., Palpant, Nathan J., Gantz, Jay A., Fugate, James A., Muskheli, Veronica, Gough, G. Michael, Vogel, Keith W., Astley, Cliff A., Hotchkiss, Charlotte E., Baldessari, Audrey, Pabon, Lil, Reinecke, Hans, Gill, Edward A., Nelson, Veronica, Kiem, Hans-Peter, Laflamme, Michael A. and Murry, Charles E. (2014). Human embryonic-stem-cell-derived cardiomyocytes regenerate non-human primate hearts. Nature, 510 (7504), 273-277. doi: 10.1038/nature13233

Human embryonic-stem-cell-derived cardiomyocytes regenerate non-human primate hearts

2013

Journal Article

Transmembrane protein 88: A Wnt regulatory protein that specifies cardiomyocyte development

Palpant, Nathan J., Pabon, Lil, Rabinowitz, Jeremy S., Hadland, Brandon K., Stoick-Cooper, Cristi L., Paige, Sharon L., Bernstein, Irwin D., Moon, Randall T. and Murry, Charles E. (2013). Transmembrane protein 88: A Wnt regulatory protein that specifies cardiomyocyte development. Development (Cambridge), 140 (18), 3799-3808. doi: 10.1242/dev.094789

Transmembrane protein 88: A Wnt regulatory protein that specifies cardiomyocyte development

2013

Journal Article

Cardiopoietry in motion

Murry, Charles E., Palpant, Nathan J. and MacLellan, W. Robb (2013). Cardiopoietry in motion. Journal of the American College of Cardiology, 61 (23), 2339-2340. doi: 10.1016/j.jacc.2013.03.028

Cardiopoietry in motion

2013

Book Chapter

Human dignity in the throes?: An introduction to the volume

Dilley, Stephen and Palpant, Nathan J. (2013). Human dignity in the throes?: An introduction to the volume. Human Dignity in Bioethics: From Worldviews to the Public Square. (pp. 3-18) New York, NY United States: Taylor and Francis. doi: 10.4324/9780203075005

Human dignity in the throes?: An introduction to the volume

2013

Book

Human dignity in bioethics: From worldviews to the public square

Dilley, Stephen and Palpant, Nathan J. (2013). Human dignity in bioethics: From worldviews to the public square. New York, United States: Routledge. doi: 10.4324/9780203075005

Human dignity in bioethics: From worldviews to the public square

2013

Book Chapter

Human dignity and the debate over early human embryos

Palpant, Nathan J. and Holland, Suzanne (2013). Human dignity and the debate over early human embryos. Human dignity in bioethics: from worldviews to the public square. (pp. 239-263) New York, NY, United States: Routledge. doi: 10.4324/9780203075005

Human dignity and the debate over early human embryos

2013

Journal Article

Zinc finger nucleases: looking toward translation

Palpant, N. J. and Dudzinski, D. (2013). Zinc finger nucleases: looking toward translation. Gene Therapy, 20 (2), 121-127. doi: 10.1038/gt.2012.2

Zinc finger nucleases: looking toward translation

2012

Journal Article

Targeted genomic integration of a selectable floxed dual fluorescence reporter in human embryonic stem cells

Gantz, Jan A., Palpant, Nathan J., Welikson, Robert E., Hauschka, Stephen D., Murry, Charles E. and Laflamme, Michael A. (2012). Targeted genomic integration of a selectable floxed dual fluorescence reporter in human embryonic stem cells. PLoS ONE, 7 (10) e46971, 1-9. doi: 10.1371/journal.pone.0046971

Targeted genomic integration of a selectable floxed dual fluorescence reporter in human embryonic stem cells

2012

Journal Article

Human ES-cell-derived cardiomyocytes electrically couple and suppress arrhythmias in injured hearts

Shiba, Yuji, Fernandes, Sarah, Zhu, Wei-Zhong, Filice, Dominic, Muskheli, Veronica, Kim, Jonathan, Palpant, Nathan J., Gantz, Jay, Moyes, Kara W., Reinecke, Hans, Van Biber, Benjamin, Dardas, Todd, Mignone, John L., Izawa, Atsushi, Hanna, Ramy, Viswanathan, Mohan, Gold, Joseph D., Kotlikoff, Michael I., Sarvazyan, Narine, Kay, Matthew W., Murry, Charles E. and Laflamme, Michael A. (2012). Human ES-cell-derived cardiomyocytes electrically couple and suppress arrhythmias in injured hearts. Nature, 489 (7415), 322-325. doi: 10.1038/nature11317

