ITCH deficiency clinical phenotype expansion and mitochondrial dysfunction-Reference-Cited by-同舟云学术

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ITCH deficiency clinical phenotype expansion and mitochondrial dysfunction

Published:2022-12 Issue: Volume:33 Page:100932
ISSN:2214-4269
Container-title:Molecular Genetics and Metabolism Reports
language:en
Short-container-title:Molecular Genetics and Metabolism Reports

Author:

Wolfe Rachel,Heiman Paige,D'Annibale Olivia,Karunanidhi Anuradha,Powers Alyssa,Mcguire Marianne,Seminotti Bianca,Dobrowolski Steven F.,Reyes-Múgica Miguel,Torok Kathryn S.,Mohsen Al-Walid,Vockley Jerry,Ghaloul-Gonzalez Lina

Funder

National Human Genome Research Institute

National Institutes of Health

Publisher

Elsevier BV

Subject

Endocrinology,Genetics,Molecular Biology

Reference36 articles.

1. The ubiquitin system for protein degradation and some of its roles in the control of the cell division cycle;Hershko;Cell Death Differ.,2005

2. Intracellular protein degradation: from a vague idea thru the lysosome and the ubiquitin-proteasome system and onto human diseases and drug targeting;Ciechanover;Cell Death Differ.,2005

3. Molecular genetic characterization of six recessive viable alleles of the mouse agouti locus;Hustad;Genetics,1995

4. Itchy mice: the identification of a new pathway for the development of autoimmunity;Matesic;Curr. Top. Microbiol. Immunol.,2008

5. Itch−/− alphabeta and gammadelta T cells independently contribute to autoimmunity in itchy mice;Parravicini;Blood,2008

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