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Staff Profile

Dr Brian Ortmann

NUAcT Fellow: Ageing and Health

  • Email: brian.ortmann@ncl.ac.uk
  • Address: Centre for Cancer
    Paul O'Gorman Building
    Framlington Place
    Newcastle upon Tyne
    NE2 4AD
Background

I am a Newcastle University Academic Track (NUAcT) fellow within the Biosciences Institute.


Past Positions:

University of Cambridge - Postdoctoral Research Assistant (2016-2022)

University of Dundee - PhD student (2011-2015)


Qualifications:

PhD in Cell Biology, University of Dundee, 2015

BSc (Hons) Biomedical Sciences, University of Dundee, 2011


Research

Cells in the human body are constantly exposed to fluctuating oxygen levels, making oxygen availability a pivotal factor in regulating cellular function and fate. Hypoxia—defined by a reduction in oxygen supply—drives the progression of diseases such as cancer and inflammation, fuelling critical processes like metastasis and immune response resulting in poor patient outcome. Therefore, understanding how cells adapt to hypoxic conditions is vital for uncovering novel therapeutic targets and improving treatment effectiveness.


The Hypoxia-Inducible Factor (HIF) family of transcription factors play a central role in the body’s response to low oxygen. Under hypoxic conditions, HIF stabilises and activates a transcriptional programme that supports cellular survival and adaptation. However, in tumours, dysregulated HIF activity accelerates disease progression, positioning HIF as both a promising and complex therapeutic target. Despite the availability of several HIF inhibitors, the risk of systemic toxicity from blanket inhibition highlights the need for more refined, targeted approaches.


A key question in the field is how HIF activity is precisely regulated across different cellular contexts. Our research has identified SET1B, a histone methyltransferase, as a crucial HIF coactivator, suggesting that targeting co-regulators could offer a more selective means of modulating HIF. SET1B is part of a larger family of methyltransferases and demethylases—many of which are oxygen-sensitive and HIF-regulated—that modify proteins through methylation, altering their function. This indicates that methylation could play a central role in the broader hypoxia response.

While HIF activation is a critical component of the cellular response to hypoxia, it is inherently slow as a transcriptional programme and cannot account for the rapid changes’ cells need to survive in low-oxygen environments. In contrast, methylation is a fast, reversible post-translational modification capable of swiftly altering protein function. Despite its potential as a key regulator of hypoxia adaptation, the broader role of methylation in both HIF-dependent and independent pathways remains largely unexplored.


My research group uses innovative forward genetic screening and proteomics to interrogate how methylation regulates the cellular response to hypoxia. The ultimate goal of the lab is to identify new therapeutic targets to treat cancer, autoimmunity, and neurodegeneration.


I am always open to inquiries from prospective undergraduate and PhD students as well postdoctoral researchers.


Current lab members:

Dr Nikita Dhillon (Post Doctoral Researcher)

Lukasz Marzec (PhD Student)

Alexander Handyside (PhD Student)

Meagan Farrington (MRes Student)


Publications