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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.

Publications

Citation

BibTex format

@article{Mielcarek:2017:10.3389/fphys.2017.00127,
author = {Mielcarek, M and Smolenski, RT and Isalan, M},
doi = {10.3389/fphys.2017.00127},
journal = {Frontiers in Physiology},
title = {Transcriptional signature of an altered purine metabolism in the skeletal muscle of a Huntington’s disease mouse model},
url = {http://dx.doi.org/10.3389/fphys.2017.00127},
volume = {8},
year = {2017}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Huntington’s disease (HD) is a fatal neurodegenerative disorder,caused by a polyglutamine expansion in the huntingtin protein (HTT).HD has a peripheral component to its pathology: skeletal musclesare severely affected, leading to atrophy and malfunction in both pre-clinical and clinical settings. We previously used two symptomatic HD mouse models to demonstrate the impairment of the contractile characteristics of the hind limb muscles, which was accompanied by a significant loss of function of motor units. The mice displayed a significant reduction in muscle force, likely because of deteriorationsin energy metabolism, decreased oxidation and altered purine metabolism. There is growing evidence suggesting that HD-related skeletal muscle malfunction might be partially or completely independent of CNS degeneration. The pathology might arise from mutant HTT within muscle (loss or gain of function). Hence, it is vital to identify novel peripheral biomarkers that will reflect HD skeletal muscle atrophy. These will be important for upcoming clinical trials that may target HD peripherally. In order to identify potential biomarkers that might reflect muscle metabolic changes, we used qPCR to validate key gene transcripts in different skeletal muscle types. Consequently, we report a number of transcript alterations that are linked to HD muscle pathology.
AU - Mielcarek,M
AU - Smolenski,RT
AU - Isalan,M
DO - 10.3389/fphys.2017.00127
PY - 2017///
SN - 1664-042X
TI - Transcriptional signature of an altered purine metabolism in the skeletal muscle of a Huntington’s disease mouse model
T2 - Frontiers in Physiology
UR - http://dx.doi.org/10.3389/fphys.2017.00127
UR - http://hdl.handle.net/10044/1/44817
VL - 8
ER -

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Work in the IC-CSynB is supported by a wide range of Research Councils, Learned Societies, Charities and more.