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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{Nousbeck:2021:10.1111/bjd.19254,
author = {Nousbeck, J and McAleer, MA and Hurault, G and Kenny, E and Harte, K and Kezic, S and Tanaka, RJ and Irvine, AD},
doi = {10.1111/bjd.19254},
journal = {British Journal of Dermatology},
pages = {514--523},
title = {miRNA analysis of childhood atopic dermatitis reveals a role for miR-451a},
url = {http://dx.doi.org/10.1111/bjd.19254},
volume = {184},
year = {2021}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - BACKGROUND: MicroRNAs (miRNAs), important regulators of gene expression, have been implicated in a variety of disorders. The expression pattern of miRNAs in pediatric atopic dermatitis (AD) has not been well studied. OBJECTIVE: We sought to investigate miRNA expression profiles in different blood compartments of infants with AD. METHODS: Small RNA and HTG-Edge sequencing were performed to identify differentially expressed miRNAs in PBMCs and plasma of AD infants versus age-matched healthy controls, with reverse transcription quantitative real-time PCR used for validation and measurement of miRNA targets. Logistic regression models with AUROC estimation was used to evaluate the diagnostic potential of chosen miRNAs for AD. RESULTS: RNA sequencing was performed to access miRNA expression profile in pediatric AD. We identified ten differentially expressed miRNAs in PBMCs and eight dysregulated miRNAs in plasma of AD infants compared to controls. Upregulated miRNAs in PBMCs included miRNAs known to be involved in inflammation: miR-223-3p, miR-126-5p and miR-143-3p. Differential expression of only one miRNA, miR-451a, was observed in both PBMCs and plasma of children with AD. Dysregulation of three miRNAs: miR-451a, miR-143-3p and miR-223-3p was validated in larger number of samples and miR-451a was identified as a predictive biomarker for the early diagnosis of the disease. Experimentally verified targets of miR-451a, IL6R and PSMB8, were increased in AD patients, negatively correlated with miR-451a levels and upregulated following inhibition of miR-451a in PBMCs. CONCLUSION: In infants with AD, a distinct peripheral blood miRNA signature is seen, highlighting the systemic effects of the disease. miR-451a is uniquely expressed in different blood compartments of AD patients and may serve as a promising novel biomarker for the early diagnosis of AD.
AU - Nousbeck,J
AU - McAleer,MA
AU - Hurault,G
AU - Kenny,E
AU - Harte,K
AU - Kezic,S
AU - Tanaka,RJ
AU - Irvine,AD
DO - 10.1111/bjd.19254
EP - 523
PY - 2021///
SN - 0007-0963
SP - 514
TI - miRNA analysis of childhood atopic dermatitis reveals a role for miR-451a
T2 - British Journal of Dermatology
UR - http://dx.doi.org/10.1111/bjd.19254
UR - https://www.ncbi.nlm.nih.gov/pubmed/32478410
UR - https://onlinelibrary.wiley.com/doi/abs/10.1111/bjd.19254
UR - http://hdl.handle.net/10044/1/79973
VL - 184
ER -

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