atrogin-1

atrogin-1

An E3 ubiquitin ligase expressed in cardiac and skeletal muscle that directs muscle protein degradation after the muscle atrophy response has been triggered by Akt1-induced phosphorylation of FOXO, a transcription factor which also activates ubiquitin ligases and MuRF-1. Atrogin-deficient mice are resistant to muscle atrophy.
References in periodicals archive ?
Methods: TGF-[beta]1 and atrogin-1 expression was evaluated by RT-qPCR and/or ELISA; Smad3 phosphorylation by western blot; Smad4 nuclear translocation by indirect immunofluorescence; and ROS levels by DCF probe fluorescent measurements.
Taqman quantitative real-time PCR, were performed using pre-designed primer sets for mouse TGF-[beta]l, atrogin-1 and housekeeping gene GAPDH (Taqman Assays-on-Demand, Applied Biosystems by Life Technologies, Carlsbad, CA, USA).
TGF-[beta]1 and atrogin-1 expression, and p3TP-lux activity induced by TGF-[beta] are dependent on NOX-derived ROS production in skeletal muscle cells
In addition, NOX-induced ROS in response to TGF-[beta] are able to modulate the canonical Smad signalling and another gene expression that is modulated by TGF-[beta] such as p3TP-lux activity and atrogin-1 gene expression.
Our data show that the expression of atrogin-1, an E3 ligase involved in skeletal muscle atrophy, is induced by TGF-[beta]1 and also modulated by ROS in skeletal muscle cells.
Briefly, IGF-1 upregulates multiple intracellular signals that inhibit the secretion of several ubiquitin-proteins, including atrogin-1, FOX-1 and MuRF1, that have been suggested as primary factors evoking skeletal muscle atrophy [1].
2009) Eicosapentaenoic acid attenuates arthritis-induced muscle wasting acting on atrogin-1 and on myogenic regulatory factors.
There was no age-related difference in expression of atrogin-1.
The changes in MuRF-1 and atrogin-1 after exercise did not differ significantly between the younger and older men.
from the Department of Cell Biology, Harvard Medical School, Boston, Massachusetts, presenting "Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy.
IGF-1 prevents ANG II-induced skeletal muscle atrophy via Akt- and Foxo-dependent inhibition of the ubiquitin ligase atrogin-1 expression.
Of which, muscle RING-finger protein-1 (MURF1) and ubiquitin ligase atrogin-1 F-box (Fbx32) is the two limiting constituents of ubiquitin proteasome system (Bodine et al.