2026-10-14T14:19:22Z https://api.figshare.com/v2/oai

oai:figshare.com:article/33842451 2026-09-16T11:06:34Z category_4 category_7 category_12 category_13 category_14 category_15 category_734 portal_63 item_type_3 month_year_09_2026

Altered Membrane Protein Abundance in the Cerebral Cortex of the JNPL3 Mouse Model of Tauopathy Sabrina Petralla (5681105) Jooseppi Hyvärinen (24976143) Mikko Gynther (2371981) Alexey Afonin (6253355) Marko Lehtonen (570178) Seppo Auriola (724269) Maria Panayotova (24976146) Katja M. Kanninen (8998832) Gert Fricker (308126) Elena Puris (2821660) Biochemistry Medicine Cell Biology Genetics Molecular Biology Neuroscience Biological Sciences not elsewhere classified provide novel information membrane proteins constitute including frontotemporal dementia essential cellular processes drug delivery targets different altered pathways associated neurodegenerative diseases jnpl3 mouse model female mouse models membrane proteomic changes membrane proteins involved membrane protein abundances female jnpl3 mice male jnpl3 mice jnpl3 mice associated changes female groups prefrontal cortex matched wild large proportion key roles independent acquisition human tauopathy examined alterations developing treatments current therapeutic could aid complex pathogeneses cerebral cortex alzheimer ’ Developing effective therapeutic approaches for tau-associated neurodegenerative diseases, including frontotemporal dementia and Alzheimer’s disease, remains extremely challenging due to their complex pathogeneses. Membrane proteins constitute a large proportion of current therapeutic and drug delivery targets because of their key roles in essential cellular processes. Here, we examined alterations in membrane protein abundances in the prefrontal cortex of male and female mouse models of human tauopathy, JNPL3 mice, compared with sex-matched wild-type (WT) mice using quantitative proteomics. The data-independent acquisition (DIA) proteomics analysis revealed various alterations in membrane proteins involved in different altered pathways in male JNPL3 mice (e.g., nucleotide metabolism and translation) and female JNPL3 mice (e.g., mitochondrial function). In addition, we found sex-associated changes in the abundances of several proteins previously reported to be involved in tau pathology, such as Reelin, DARPP-32, Zyxin, Tbce, and Gng5, in JNPL3 mice. Our multiple-reaction monitoring absolute quantitative analysis of transporter proteins revealed reduced abundance of the main drug efflux transporter ABCB1 in male JNPL3 mice compared with WT animals, with no changes in female groups. All in all, we provide novel information on membrane proteomic changes in male and female mouse models of human tauopathy, JNPL3 mice, which could aid in developing treatments for tau-associated neurodegenerative diseases and facilitate the prediction of neuropharmacokinetics in female and male patients. 2026-09-16T00:00:00Z Dataset Dataset 10.1021/acs.jproteome.6c00679.s002 https://figshare.com/articles/dataset/Altered_Membrane_Protein_Abundance_in_the_Cerebral_Cortex_of_the_JNPL3_Mouse_Model_of_Tauopathy/33842451 CC BY-NC 4.0