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Biological Sciences
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(023) 8059 4296
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sergio.regufedamota@soton.ac.uk

Dr Sergio Miguel Regufe da Mota PhD

Research Fellow in Proteomics

Dr Sergio Miguel Regufe da Mota's photo

Dr Sergio Regufe da Mota is a Post-doctoral Research Fellow in Proteomics within Biological Sciences at the University of Southampton. His current research focuses in Functional Skin Proteomics and in the study of skin proteins modified by sensitising chemicals.

As a molecular biologist my interests lie in the understanding of different cellular processes and how external factors can affect cellular homeostasis

Dr Sergio Regufe da Mota graduated from the University of Lisbon, Portugal in 2002. He went to complete his PhD with the Institute of Tropical Medicine of the New University of Lisbon in 2009. His research was focussed on the study of the changes in the cellular proteome caused by the replication of the Hepatitis Delta Virus.

He then moved to the UK to join Dr Tracey Newman’s team in Southampton where he worked with biocompatible targeted nanoparticles for drug delivery to the central nervous system. In 2011 he moved to Professor Chris Proud’s group where he studied the regulation of the eukaryotic elongation factor 2 kinase and how its activity/regulation enables the cells to survive stress conditions present in a cancer setting.

In 2014 he joined Dr Simon Crabb group that studies novel molecular targets for the treatment of castration resistant prostate cancer where he showed that inhibition of the LSD1 attenuates androgen receptor (AR) driven prostate cancer resistant to next generation AR antagonists.

Currently he joined the Centre for Proteomic Research under Dr Paul Skipp where he is working on the study of skin proteins modified by sensitising chemicals.

Career History

2017-current: Post-Doctoral Research Fellow in Proteomics with Dr Paul Skipp, Centre for Biological Sciences, University of Southampton, UK.
2015-2017: CRUK Post-Doctoral Research Fellow with Dr Simon Crabb and Professor Graham Packham, Cancer Sciences, University of Southampton, UK.
2014-2015: PCUK Post-Doctoral Research Fellow with Dr Simon Crabb and Professor Graham Packham, Cancer Sciences, University of Southampton, UK.
2013-2014: Post-Doctoral Research Fellow with Professor Chris Proud, Centre for Biological Sciences, University of Southampton, UK.
2011-2013: Research Assistant with Professor Chris Proud, Centre for Biological Sciences, University of Southampton, UK.
2010-2011: Post-Doctoral Research Fellow with Dr Tracey Newman and Professor Hugh Perry, Centre for Biological Sciences, University of Southampton, UK.
2003-2009: PhD Student, Institute of Tropical Medicine of the New University of Lisbon, Portugal.

Academic Qualifications

2009: PhD, Biomedical Sciences – Molecular and Cellular Biology, Institute of Topical Medicine of the Nova University of Lisbon, Portugal.
2002: University degree, Biology – Microbiology and Genetics, Faculty of Science at the University of Lisbon, Portugal.

Research

Publications

Teaching

Contact

Research interests

Current research project:

Functional Skin Proteomics

His current research focuses in Functional Skin Proteomics and in the study of skin proteins modified by sensitising chemicals.

Previous research projects:

Therapeutic inhibition of LSD1 to attenuate androgen receptor signalling in castration resistant prostate cancer

Prostate cancer is one of the main causes of cancer related death in men. Treatment is critically reliant on androgen receptor (AR) signalling inhibition but virtually all patients become resistant to initial androgen deprivation (castration resistant prostate cancer, CRPC). Subsequent treatment options exist but the disease remains lethal (median 2-3 years) after transition to CRPC. CRPC therapeutic options include the ‘new generation’ AR antagonist enzalutamide. However despite proven efficacy virtually all patients develop clinical resistance. Enzalutamide/AR antagonist resistance mechanisms include activating AR splice variants and point mutations. Lysine (K)-specific demethylase 1A (LSD1), is an epigenetic AR co-activator which modifies chromatin structure at AR target genes. Our data show that LSD1 chemical inhibition suppresses prostate cancer cell growth and inhibits AR signalling. Critically, in AR response element reporter assays, we have now found that LSD1 inhibition reduces activation of both wild type AR and the enzalutamide resistant variant. We therefore hypothesise that LSD1 co-activation of the AR is retained and is therapeutically targetable in CRPC despite resistance to new generation hormonal therapy.

Structure, function and regulation of eukaryotic elongation factor 2 kinase (eEF2K)

Eukaryotic elongation factor 2 kinase phosphorylates and inactivates eEF2, a protein which mediates ribosomal translocation during elongation of the new polypeptide chain. This kinase belongs to a small family of kinases distinct from the main kinase superfamily. We are working to elucidate its structure and control, using a range of biophysical and structural approaches. The activity and expression levels of eEF2K are tightly controlled by many signalling pathways, including mTOR. We are investigating how these control mechanisms operate and their importance for regulating protein synthesis in a wide range of settings present in cancer (hypoxia, nutrient starvation).

Targeted nanoparticle as vehicle to deliver drugs to the centre nervous system

The treatment of neurodegenerative diseases is hampered by the current strategies used for drug delivery to neurons and the central nervous system. In this work we used polymersomes produced from non-toxic amphiphilic block copolymers functionalized with the tetanus toxin peptide (tet1) to target neuronal cells and to circumvent these obstacles. Targeting nanoparticles loaded with BSA-FITC and sodium valproate were used as a model to analyse the uptake into neuronal cell lines and to induce biological changes in neuronal “like” cells.

Gene expression changes during hepatitis delta virus infection. I. Analysis of the cellular proteome.

The Hepatitis Delta Virus (HDV) is the causative agent of delta hepatitis, one of the most severe forms of virus hepatitis. The HDV increases the risk of fulminant hepatitis, and development of liver cirrhosis. Despite being a small and simple virus, many questions remain answered concerning virus-host interactions and pathogenesis. Namely, it is not clear at all which are the cellular factors involved in each step of virus replication, and which are the mechanisms responsible for the worsening of symptoms and prognosis. We aim to contribute to a deeper and detailed knowledge of changes in gene expression at the protein level, as a result of HDV infection. We believe that this may represent an important contribution to the identification of potential targets for a specific antivirus therapy. Our approach is based on the analysis of the proteome of liver cells that express the HDV, and each of the virus components separately (S-HDAg, L-HDAg, genomic RNA, antigenomic RNA). Proteins that will display a different expression pattern will be identified by mass spectrometry. This approach allowed the identification of potential targets for a specific antivirus therapy.

 

Research group

Molecular and Cellular Biosciences

Affiliate research group

Centre for Protemic Research

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Dr Sergio Miguel Regufe da Mota
School of Biological Sciences
Faculty of Environmental and Life Sciences
Life Sciences Building 85
University of Southampton
Highfield Campus
Southampton
SO17 1BJ

Room Number: 85/4041/M55

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