ArticleMolecular brain2020
Protrudin-deficient mice manifest depression-like behavior with abnormalities in activity, attention, and cued fear-conditioning.
Article in Molecular brain, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- PDZD8-deficient mice manifest behavioral abnormalities related to emotion, cognition, and adaptation due to dyslipidemia in the brain.Molecular brain · 2023Article
- Effect of brain acidification on depression-related behaviors in diabetes mellitus.Frontiers in psychiatry · 2023Article
- PDZD8-deficient mice accumulate cholesteryl esters in the brain as a result of impaired lipophagy.iScience · 2022Article
- Protrudin regulates FAK activation, endothelial cell migration and angiogenesis.Cellular and molecular life sciences : CMLS · 2022Article
- Lipid Transfer-Dependent Endosome Maturation Mediated by Protrudin and PDZD8 in Neurons.Frontiers in cell and developmental biology · 2020Review
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protrudin is a protein that resides in the membrane of the endoplasmic reticulum and is highly expressed in the nervous system. Although mutations in the human protrudin gene (ZFYVE27, also known as SPG33) give rise to hereditary spastic paraplegia (HSP), the physiological role of the encoded protein has been largely unclear. We therefore generated mice deficient in protrudin and subjected them to a battery of behavioral tests designed to examine their intermediate phenotypes. The protrudin-deficient mice were found to have a reduced body size and to manifest pleiotropic behavioral abnormalities, including hyperactivity, depression-like behavior, and deficits in attention and fear-conditioning memory. They exhibited no signs of HSP, however, consistent with the notion that HSP-associated mutations of protrudin may elicit neural degeneration, not as a result of a loss of function, but rather as a result of a gain of toxic function. Overall, our results suggest that protrudin might play an indispensable role in normal neuronal development and behavior.
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