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FBXO32 encodes a member of the F-box protein family which is characterized by an approximately 40 amino acid motif, the F-box. Additionally we are shipping FBXO32 Antibodies (75) and FBXO32 Proteins (9) and many more products for this protein.
Showing 10 out of 29 products:
Atrogin-1 inactivation leads to progressive impairment of heart and skeletal muscle function and structure. Autophagy is severely impaired in Atrogin-1-deficient zebrafish embryos.
Results suggest that the up-regulation of FBXO32 is associated with skeletal and smooth muscle atrophy that occurs during fasting.
These results have revealed the roles for atrogin-1 in the regulation of smooth muscle contractility through enhancement of myocardin (show MYOCD ELISA Kits) ubiquitylation/degradation and its transcriptional activity.
Our results indicate that abnormal SCF (show KITLG ELISA Kits) activity with subsequent impairment of the autophagic flux due to a novel FBXO32 mutation is implicated in the pathogenesis of Dilated cardiomyopathy .
Our data suggest that FBXO32 is a candidate gene for recessive familial dilated cardiomyopathy. Acting as a cardiac ubiquitin ligase, mutated FBXO32 could perturb the degradation of target proteins in the ubiquitin proteasome system.
Vitamin D3 might have an inhibitory effect on the expression of MAFbx and MuRF1 (show TRIM63 ELISA Kits) in skeletal muscle.
Atrogin-1 expression tended to be increased in the skeletal muscle of patients with malignant disease even before c (show TNF ELISA Kits)ancer related cachexia weight loss.
Expression of USP19 (show USP19 ELISA Kits) correlates with that of MuRF1 (show TRIM63 ELISA Kits) and MAFbx/atrogin-1 in skeletal muscles
FBXO32 targets Lys (show LYZ ELISA Kits)-326 of c-Myc (show MYC ELISA Kits) to form polyubiquitin (show UBB ELISA Kits) chains, resulting in inhibition of cell proliferation.
In conclusion, atrogin-1, MuRF1 (show TRIM63 ELISA Kits), FOXO1 (show FOXO1 ELISA Kits)/3A, and eIF3 (show EIF3A ELISA Kits)-f mRNA, and protein levels, are differentially regulated by exercise contraction mode but not WPH supplementation combined with hypertrophy-inducing training.
MAFbx not only regulates protein degradation, but also reduces protein synthesis, exerting a dual role in regulating cardiac mass and preventing from cardiac hypertrophy.
FBXO32 methylation status and protein expression were independently associated with survival in ESCC. FBXO32 may be a functional tumor suppressor. Its inactivation through promoter methylation could play an important role in ESCC carcinogenesis.
this study shows that aspartate suppresses lipopolysaccharide-induced MAFbx expression in skeletal muscle via activation of Akt (show AKT1 ELISA Kits) signaling, and inhibition of AMPKa and FOXO1 (show FOXO1 ELISA Kits) signaling
Porcine congenital splayleg (PCS) is a condition characterized by extensive fibre atrophy and raised fibre density. The combined differential expression of MAFbx and P311 (show C5orf13 ELISA Kits) is of potential in the diagnosis of subclinical PCS.
A study on the variability of bovine FBXO32 gene that is predictive of genetic potential for body length phenotype.
Valproic acid attenuated muscle wasting and myotube atrophy and reduced C/EBPbeta (show CEBPB ELISA Kits) binding to atrogin1 promoter locus in the myotubes.
educed PABPN1 levels caused a consistent decline in distal PAS utilization in the 3'-UTR of a subset of OPMD-dysregulated genes. This alternative PAS utilization led to up-regulation of Atrogin-1, a key muscle atrophy regulator, but down regulation of proteasomal genes. Additionally reduced PABPN1 levels caused a reduction in proteasomal activity, and transition in MyHC isotope expression pattern in myofibers.
Iron-induced skeletal muscle atrophy is suggested to involve the E3 ubiquitin ligase mediated by the reduction of Akt (show AKT1 ELISA Kits)-FOXO3a (show FOXO3 ELISA Kits) signaling by oxidative stress.
MAFbx mRNA expression was decreased in old mice relative to adult mice, whereas MuRF1 (show TRIM63 ELISA Kits) mRNA expression was less affected by ageing
Suggest role for atrogin-1 up-regulation in simvastatin-induced heart mitochondria dysfunction.
Atrogin1 was upregulated in cancer cachexia mice. Atrogin1 knockdown protected skeletal muscle cells from TNF-alpha (show TNF ELISA Kits) induced atrophy.
mechanical vibration strongly down-regulates atrophy genes myostatin (show MSTN ELISA Kits) and atrogin-1 both in vivo and in vitro.
This gene encodes a member of the F-box protein family which is characterized by an approximately 40 amino acid motif, the F-box. The F-box proteins constitute one of the four subunits of the ubiquitin protein ligase complex called SCFs (SKP1-cullin-F-box), which function in phosphorylation-dependent ubiquitination. The F-box proteins are divided into 3 classes: Fbws containing WD-40 domains, Fbls containing leucine-rich repeats, and Fbxs containing either different protein-protein interaction modules or no recognizable motifs. The protein encoded by this gene belongs to the Fbxs class and contains an F-box domain. This protein is highly expressed during muscle atrophy, whereas mice deficient in this gene were found to be resistant to atrophy. This protein is thus a potential drug target for the treatment of muscle atrophy. Alternative splicing results in multiple transcript variants encoding different isoforms.
F-box only protein 32
, F-box protein 32
, F-box only protein 32-like
, atrogin 1
, muscle atrophy F-box protein
, atrophy gene 1