anti-F-Box Protein 32 (FBXO32) Antibodies

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), which is required for its stability and nuclear retention.

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

3. role of the muscle specific E3s MuRF-1 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 through IkappaBalpha 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.

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 ubiquitylation/degradation and its transcriptional activity.

9. Our results indicate that abnormal SCF 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.

11. Vitamin D3 might have an inhibitory effect on the expression of MAFbx and MuRF1 in skeletal muscle.

12. Atrogin-1 expression tended to be increased in the skeletal muscle of patients with malignant disease even before cancer related cachexia weight loss.

13. Expression of USP19 correlates with that of MuRF1 and MAFbx/atrogin-1 in skeletal muscles

14. FBXO32 targets Lys-326 of c-Myc to form polyubiquitin chains, resulting in inhibition of cell proliferation.

15. In conclusion, atrogin-1, MuRF1, FOXO1/3A, and eIF3-f mRNA, and protein levels, are differentially regulated by exercise contraction mode but not WPH supplementation combined with hypertrophy-inducing training.

16. MAFbx not only regulates protein degradation, but also reduces protein synthesis, exerting a dual role in regulating cardiac mass and preventing from cardiac hypertrophy.

17. 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.

18. both MuRF1 and MAFbx are enriched in skeletal, cardiac, and smooth muscle--REVIEW

19. EZH2 is a key factor in the proliferation and survival of PAX3-FOXO1 alveolar RMS cells working, at least in part, by repressing FBXO32

20. ATROGIN1 gene expression is increased in patients with severe burn injury.

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 pathway

2. this study shows that aspartate suppresses lipopolysaccharide-induced MAFbx expression in skeletal muscle via activation of Akt signaling, and inhibition of AMPKa and FOXO1 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. The results indicate that FBXO-32 contributes to SK2 down-regulation and that the F-box domain is essential for FBXO-32 function.

2. These findings suggest that the circadian clock controls the day-night oscillation of Atrogin1 expression and the therapeutic effects of weight-bearing are dependent on its timing.

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

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

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.

6. Valproic acid attenuated muscle wasting and myotube atrophy and reduced C/EBPbeta binding to atrogin1 promoter locus in the myotubes.

7. These results have revealed the roles for atrogin-1 in the regulation of smooth muscle contractility through enhancement of myocardin ubiquitylation/degradation and its transcriptional activity.

8. 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.

9. Iron-induced skeletal muscle atrophy is suggested to involve the E3 ubiquitin ligase mediated by the reduction of Akt-FOXO3a signaling by oxidative stress.

10. MAFbx mRNA expression was decreased in old mice relative to adult mice, whereas MuRF1 mRNA expression was less affected by ageing

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

12. Atrogin1 was upregulated in cancer cachexia mice. Atrogin1 knockdown protected skeletal muscle cells from TNF-alpha induced atrophy.

13. Expression of USP19 correlates with that of MuRF1 and MAFbx/atrogin-1 in skeletal muscles

14. MAFbx not only regulates protein degradation, but also reduces protein synthesis, exerting a dual role in regulating cardiac mass and preventing from cardiac hypertrophy.

15. mechanical vibration strongly down-regulates atrophy genes myostatin and atrogin-1 both in vivo and in vitro.

16. mTORC1 promotes denervation-induced muscle atrophy through a mechanism involving the activation of FoxO and E3 ubiquitin ligases.

17. atrogin-1 promotes cardiomyocyte health through mediating the interplay between the ubiquitin/proteasome system and autophagy/lysosome system and its alteration promotes development of cardiomyopathies

18. Smad3 expression is sufficient to stimulate atrogin-1 promoter activity, inhibit Akt/mTOR signaling and protein synthesis, and induce muscle fiber atrophy.

19. Loss of SPARC not only upregulates atrogin 1 expression but also enhances transforming growth factor (TGF)beta signaling, which may in turn cause muscle atrophy.

20. The muscle wasting effects of the myostatin-atrogin-1 axis are not only limited to the degradation of MyoD and eukaryotic translation initiation factor 3 subunit f, but also encompass several other muscle proteins.