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Profil bibliographique

Georgina F Osborne

Informations fournies par OpenAlex. Research Africa ne déduit ni nationalité, ni poste, ni coordonnées personnelles.

39Publications signalées
1157Citations signalées
4Affiliations récentes

Les institutions déclarées

Les domaines associés

Genetic Neurodegenerative DiseasesMitochondrial Function and PathologyMuscle Physiology and DisordersNeurological disorders and treatmentsCardiomyopathy and Myosin Studies

Les publications récentes

2026 article OpenAlex

Blocking somatic repeat expansion and lowering huntingtin by RNAi synergize to attenuate Huntington’s disease pathogenesis in mice

Jillian Belgrad, Ashley Summers, Christian Landles, Jonathan Greene et autres

Huntington's disease (HD) is a progressive neurodegenerative disorder with no approved therapies. Despite multiple clinical trials, huntingtin (HTT)-lowering strategies have yet to show meaningful clinical benefit. Both somatic expansion and toxic HTT species are key molecular drivers of HD, yet therapeutic strategies …

us, gb (code pays fourni par la source)

0 citations Science Translational Medicine
Accès ouvert 2026 article OpenAlex

Human-specific sequence features in HTT exon 1 promote toxic misprocessing via splicing factor SRSF7

Camilla Maffezzini, Raffaele Iennaco, Andrea Scolz, Simone Maestri et autres

Expansion of CAG repeats in HTT exon 1 is the acknowledged driver of Huntington’s disease. Alternative processing of HTT pre-mRNA generates the truncated HTT1a transcript, translated into a toxic peptide. While its dependence on CAG length is well documented, the role of …

it, gb, se, us (code pays fourni par la source)

0 citations Nature Communications
Accès ouvert 2026 article OpenAlex

Enhancing the detection of HTT1a with neoepitope antibodies in mouse models of Huntington’s disease

Georgina F Osborne, Edward J. Smith, Kirupa Sathasivam, Xinin Kang et autres

Abstract Huntington’s disease is an inherited neurodegenerative disorder caused by a CAG repeat expansion in exon 1 of the huntingtin (HTT) gene, encoding an expanded polyglutamine tract in the huntingtin (HTT) protein. The pathogenic CAG repeat of HTT is unstable and undergoes …

gb (code pays fourni par la source)

0 citations Brain Communications
Accès ouvert 2025 preprint OpenAlex

Selective targeting of mutant huntingtin intron-1 improves rescue provided by antisense oligonucleotides

Robert M. Bragg, Christian Landles, E. J. Smith, Georgina F Osborne et autres

Abstract Huntington’s disease (HD) arises from the toxic gain of function caused by a CAG expansion in the coding region of the HTT gene. HD is increasingly appreciated to emerge from multiple pathogenic processes, including somatic instability in mutant HTT’s ( mHTT …

us, gb (code pays fourni par la source)

3 citations bioRxiv (Cold Spring Harbor Laboratory)
Accès ouvert 2025 preprint OpenAlex

Blocking somatic repeat expansion and lowering huntingtin via RNA interference synergize to prevent Huntington’s disease pathogenesis in mice

Jillian Belgrad, Ashley Summers, Christian Landles, Jonathan Greene et autres

Huntington's disease (HD) is a progressive neurodegenerative disorder with no approved therapies. Two major molecular drivers-somatic expansion of inherited CAG repeats and toxic mutant HTT (mHTT) variants-lead to neuronal dysfunction. Despite multiple trials, HTT-lowering strategies have not shown meaningful clinical benefit. Using …

us, gb (code pays fourni par la source)

8 citations bioRxiv (Cold Spring Harbor Laboratory)
Accès ouvert 2025 preprint OpenAlex

Lowering the HTT1a transcript as an effective therapy for Huntington’s disease

Aikaterini S. Papadopoulou, Julia F. Alterman, Christian Landles, Edward J. Smith et autres

