Overexpression of UBQLN1 reduces neuropathology in the P497S UBQLN2 mouse model of ALS/FTD

Overexpression of UBQLN1 reduces neuropathology in the P497S UBQLN2 mouse model of ALS/FTD

Abstract Missense mutations in UBQLN2 cause X-linked dominant inheritance of amyotrophic lateral sclerosis with frontotemporal dementia (ALS/FTD). UBQLN2 belongs to a family of four highly homologous proteins expressed in humans that play diverse roles in maintaining proteostasis, but whether one is...

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Bibliographic Details
Main Authors: Shaoteng Wang, Micaela Tatman, Mervyn J. Monteiro
Format: Article
Language:English
Published: BMC 2020-10-01
Series:Acta Neuropathologica Communications
Subjects:
Amyotrophic lateral sclerosis
UBQLN1
UBQLN2
Motor neuron disease
Proteostasis
Online Access:http://link.springer.com/article/10.1186/s40478-020-01039-9

Internet

http://link.springer.com/article/10.1186/s40478-020-01039-9

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