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Synthetic Biology underpins advances in the bioeconomy

Biological systems - including the simplest cells - exhibit a broad range of functions to thrive in their environment. Research in the Imperial College Centre for Synthetic Biology is focused on the possibility of engineering the underlying biochemical processes to solve many of the challenges facing society, from healthcare to sustainable energy. In particular, we model, analyse, design and build biological and biochemical systems in living cells and/or in cell extracts, both exploring and enhancing the engineering potential of biology. 

As part of our research we develop novel methods to accelerate the celebrated Design-Build-Test-Learn synthetic biology cycle. As such research in the Centre for Synthetic Biology highly multi- and interdisciplinary covering computational modelling and machine learning approaches; automated platform development and genetic circuit engineering ; multi-cellular and multi-organismal interactions, including gene drive and genome engineering; metabolic engineering; in vitro/cell-free synthetic biology; engineered phages and directed evolution; and biomimetics, biomaterials and biological engineering.



BibTex format

author = {Toczek, M and Kutryb-Zajac, B and Zukowska, P and Slominska, E and Isalan, M and Mielcarek, M and Smolenski, R},
doi = {10.1080/15257770.2016.1154969},
journal = {Nucleosides, Nucleotides and Nucleic Acids},
pages = {707--712},
title = {Changes in cardiac nucleotide metabolism in Huntington’s disease},
url = {},
volume = {35},
year = {2016}

RIS format (EndNote, RefMan)

AB - Huntington’s disease (HD) is a monogenic neurodegenerative disorder with a significant peripheralcomponent to the disease pathology. This includes an HD-related cardiomyopathy, with an unknownpathological mechanism. In this study, we aimed to define changes in the metabolism of cardiacnucleotides using the well-established R6/2 mouse model. In particular, we focused on measuring theactivity of enzymes that control ATP and other adenine nucleotides in the cardiac pool, includingeNTPD, AMPD, e5'NT, ADA and PNP. We employed HPLC to assay the activities of these enzymes bymeasuring the concentrations of adenine nucleotide catabolites in the hearts of symptomatic R6/2 mice.We found a reduced activity of AMPD (12.9 ± 1.9 nmol/min/mg protein in control; 7.5 ± 0.5nmol/min/mg protein in R6/2) and e5'NT (11.9 ± 1.7 nmol/min/mg protein in control; 6.7 ± 0.7nmol/min/mg protein in R6/2). Moreover, we detected an increased activity of ADA (1.3 ± 0.2nmol/min/mg protein in control; 5.2 ± 0.5 nmol/min/mg protein in R6/2), while no changes in eNTPDand PNP activities were detected. Analysis of cardiac adenine nucleotide catabolite levels revealed anincreased inosine level (0.7 ± 0.01 nmol/mg dry tissue in control; 2.7 ±0.8 nmol/mg dry tissue in R6/2)and a reduced concentration of cardiac adenosine (0.9 ± 0.2 nmol/mg dry tissue in control; 0.2 ± 0.08nmol/mg dry tissue in R6/2). This study highlights a decreased rate of degradation of cardiac nucleotidesin HD mouse model hearts, and an increased capacity for adenosine deamination, that may alteradenosine signaling.
AU - Toczek,M
AU - Kutryb-Zajac,B
AU - Zukowska,P
AU - Slominska,E
AU - Isalan,M
AU - Mielcarek,M
AU - Smolenski,R
DO - 10.1080/15257770.2016.1154969
EP - 712
PY - 2016///
SN - 1525-7770
SP - 707
TI - Changes in cardiac nucleotide metabolism in Huntington’s disease
T2 - Nucleosides, Nucleotides and Nucleic Acids
UR -
UR -
VL - 35
ER -