Loss of TMEM 106B potentiates lysosomal and FTLD ‐like pathology in progranulin‐deficient mice-Reference-Cited by-同舟云学术

Loss of TMEM 106B potentiates lysosomal and FTLD ‐like pathology in progranulin‐deficient mice

Published:2020-09-14 Issue:10 Volume:21 Page:
ISSN:1469-221X
Container-title:EMBO reports
language:en
Short-container-title:EMBO Rep

Author:

Werner Georg¹^ORCID,Damme Markus²,Schludi Martin³,Gnörich Johannes⁴,Wind Karin⁴,Fellerer Katrin¹,Wefers Benedikt³⁵,Wurst Wolfgang³⁵⁶,Edbauer Dieter³^ORCID,Brendel Matthias⁴,Haass Christian¹³⁶^ORCID,Capell Anja¹^ORCID

Affiliation:

1. Metabolic Biochemistry Biomedical Center (BMC) Faculty of Medicine Ludwig‐Maximilians‐Universität München Munich Germany

2. Institute of Biochemistry Kiel University Kiel Germany

3. German Center for Neurodegenerative Diseases (DZNE) Munich Germany

4. Department of Nuclear Medicine University Hospital Ludwig‐Maximilians‐Universität München Munich Germany

5. Institute of Developmental Genetics Helmholtz Zentrum München German Research Center for Environmental Health Neuherberg Germany

6. Munich Cluster for Systems Neurology (SyNergy) Munich Germany

Funder

Deutsche Forschungsgemeinschaft

Helmholtz-Gemeinschaft

Publisher

EMBO

Subject

Genetics,Molecular Biology,Biochemistry

Link

https://onlinelibrary.wiley.com/doi/pdf/10.15252/embr.202050241

Reference86 articles.

1. Accelerated Lipofuscinosis and Ubiquitination in Granulin Knockout Mice Suggest a Role for Progranulin in Successful Aging

2. Portuguese family with the co-occurrence of frontotemporal lobar degeneration and neuronal ceroid lipofuscinosis phenotypes due to progranulin gene mutation

3. Partial Tmem106b reduction does not correct abnormalities due to progranulin haploinsufficiency

4. Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17

5. A Brief Overview of Progranulin in Health and Disease

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