Human ES-cell-derived cardiomyocytes electrically couple and suppress arrhythmias in injured hearts

2012

Journal Article

Diastolic dysfunction and thin filament dysregulation resulting from excitation-contraction uncoupling in a mouse model of restrictive cardiomyopathy

Davis, J., Yasuda, S., Palpant, N.J., Martindale, J., Stevenson, T., Converso, K. and Metzger, J.M. (2012). Diastolic dysfunction and thin filament dysregulation resulting from excitation-contraction uncoupling in a mouse model of restrictive cardiomyopathy. Journal of Molecular and Cellular Cardiology, 53 (3), 446-457. doi: 10.1016/j.yjmcc.2012.05.018

Diastolic dysfunction and thin filament dysregulation resulting from excitation-contraction uncoupling in a mouse model of restrictive cardiomyopathy

2012

Journal Article

Regenerative medicine: reprogramming the injured heart

Palpant, Nathan J. and Murry, Charles E. (2012). Regenerative medicine: reprogramming the injured heart. Nature, 485 (7400), 585-586. doi: 10.1038/485585a

Regenerative medicine: reprogramming the injured heart

2012

Journal Article

pH-responsive titratable inotropic performance of histidine-modified cardiac troponin i

Palpant, Nathan J., Houang, Evelyne M., Sham, Yuk Y. and Metzger, Joseph M. (2012). pH-responsive titratable inotropic performance of histidine-modified cardiac troponin i. Biophysical Journal, 102 (7), 1570-1579. doi: 10.1016/j.bpj.2012.01.024

pH-responsive titratable inotropic performance of histidine-modified cardiac troponin i

2011

Journal Article

Cardiac disease in mucopolysaccharidosis type I attributed to catecholaminergic and hemodynamic deficiencies

Palpant, Nathan J., Bedada, Fikru B., Peacock, Brandon, Blazar, Bruce R., Metzger, Joseph M. and Tolar, Jakub (2011). Cardiac disease in mucopolysaccharidosis type I attributed to catecholaminergic and hemodynamic deficiencies. American Journal of Physiology - Heart and Circulatory Physiology, 300 (1), H356-H365. doi: 10.1152/ajpheart.00774.2010

Cardiac disease in mucopolysaccharidosis type I attributed to catecholaminergic and hemodynamic deficiencies

2010

Journal Article

Influence of genetic background on ex vivo and in vivo cardiac function in several commonly used inbred mouse strains

Barnabei, Matthew S., Palpant, Nathan J. and Metzger, Joseph M. (2010). Influence of genetic background on ex vivo and in vivo cardiac function in several commonly used inbred mouse strains. Physiological Genomics, 42A (2), 103-113. doi: 10.1152/physiolgenomics.00071.2010

Influence of genetic background on ex vivo and in vivo cardiac function in several commonly used inbred mouse strains

2010

Journal Article

Pathogenic peptide deviations support a model of adaptive evolution of chordate cardiac performance by troponin mutations

Palpant N.J., Houang E.M., Delport W., Hastings K.E.M., Onufriev A.V., Sham Y.Y. and Metzger J.M. (2010). Pathogenic peptide deviations support a model of adaptive evolution of chordate cardiac performance by troponin mutations. Physiological Genomics, 42 (2), 287-299. doi: 10.1152/physiolgenomics.00033.2010

Pathogenic peptide deviations support a model of adaptive evolution of chordate cardiac performance by troponin mutations

2010

Journal Article

Aesthetic cardiology: adipose-derived stem cells for myocardial repair

Palpant, N.J. and Metzger, J.M. (2010). Aesthetic cardiology: adipose-derived stem cells for myocardial repair. Current Stem Cell Research and Therapy, 5 (2), 145-152. doi: 10.2174/157488810791268654

Aesthetic cardiology: adipose-derived stem cells for myocardial repair

2009

Journal Article

Artificial selection for whole animal low intrinsic aerobic capacity co-segregates with hypoxia-induced cardiac pump failure

