ER strikes again: Proteostasis Dysfunction In ALS


Autoria(s): Maharjan, Niran; Saxena, Smita
Data(s)

11/03/2016

Resumo

The precise contribution of endoplasmic reticulum (ER) chaperone protein disulfide isomerase (PDI) variants in human amyotrophic lateral sclerosis (ALS) patients to the pathogenesis of ALS remained unclear. In the present study, Woehlbier et al (2016) demonstrated that these PDI variants are capable of altering motor neuron morphology, impairing the expression of synaptic proteins, and compromising neuromuscular junction (NMJ) integrity.

Formato

application/pdf

Identificador

http://boris.unibe.ch/79961/1/EMBO%20J.pdf

Maharjan, Niran; Saxena, Smita (2016). ER strikes again: Proteostasis Dysfunction In ALS. EMBO journal, 35(8), pp. 798-800. Nature Publishing Group 10.15252/embj.201694117 <http://dx.doi.org/10.15252/embj.201694117>

doi:10.7892/boris.79961

info:doi:10.15252/embj.201694117

info:pmid:26968985

urn:issn:0261-4189

Idioma(s)

eng

Publicador

Nature Publishing Group

Relação

http://boris.unibe.ch/79961/

Direitos

info:eu-repo/semantics/restrictedAccess

Fonte

Maharjan, Niran; Saxena, Smita (2016). ER strikes again: Proteostasis Dysfunction In ALS. EMBO journal, 35(8), pp. 798-800. Nature Publishing Group 10.15252/embj.201694117 <http://dx.doi.org/10.15252/embj.201694117>

Palavras-Chave #570 Life sciences; biology #610 Medicine & health
Tipo

info:eu-repo/semantics/article

info:eu-repo/semantics/publishedVersion

PeerReviewed