Abstract Lowering the levels of HTT transcripts has been a major focus of therapeutic development for Huntington’s disease (HD), but which transcript should be lowered? HD is caused by a CAG repeat expansion in exon 1 of the HTT gene, and the …

gb, in, us, pk (code pays fourni par la source)

4 citations bioRxiv (Cold Spring Harbor Laboratory)
Accès ouvert 2024 conference-abstract OpenAlex

B005 Characterisation of mouse embryonic fibroblast models of Huntington’s disease and their application as screening tools for therapeutic agents

Casandra Gomez-Paredes, Kirupa Sathasivam, Aikaterini S. Papadopoulou, Sandra Fieńko et autres

Background Mouse embryonic fibroblasts (MEFs) have been isolated from the widely studied Huntington’s disease (HD) mouse models zQ175 and YAC128. zQ175 knock-in mice contain a mutated version of human HTT exon 1 integrated into mouse Htt and carry approximately 175-200 CAGs. YAC128 …

gb (code pays fourni par la source)

0 citations
Accès ouvert 2024 conference-paper OpenAlex

A015 Mutant Huntingtin protein levels decrease with CAG repeat expansion: implications for therapeutics and bioassays

Christian Landles, Georgina F Osborne, Jemima Phillips, Maria Canibano Pico et autres

Background The Huntington’s disease CAG repeat expansion is unstable and expands in brain and peripheral tissues throughout life. The rate of somatic expansion drives the age of onset and rate of disease progression. Mutant HTT pre-mRNA can be alternatively processed to generate …

gb (code pays fourni par la source)

0 citations
Accès ouvert 2024 conference-abstract OpenAlex

A002 A CAG repeat threshold for therapeutics targeting somatic instability in mouse models of Huntington’s disease

Sarah G. Aldous, Edward J. Smith, Christian Landles, Georgina F Osborne et autres

Background The Huntington’s disease (HD) mutation is a CAG repeat expansion that encodes for an expanded polyglutamine tract. The CAG repeat is unstable, and expansions of hundreds of CAGs have been detected in HD post-mortem brains. Mismatch repair genes, including MSH3, known …

gb, us (code pays fourni par la source)

0 citations
Accès ouvert 2024 conference-paper OpenAlex

A021 Early detection of exon 1 Huntingtin aggregation in zQ175 brains by molecular and histological approaches

E. J. Smith, Kirupa Sathasivam, Christian Landles, Georgina F Osborne et autres

Background Huntington-lowering approaches are a major focus for therapeutic intervention for Huntington’s disease. In evaluating these treatments, it will be important to understand how the targeting strategy affects (1) levels of the HTT1a and full-length HTT transcripts, (2) the soluble HTTexon1 and …

gb (code pays fourni par la source)

0 citations
Accès ouvert 2024 article OpenAlex

Exon 1-targeting miRNA reduces the pathogenic exon 1 HTT protein in Huntington's disease models

Marina Sogorb-González, Christian Landles, Nicholas S. Caron, Anouk Stam et autres

Huntington's disease (HD) is a fatal neurodegenerative disease caused by a trinucleotide repeat expansion in exon 1 of the huntingtin gene (HTT) that results in toxic gain of function and cell death. Despite its monogenic cause, the pathogenesis of HD is highly …

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27 citations Brain
Accès ouvert 2024 preprint OpenAlex

Mutant HTT protein decreases with CAG repeat expansion: implications for therapeutics and bioassays

Christian Landles, Georgina F Osborne, Jemima Phillips, Maria Canibano Pico et autres

ABSTRACT Huntington’s disease is an inherited neurodegenerative disorder caused by a CAG repeat expansion that encodes a polyglutamine tract in the HTT protein. The mutant CAG repeat is unstable and expands in specific brain cells and peripheral tissues throughout life. Genes involved …

gb, us (code pays fourni par la source)

1 citation bioRxiv (Cold Spring Harbor Laboratory)

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