Palpant, Nathan J., Szatkowski, Michael L., Wang, Wang, Townsend, DeWayne, Bedada, Fikru B., Koch, Lauren G., Britton, Steven L. and Metzger, Joseph M. (2009). Artificial selection for whole animal low intrinsic aerobic capacity co-segregates with hypoxia-induced cardiac pump failure. PLoS One, 4 (7) e6117, e6117. doi: 10.1371/journal.pone.0006117

Artificial selection for whole animal low intrinsic aerobic capacity co-segregates with hypoxia-induced cardiac pump failure

Funding

Current funding

  • 2024 - 2028
    Spider venom peptides: precision therapy for genetic epilepsies
    NHMRC MRFF Stem Cells Therapies Mission
    Open grant
  • 2024 - 2028
    The HEART REHAB Clinical Trials: Therapeutics to Protect the Human Heart
    MRFF Frontier Health and Medical Research Program administered by AusIndustry
    Open grant
  • 2024 - 2026
    Glycaemic variability: A culprit cause of heart disease in diabetes
    MRFF Targeted Translation Research Accelerator
    Open grant
  • 2024 - 2026
    ALL IN - AI and Laboratory Led IdentificatioN of PASC
    NHMRC MRFF Post-Acute Sequalae of COVID-19
    Open grant
  • 2024 - 2025
    Characterization of Tnnc1 variant in cardiac and skeletal muscle function
    Australian Functional Genomics Network
    Open grant
  • 2023 - 2026
    Molecular definition of cellular states in the vascular endothelium
    ARC Discovery Projects
    Open grant
  • 2022 - 2026
    TRIAGE: A disease agnostic computational and modelling platform to accelerate variant classification
    NHMRC MRFF Genomics Health Futures Mission
    Open grant
  • 2021 - 2025
    Development of drugs to prevent ischemic injuries of the heart and brain
    NHMRC MRFF - Cardiovascular Health Mission
    Open grant
  • 2021 - 2026
    Induced pluripotent stem cell derived cardiomyocytes: a new therapy for 'no-option' end stage heart failure (MRFF Stem Cell Therapies grant from University of Sydney).
    University of Sydney
    Open grant
  • 2021 - 2026
    The Australian Functional Genomics Network (Administered by Murdoch Children's Research Institute)
    Murdoch Childrens Research Institute
    Open grant
  • 2021 - 2024
    ASIC1a, a new therapeutic drug target for cardiac ischemia
    NHMRC IDEAS Grants
    Open grant
  • 2021 - 2024
    Development of a first-in-class therapeutic for protecting the ischemic heart
    NHMRC Development Grant
    Open grant

Past funding

  • 2023 - 2024
    Studying the basis of and developing new therapies to treat heart disease
    IPF Healthy - Medical Research
    Open grant
  • 2022 - 2023
    Knock-in genetic barcodes for multiplex single-cell sequencing
    UniQuest Pty Ltd
    Open grant
  • 2022
    Assessment of pathogenicity of VUS in MYBPC3 using CRISPR interference with high-throughput variant expression &functional characterisation (NHMRC Aus Genomics Grant Program administered through VCCRI
    Victor Chang Cardiac Research Institute Limited
    Open grant
  • 2021
    TRIAGE and cell barcoding
    UniQuest Pty Ltd
    Open grant
  • 2020
    Electrophysiology Platform for Ion-channel Characterisation
    ARC Linkage Infrastructure, Equipment and Facilities
    Open grant
  • 2020 - 2023
    Use of TRIAGE to screen for non-coding RNA targets governing organ specific fibrosis
    UniQuest Pty Ltd
    Open grant
  • 2019 - 2020
    Venom peptides for stem cell applications
    Innovation Connections
    Open grant
  • 2019
    Vevo 3100 Imaging System for ultrahigh resolution and frame rate echocardiographic assessment of small animals.
    UQ Major Equipment and Infrastructure
    Open grant
  • 2018 - 2021
    Role of common genetic variation in single cell transcriptional heterogeneity across the cardiomyocyte lineage (NHMRC Project Grant administered by UNSW)
    University of New South Wales
    Open grant
  • 2018 - 2021
    Cardiovascular Development and Disease: Discovery science to translational applications
    National Heart Foundation Future Leader Fellowship
    Open grant
  • 2018
    Controlling cardiac differentiation from human pluripotent stem cells
    UQ Foundation Research Excellence Awards - DVC(R) Funding
    Open grant
  • 2018
    High-throughput ion channel pharmacology
    UQ Major Equipment and Infrastructure
    Open grant
  • 2018
    Role of common genetic variation driving single cell transcriptional heterogeneity across the cardiomyocyte lineage
    NHMRC Project Grant
    Open grant
  • 2017 - 2024
    ACRF Cancer Ultrastructure and Function Facility
    Australian Cancer Research Foundation
    Open grant
  • 2017 - 2019
    Investigating a novel genetic regulator of cardiac rhythm
    NHMRC Project Grant
    Open grant
  • 2017 - 2019
    Understanding the differentiation of the endocardium
    ARC Discovery Projects
    Open grant
  • 2016
    Single Cell Transcriptomic Laboratory
    UQ Major Equipment and Infrastructure
    Open grant
  • 2011 - 2019
    Stem Cells Australia (ARC Special Research Initiative administered by the University of Melbourne)
    University of Melbourne
    Open grant

