scispace - formally typeset
G

Gabriella Forte

Researcher at University of Manchester

Publications -  23
Citations -  2188

Gabriella Forte is an academic researcher from University of Manchester. The author has contributed to research in topics: Aicardi–Goutières syndrome & Medicine. The author has an hindex of 12, co-authored 19 publications receiving 1679 citations. Previous affiliations of Gabriella Forte include Central Manchester University Hospitals NHS Foundation Trust & Manchester Academic Health Science Centre.

Papers
More filters
Journal ArticleDOI

Mutations in ADAR1 cause Aicardi-Goutières syndrome associated with a type I interferon signature

Gillian I. Rice, +53 more
- 01 Nov 2012 - 
TL;DR: It is shown that mutations in ADAR1 cause the autoimmune disorder Aicardi-Goutières syndrome (AGS), and it is speculated that ADar1 may limit the cytoplasmic accumulation of the dsRNA generated from genomic repetitive elements.
Journal ArticleDOI

Characterization of human disease phenotypes associated with mutations in TREX1, RNASEH2A, RNASEH2B, RNASEH2C, SAMHD1, ADAR, and IFIH1.

Yanick J. Crow, +135 more
TL;DR: A robust relationship between mutations in all seven genes with increased type I interferon activity in cerebrospinal fluid and serum, and the increased expression of interferOn‐stimulated gene transcripts in peripheral blood is observed.
Journal ArticleDOI

Assessment of interferon-related biomarkers in Aicardi-Goutières syndrome associated with mutations in TREX1, RNASEH2A, RNASEH2B, RNASEH2C, SAMHD1, and ADAR: a case-control study

Gillian I. Rice, +56 more
- 01 Dec 2013 - 
TL;DR: AGS is consistently associated with an interferon signature, which is apparently sustained over time and can thus be used to differentiate patients with AGS from controls, and neutralisation assays suggested that measurable antiviral activity was related toInterferon α production.
Journal ArticleDOI

N-terminal acetylation inhibits protein targeting to the endoplasmic reticulum.

TL;DR: A systematic analysis of the predicted N-terminal processing of cytosolic proteins versus those destined to be sorted to the secretory pathway found an equal and opposite bias against such modification for secretory proteins.