M sp1/ ATAD 1 maintains mitochondrial function by facilitating the degradation of mislocalized tail‐anchored proteins-Reference-Cited by-同舟云学术

M sp1/ ATAD 1 maintains mitochondrial function by facilitating the degradation of mislocalized tail‐anchored proteins

Author:

Chen Yu‐Chan¹,Umanah George K E²³,Dephoure Noah⁴,Andrabi Shaida A²³,Gygi Steven P⁴,Dawson Ted M²³⁵⁶,Dawson Valina L²³⁵⁷,Rutter Jared¹

Affiliation:

1. Department of Biochemistry University of Utah School of Medicine Salt Lake City UT USA

2. Neuroregeneration and Stem Cell Programs Institute for Cell Engineering Johns Hopkins University School of Medicine Baltimore MD USA

3. Department of Neurology Johns Hopkins University School of Medicine Baltimore MD USA

4. Department of Cell Biology Harvard Medical School Boston MA USA

5. Solomon H. Snyder Department of Neuroscience Johns Hopkins University School of Medicine Baltimore MD USA

6. Departments of Pharmacology and Molecular Sciences Johns Hopkins University School of Medicine Baltimore MD USA

7. Department of Physiology Johns Hopkins University School of Medicine Baltimore MD USA

Publisher

EMBO

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,Molecular Biology,General Neuroscience

Link

Reference60 articles.

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