News

Professor Sir Philip Cohen is recently returned from a 10-day visit to India where, as a guest of the British Council, he gave 6 lectures to audiences in Kolkata, Guwahati, and Mumbai. During his free weekend, Philip took a 5-hour taxi ride from Guwahati - in the State of Assam, in North East India - passing many famous tea plantations (called tea gardens in Assam) to the Kaziranga National Park, where he went on safari by elephant at dawn. The elephant driver is carrying a rifle in case of attack by tigers, or charging rhino or water buffalo. 

This was Philip's second ride on an elephant, the first having been at London Zoo, 61 years ago. 

 …more

Last night MRC PPU Programme Leader and Wellcome Senior Clinical Fellow, Miratul Muqit, delivered the Francis Crick Lecture at the Royal Society in front of a packed audience comprising scientists and members of the public including Parkinson’s patients.

 …more

On January 18, 2018 the MRC PPU opened its doors for a visit for people affected by Parkinson’s, organised by the Dundee Research Interest Group (DRIG).  Over 25 people spent the afternoon not only talking to MRC PPU Director Professor Dario Alessi and the many researchers working to unravel the mechanisms that cause Parkinson’s, but also going on a tour of the Centre for Translational and Interdisciplinary Research (CTIR) Mass Spectrometry facility, an immunofluorescent microscopy demonstration, and having other scientists explain their work at the bench. …more

Congratulations to MRC PPU Postdocs Giulia Saredi (Rouse lab) and Lea Wilhelm (Ganley lab) for being awarded prestigious EMBO long-term Fellowships

 …more

Calum Sutherland, a PhD student in Philip Cohen’s lab from 1993 to 1996, has been promoted to Professor of Molecular Medicine in the School of Medicine, University of Dundee.  Calum graduated with a B.Sc. in Biochemistry from the University of St Andrews in 1985, and then spent five years working with pharmaceutical company Glaxo in London before joining Philip’s lab in 1991 where he made seminal contributions to our understanding of how insulin inhibits the protein kinase GSK3 to stimulate glycogen synthesis. …more

Mutations in genes encoding PINK1 (PTEN-induced kinase 1) and the ubiquitin E3 ligase Parkin are associated with early-onset Parkinson’s disease. Several years ago the laboratory of Miratul Muqit discovered that upon mitochondrial damage, PINK1 can phosphorylate Parkin at a highly conserved residue, Serine 65 (Ser65), that lies within its N-terminal Ubiquitin-like domain (Ubl). Further, it was discovered that PINK1 can phosphorylate Ubiquitin at an equivalent Ser65 residue and this associates with Parkin in a complex to trigger maximal activation of Parkin E3 ligase activity. …more

Our flagship DSTT (Division of Signal Transduction Therapy) collaboration with pharmaceutical companies is still going remarkably strongly after 20 years. Founded in 1998, it is believed to be one of the longest continuous collaborations between academia and pharmaceutical companies.

 

 …more

As part of the Lister Prize that Yogesh Kulathu received last year, he has delivered a keynote lecture at the University of Dundee entitled “Reversing ubiquitylation: Mechanisms and functions of Deubiquitinases”. Sir Alex Markham (Chair) and Ms Kate Law (Director) of Lister Institute attended the lecture.

 

 …more
Miratul Muqit Portrait

We are delighted to announce that MRC-PPU PI Miratul Muqit has been promoted to the rank of Professor. 

Miratul joined the MRC-PPU after he completed his clinical neurology training in 2008, to investigate the role of the Parkinson's disease PINK1 protein kinase that he played a key role in uncovering during his PhD in the laboratory of Nicholas Wood (UCL).

 …more

Cyclin-dependent kinase-like 5 (CDKL5/STK9) is a poorly understood protein kinase mutated in CDKL5 disorder. This disease is characterized by seizure onset before 3 months of age, severely impaired gross motor, language and hand skills and subtle but shared physical characteristics. It is not clear why mutations in CDKL5 cause this disease, especially as the cellular processes controlled by CDKL5 remain unknown and the cellular targets of CDKL5 and the mechanisms controlling its activity are also unclear. 

 

 …more