Email: e.zeqiraj@leeds.ac.uk

Research profile and key clinical specialties

My laboratory investigates how cell signalling networks are regulated by ubiquitin and how this impacts disease conditions and future therapeutic opportunities.

Our major research interests centre on:

• How ubiquitin signalling events regulate DNA damage and repair processes.
• The structural and molecular basis by which ubiquitin modifications regulate cytokine receptor signalling.
• How metabolism controls deubiquitylase (DUB) enzyme activity and immune signalling.

Two key publications

• M. Walden, T. Lei, U. Sykora, R. Ross, E. L. Hesketh, D. Byrne, S. K. Masandi, J. Cassel, R. George, J. R. Ault, K. Pawłowski, J. Salvino, F. Del Galdo, P. Eyers, N. A. Ranson, Roger A. Greenberg and E. Zeqiraj. Metabolic control of SHMT2 oligomerization regulates ubiquitin-dependent cytokine signaling. Nature, 570:194-199. PMCID: PM.C6914362
• R. W. Hunter, C. C. Hughey, L. Lantier, E. I. Sundelin, M. Peggie, E. Zeqiraj, F. Sicheri, N. Jessen, D. H. Wasserman and K. Sakamoto Metformin reduces liver glucose production by inhibition of fructose-1-6-bisphosphatase. Nature Medicine, 24(9):1395-1406, (2018). PMCID: PMC6207338

Possible PhD projects

• Manipulation of the ubiquitin system and protein degradation machinery in autoimmunity
• Structural and molecular studies of metabolic enzymes

More information

• Full publication list

Keywords: Elton, Zeqiraj, cell, signalling, networks, ubiquitin, autoimmunity, Leeds

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