Research groups
Aminah Loonat
Postdoctoral Research Scientist
RESEARCH INTEREST
I am a postdoctoral research scientist in the group of Associate. Prof. Pawel Swietach. My research interest lies in understanding intracellular cardiac signalling pathways involved in the development of cardiac hypertrophy and heart failure. I am currently working on a BHF funded project which aims to understand H+ ion control and signalling in cardiac hypertrophy and heart failure. My key interest is how proteins change behaviour in disease conditions, and how this acts to bring about a change at the cellular level. As such I am interested in:
1. Changes in expression of proteins
2. How proteins interact with each other
3. If proteins undergo post-translational changes
4. If proteins change intracellular localisation
To address these questions, I employ a wide range of molecular and biochemical techniques such as RT-PCR, SDS-PAGE/Western blotting, Phostag gel analysis, immunocytochemistry, gene knockdown, overexpression and site directed mutagenesis.
BIOGRAPHY AND EDUCATION
I joined the Oxford Proton Signalling Group in 2016 as a postdoctoral research scientist, having previously completed my PhD at the BHF Centre of Excellence, St Thomas’ Hospital, King’s College London. My doctoral work was also focused on signalling in cardiac hypertrophy, examining the role of p38ɣ and its substrates in disease progression.
Recent publications
-
Nitric oxide modulates cardiomyocyte pH control through a biphasic effect on sodium/hydrogen exchanger-1.
Journal article
Richards MA. et al, (2020), Cardiovasc Res, 116, 1958 - 1971
-
p38γ MAPK contributes to left ventricular remodeling after pathologic stress and disinhibits calpain through phosphorylation of calpastatin
Journal article
Loonat AA. et al, (2019), The FASEB Journal, 33, 13131 - 13144
-
A high-throughput ratiometric method for imaging hypertrophic growth in cultured primary cardiac myocytes.
Journal article
Loonat AA. et al, (2019), J Mol Cell Cardiol, 130, 184 - 196
-
Iron-deficiency anemia reduces cardiac contraction by downregulating RyR2 channels and suppressing SERCA pump activity.
Journal article
Chung YJ. et al, (2019), JCI Insight, 4
-
ELUCIDATING THE ROLE OF P38 gamma IN PATHOLOGICAL CARDIAC HYPERTROPHY
Conference paper
Loonat A. et al, (2014), HEART, 100