Supervision

Availability

Associate Professor Nathan Palpant is:
Available for supervision

Before you email them, read our advice on how to contact a supervisor.

Available projects

  • Projects in Stem Cell Biology, Genomics, Cardiovascular Development, and Cell Therapeutics

    As outlined in the research interests of my lab, there are numerous projects available for students covering a range of topics. These projects are continuously changing. The following areas cover topics I use to develop projects for incoming students:

    - Use stem cells, genome engineering, and single cell RNA-sequencing to study how cells differentiate into cell types of the heart

    - Modify stem cells to generate cells with custom engineered functions to create synthetic cell states

    - Use bioinformatics approaches to analyse large scale genomic data to study what features of the genome control cell decisions

    - Study novel genes that control how heart cells respond to stress like ischemia and work with chemists to develop novel drugs that could be used to treat patients who have heart attacks

    - Use computational genomics and cell biology approaches to study how the heart adapts to extreme environments (like high altitude) to learn what genes control stress responses in cells.

    - Study the biology of how venoms of marine and terrestrial species impact heart function using cells, whole organ models, and animal models.

    Contact me for a discussion about current opportunities and specific projects available.

Supervision history

Current supervision

  • Doctor Philosophy

    Using genomic data and epigenetic annotations to identify genetic causes of cell differentiation

    Principal Advisor

    Other advisors: Dr Jian Zeng, Dr Amy Hanna

  • Doctor Philosophy

    Using signatures of cell identity to improve cell type prediction in single cell analysis pipelines

    Principal Advisor

    Other advisors: Dr Quan Nguyen, Dr Woo Jun Shim

  • Doctor Philosophy

    Understanding genetic adaptation of the heart to extreme environments

    Principal Advisor

    Other advisors: Dr Sonia Shah

  • Doctor Philosophy

    Multilineage differentiation from pluripotency reveals genetic regulators of cardiovascular physiology

    Principal Advisor

    Other advisors: Dr Quan Nguyen

  • Doctor Philosophy

    The long-term cardiovascular complications of COVID-19

    Associate Advisor

    Other advisors: Dr Helen Mayfield, Professor Colleen Lau, Dr Linda Gallo, Associate Professor Kirsty Short

  • Doctor Philosophy

    Elucidating the effects of potency biomarkers on cellular reprogramming and differentiation in adult stem cells

    Associate Advisor

    Other advisors: Dr Alex Smith, Professor Simon Cool

  • Doctor Philosophy

    Identifying the structure, function, and mechanism of action of cardiotoxic components in the venoms of box (Chironex fleckeri) and Irukandji (Carukia barnesi) jellyfish

    Associate Advisor

    Other advisors: Dr Andrew Walker, Professor Glenn King

Completed supervision

Media

Enquiries

Contact Associate Professor Nathan Palpant directly for media enquiries about:

  • bioengineering
  • cardiovascular disease
  • cardiovascular system
  • differentiation
  • genome engineering
  • genomics
  • heart development
  • heart disease
  • heart regeneration
  • human pluripotent stem cells
  • stem cells
  • vascular development

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