HDAC inhibition improves autophagic and lysosomal function to prevent loss of subcutaneous fat in a mouse model of Cockayne syndrome-Reference-Cited by-同舟云学术

HDAC inhibition improves autophagic and lysosomal function to prevent loss of subcutaneous fat in a mouse model of Cockayne syndrome

Published:2018-08-29 Issue:456 Volume:10 Page:
ISSN:1946-6234
Container-title:Science Translational Medicine
language:en
Short-container-title:Sci. Transl. Med.

Author:

Majora Marc¹^ORCID,Sondenheimer Kevin¹^ORCID,Knechten Maren¹,Uthe Ingo¹,Esser Charlotte¹,Schiavi Alfonso¹,Ventura Natascia¹²^ORCID,Krutmann Jean¹³^ORCID

Affiliation:

1. IUF-Leibniz Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany.

2. Institute of Clinical Chemistry and Laboratory Diagnostics, University of Düsseldorf, Medical Faculty, 40225 Düsseldorf, Germany.

3. Medical Faculty, University of Düsseldorf, 40225 Düsseldorf, Germany.

Abstract

The HDAC inhibitor SAHA rescues the skin phenotype in CSB-deficient mice by enhancing protein acetylation and inducing autophagy.

Funder

Deutsche Forschungsgemeinschaft

Italian Association for Cancer Research

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

Reference72 articles.

1. Cockayne syndrome: Review of 140 cases

2. Deficient repair of the transcribed strand of active genes in Cockayne's syndrome cells

3. Mitochondrial repair of 8-oxoguanine is deficient in Cockayne syndrome group B

4. Proteins of nucleotide and base excision repair pathways interact in mitochondria to protect from loss of subcutaneous fat, a hallmark of aging

5. Cockayne syndrome group B protein promotes mitochondrial DNA stability by supporting the DNA repair association with the mitochondrial membrane

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