Author

Linlin Ma

Griffith UniversityORCID 0000-0002-4716-5158Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Approach:experimental assay· 2 Assay:bulk RNA-seq· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Assay:electrophysiology· 1 Research Focus:gene regulatory network inference· 1 Organism:human· 1

Frequent Co-Authors

George D. MellickiD· 2 shared Mo CheniD· 2 shared Alex M. SykesiD· 1 shared Benjamin Garland· 1 shared Bingmiao GaoiD· 1 shared Bo GaoiD· 1 shared David J. AdamsiD· 1 shared Des Raymond RichardsoniD· 1 shared

Activity by Year

2025-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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2 shared papersNeuroscience

George D. MellickORCID

Mutual co-authors in cluster

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2 papers

Recent·Most cited

Kir4.2 deficiency drives progressive Parkinson's disease-like motor, cognitive and neuropathological phenotypes in mice

Benjamin Garland, Zhiqiang Shen, Mo Chen, Bo Gao, Kailin Mao, Des Raymond Richardson, George D. Mellick, Linlin Ma

This study shows that Kir4.2 deficiency in mice causes PD-like motor, cognitive, and neuropathological symptoms, establishing a new model for PD research.

bioRxiv · May 4, 2026 · PreprintNeuroscience

Parkinson's Disease-Linked Kir4.2 Mutation R28C Leads to Loss of Ion Channel Function

Xiaoyi Chen, Rocio K. Finol‐Urdaneta, Mo Chen, Alex M. Sykes, Bingmiao Gao, Jamila Iqbal, David J. Adams, George D. Mellick, Linlin Ma

This study investigates the impact of the Kir4.2R28C mutation on channel function and cellular processes, finding it causes loss of function and disrupts protein stability and trafficking.

The Journal of Physiology · Jun 1, 2025Peer-reviewedCell Biology