Proteomics

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Proteomic analysis of a filaggrin-deficient skin organoid model shows evidence of increased translation, keratinocyte-immune crosstalk and disordered axon guidance


ABSTRACT: Atopic eczema is an itchy inflammatory disorder characterised by skin barrier dysfunction. Loss-of-function mutations in the gene encoding filaggrin (FLG) are a major risk factor, but the mechanisms by which filaggrin haploinsufficiency leads to atopic inflammation remain incompletely understood. Skin as an organ which can be modelled using primary cells in vitro provides the opportunity for selected genetic effects to be investigated in detail.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Keratinocyte, Skin

DISEASE(S): Eczema

SUBMITTER: Sara ten Have  

LAB HEAD: Sara Brown

PROVIDER: PXD014875 | Pride | 2019-08-14

REPOSITORIES: Pride

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Publications

Functional and proteomic analysis of a full thickness filaggrin-deficient skin organoid model.

Elias Martina S MS   Wright Sheila C SC   Nicholson William V WV   Morrison Kimberley D KD   Prescott Alan R AR   Ten Have Sara S   Whitfield Phillip D PD   Lamond Angus I AI   Brown Sara J SJ  

Wellcome open research 20191126


<b>Background:</b> Atopic eczema is an itchy inflammatory disorder characterised by skin barrier dysfunction. Loss-of-function mutations in the gene encoding filaggrin ( <i>FLG</i>) are a major risk factor, but the mechanisms by which filaggrin haploinsufficiency leads to atopic inflammation remain incompletely understood. Skin as an organ that can be modelled using primary cells <i>in vitro</i> provides the opportunity for selected genetic effects to be investigated in detail. <b>Methods:</b> P  ...[more]

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