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Mr Kritarth Singh
138, Duchen-Szabadkai Lab
Department of Cell and Developmental Biology
University College London, Gower Street
London
UK
WC1E 6BT
Appointment
  • Research Fellow
  • Cell & Developmental Biology
  • Div of Biosciences
  • Faculty of Life Sciences
Biography

I studied Biochemistry at the University of Burdwan, India, completing my post-graduation in 2011. Subsequently, I joined the Institute of Advanced Research, India as a Research Fellow in 2013 and later moved to Department of Biochemistry at The Maharaja Sayajirao University of Baroda, India, completing my PhD 'Study the role of NLRX1 in regulation of TNF-α-induced cancer cell death and metabolism' (supervised by Prof. Rajesh Singh) in 2019. During my PhD, I worked with Department of Pharmacology in design/synthesis of nano-conjugates and its application to glioblastoma. I also worked at the Seoul National University, South Korea, exploring the quantitative mitochondrial proteome of breast cancer cells.


Currently, I am working as a Postdoctoral research fellow with Prof. Michael Duchen (Principle Investigator) at the University College London and Prof. Heinz Jungbluth and Dr Manolis Fanto (Project collaborators) at the King's College London. In general, my research focuses on  understanding the crosstalk between mitochondrial dysfunction and impaired autophagy pathway in the pathophysiology of neurodegenerative disorders.

Research Summary

As a cell biologist, I have been always fascinated by the various cellular mechanisms that maintain an optimal mitochondrial form and function in a narrow physiological range, contributing to cellular homeostasis. How the subtle changes in mitochondrial form and function reaches its point of inflection, thus affecting cell physiology in normal and diseased conditions ranging from cancer to cardiovascular to neurodegenerative disorders.

To answer this, our primary aims are to investigate the role and mechanisms of mitochondrial dysfunction in the pathophysiology of Vici syndrome- a rare multisystem autophagy disorder with neurodegeneration. We further aim to characterize the extent to which mitochondrial dysfunction and impaired energy supply contribute to Vici syndrome related to EPG5 mutations.

The ongoing work is attempting to characterize the mitochondrial bioenergetic function and calcium signalling in cellular models of  Vici syndrome. The long-term goal to identify the pharmacologically targeted pathways that couple EPG5 mutations associated with dysfunctional autophagy to impaired mitochondrial function with potential patient benefit.

Appointments
11-FEB-2019 Research Associate Cell and Developmental Biology University College London, United Kingdom
Academic Background
2019   Doctor of Philosophy Maharaja Sayajirao University of Baroda
2011   Master of Science University of Burdwan
2009   Bachelor of Science Saurashtra University, Rajkot
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