Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/83416
Title: [Retracted] The ubiquitin ligase Mul1 induces mitophagy in skeletal muscle in response to muscle-wasting stimuli
Authors: Gluckman, Peter D.
McFarlane, Craig
Sharma, Mridula
Kambadur, Ravi
Lokireddy, Sudarsanareddy
Wijesoma, Isuru Wijerupage
Teng, Serena
Bonala, Sabeera
Keywords: DRNTU::Science::Biological sciences
Issue Date: 2012
Source: Lokireddy, S., Wijesoma, I., Teng, S., Bonala, S., Gluckman, P., McFarlane, C., Sharma, M.,& Kambadur, R. (2012). The Ubiquitin Ligase Mul1 Induces Mitophagy in Skeletal Muscle in Response to Muscle-Wasting Stimuli. Cell Metabolism, 16(5), 613-624. [Retracted]
Series/Report no.: Cell metabolism
Abstract: Recent research reveals that dysfunction and subsequent loss of mitochondria (mitophagy) is a potent inducer of skeletal muscle wasting. However, the molecular mechanisms that govern the deregulation of mitochondrial function during muscle wasting are unclear. In this report, we show that different muscle-wasting stimuli upregulated mitochondrial E3 ubiquitin protein ligase 1 (Mul1), through a mechanism involving FoxO1/3 transcription factors. Overexpression of Mul1 in skeletal muscles and myoblast cultures was sufficient for the induction of mitophagy. Consistently, Mul1 suppression not only protected against mitophagy but also partially rescued the muscle wasting observed in response to muscle-wasting stimuli. In addition, upregulation of Mul1, while increasing mitochondrial fission, resulted in ubiquitination and degradation of the mitochondrial fusion protein Mfn2. Collectively, these data explain the molecular basis for the loss of mitochondrial number during muscle wasting.
URI: https://hdl.handle.net/10356/83416
http://hdl.handle.net/10220/12909
ISSN: 1550-4131
DOI: 10.1016/j.cmet.2012.10.005
Fulltext Permission: none
Fulltext Availability: No Fulltext
Appears in Collections:SBS Journal Articles

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