F-Box Protein 32 (FBXO32) ELISA Kits

Zebrafish F-Box Protein 32 (FBXO32) interaction partners

1. 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.

Rainbow Trout (Oncorhynchus mykiss) F-Box Protein 32 (FBXO32) interaction partners

1. Results suggest that the up-regulation of FBXO32 is associated with skeletal and smooth muscle atrophy that occurs during fasting.

Human F-Box Protein 32 (FBXO32) interaction partners

1. F-box only protein 32 (FBXO32) directly ubiquitinates C-terminal binding protein 1 (CtBP1 (show CTBP1 ELISA Kits)), which is required for its stability and nuclear retention.

2. Authors found that the FBXO32 and SMAD4 (show SMAD4 ELISA Kits) levels were higher in normal tissues than in CRC (show CALR ELISA Kits) tissues. The expressions of FBXO32 and SMAD4 (show SMAD4 ELISA Kits) were related to clinicopathological parameters in CRC (show CALR ELISA Kits).

3. role of the muscle specific E3s MuRF-1 (show TRIM63 ELISA Kits) and MAFbx in skeletal muscle wasting during various pathologies, as well as their regulation by modifiable lifestyle factors, were explored (review)

4. FBXO32 activates NF-kappaB (show NFKB1 ELISA Kits) through IkappaBalpha (show NFKBIA ELISA Kits) degradation in inflammatory and genotoxic stress

5. Transcriptional analysis of endophilin-A mutant mice, complemented by proteomics, highlighted ataxia- and protein-homeostasis-related genes and revealed upregulation of the E3-ubiquitin ligase FBXO32/atrogin-1 and its transcription factor FOXO3A (show FOXO3 ELISA Kits).

6. Low FBXO32 expression is associated with breast cancer tumorigenesis.

7. the involvement of oxidative stress in the atrophy of COPD peripheral muscle cells in vitro, via the FoxO1/MuRF1/atrogin-1 signaling pathway of the ubiquitin/proteasome system

8. 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.

9. 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 .

10. 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.

Pig (Porcine) F-Box Protein 32 (FBXO32) interaction partners

1. we speculated that the overexpression of FBXO32 is responsible for congenital splay leg syndrome and it plays an important role in the PI3K-Akt (show AKT1 ELISA Kits) pathway

2. 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

3. Porcine congenital splayleg (PCS) is a condition characterized by extensive fibre atrophy and raised fibre density. The combined differential expression of MAFbx and P311 is of potential in the diagnosis of subclinical PCS.

Cow (Bovine) F-Box Protein 32 (FBXO32) interaction partners

1. A study on the variability of bovine FBXO32 gene that is predictive of genetic potential for body length phenotype.

Mouse (Murine) F-Box Protein 32 (FBXO32) interaction partners

1. Oligonol-mediated downregulation of Atrogin-1 and MuRF1 (show TRIM63 ELISA Kits) gene expression alleviates muscle loss and improves the impaired myotube formation, indicating that oligonol supplementation may be useful for the attenuation of myotube loss.

2. Indoxyl sulfate enhanced the production of atrogin-1 by enhancing oxidative stress in skeletal muscle, leading to muscle atrophy.

3. Transcriptional analysis of endophilin-A mutant mice, complemented by proteomics, highlighted ataxia- and protein-homeostasis-related genes and revealed upregulation of the E3-ubiquitin ligase FBXO32/atrogin-1 and its transcription factor FOXO3A (show FOXO3 ELISA Kits).

4. Valproic acid attenuated muscle wasting and myotube atrophy and reduced C/EBPbeta (show CEBPB ELISA Kits) binding to atrogin1 promoter locus in the myotubes.

5. 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.

6. 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.

7. 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.

8. 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

9. Suggest role for atrogin-1 up-regulation in simvastatin-induced heart mitochondria dysfunction.

10. Atrogin1 was upregulated in cancer cachexia mice. Atrogin1 knockdown protected skeletal muscle cells from TNF-alpha (show TNF ELISA Kits) induced atrophy.