Alison L. Hogan

2 Technology Place
North Ryde, NSW 2109, Australia

Last Updated: 09/26/2026

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Found 23 publications

Human TDP-43 overexpression in zebrafish motor neurons triggers MND-like phenotypes through gain-of-function mechanism.

Human TDP-43 overexpression in zebrafish motor neurons triggers MND-like phenotypes through gain-of-function mechanism.

Journal: bioRxiv : the preprint server for biology

Published: July 17, 2025

Human TDP-43 overexpression in zebrafish motor neurons triggers MND-like phenotypes through gain-of-function mechanism.

Human TDP-43 overexpression in zebrafish motor neurons triggers MND-like phenotypes through gain-of-function mechanism.

Journal: Acta neuropathologica communications

Published: July 11, 2025

Protocol for characterizing biomolecular condensates through live-cell imaging and analysis.

Protocol for characterizing biomolecular condensates through live-cell imaging and analysis.

Journal: STAR protocols

Published: April 13, 2025

Critical impact of lysine 136 in TDP-43 phase separation, compartmentalization, and aggregation in living vertebrates.

Critical impact of lysine 136 in TDP-43 phase separation, compartmentalization, and aggregation in living vertebrates.

Journal: iScience

Published: November 19, 2024

Cyclin F can alter the turnover of TDP-43.

Cyclin F can alter the turnover of TDP-43.

Journal: Neurobiology of disease

Published: October 23, 2023

RNA-binding properties orchestrate TDP-43 homeostasis through condensate formation in vivo.

RNA-binding properties orchestrate TDP-43 homeostasis through condensate formation in vivo.

Journal: Nucleic acids research

Published: June 23, 2023

Cyclin F, Neurodegeneration, and the Pathogenesis of ALS/FTD.

Cyclin F, Neurodegeneration, and the Pathogenesis of ALS/FTD.

Journal: The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry

Published: September 05, 2022

Co-deposition of SOD1, TDP-43 and p62 proteinopathies in ALS: evidence for multifaceted pathways underlying neurodegeneration.

Co-deposition of SOD1, TDP-43 and p62 proteinopathies in ALS: evidence for multifaceted pathways underlying neurodegeneration.

Journal: Acta neuropathologica communications

Published: July 28, 2022

Altered SOD1 maturation and post-translational modification in amyotrophic lateral sclerosis spinal cord.

Altered SOD1 maturation and post-translational modification in amyotrophic lateral sclerosis spinal cord.

Journal: Brain : a journal of neurology

Published: December 14, 2021

Flow cytometry allows rapid detection of protein aggregates in cellular and zebrafish models of spinocerebellar ataxia 3.

Flow cytometry allows rapid detection of protein aggregates in cellular and zebrafish models of spinocerebellar ataxia 3.

Journal: Disease models & mechanisms

Published: March 18, 2021

Splicing factor proline and glutamine rich intron retention, reduced expression and aggregate formation are pathological features of amyotrophic lateral sclerosis.

Splicing factor proline and glutamine rich intron retention, reduced expression and aggregate formation are pathological features of amyotrophic lateral sclerosis.

Journal: Neuropathology and applied neurobiology

Published: December 03, 2020

Unbiased Label-Free Quantitative Proteomics of Cells Expressing Amyotrophic Lateral Sclerosis (ALS) Mutations in CCNF Reveals Activation of the Apoptosis Pathway: A Workflow to Screen Pathogenic Gene Mutations.

Unbiased Label-Free Quantitative Proteomics of Cells Expressing Amyotrophic Lateral Sclerosis (ALS) Mutations in CCNF Reveals Activation of the Apoptosis Pathway: A Workflow to Screen Pathogenic Gene Mutations.

Journal: Frontiers in molecular neuroscience

Published: November 10, 2020

Showing 1-12 of 23

Last Updated: 09/26/2026