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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 Kits (21) and FBXO32 Proteins (8) and many more products for this protein.
Showing 10 out of 70 products:
Human Polyclonal FBXO32 Primary Antibody for EIA, WB - ABIN492795
Bodine, Latres, Baumhueter, Lai, Nunez, Clarke, Poueymirou, Panaro, Na, Dharmarajan, Pan, Valenzuela, DeChiara, Stitt, Yancopoulos, Glass: Identification of ubiquitin ligases required for skeletal muscle atrophy. in Science (New York, N.Y.) 2001
Show all 5 references for ABIN492795
Human Polyclonal FBXO32 Primary Antibody for ELISA, WB - ABIN451805
Hanai, Cao, Tanksale, Imamura, Koshimizu, Zhao, Kishi, Yamashita, Phillips, Sukhatme, Lecker: The muscle-specific ubiquitin ligase atrogin-1/MAFbx mediates statin-induced muscle toxicity. in The Journal of clinical investigation 2007
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.
Our results indicate that abnormal SCF (show KITLG Antibodies) 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 Antibodies) in skeletal muscle.
Atrogin-1 expression tended to be increased in the skeletal muscle of patients with malignant disease even before c (show TNF Antibodies)ancer related cachexia weight loss.
Expression of USP19 (show USP19 Antibodies) correlates with that of MuRF1 (show TRIM63 Antibodies) and MAFbx/atrogin-1 in skeletal muscles
FBXO32 targets Lys (show LYZ Antibodies)-326 of c-Myc (show MYC Antibodies) to form polyubiquitin (show UBB Antibodies) chains, resulting in inhibition of cell proliferation.
In conclusion, atrogin-1, MuRF1 (show TRIM63 Antibodies), FOXO1 (show FOXO1 Antibodies)/3A, and eIF3 (show EIF3A Antibodies)-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.
both MuRF1 (show TRIM63 Antibodies) and MAFbx are enriched in skeletal, cardiac, and smooth muscle--REVIEW
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 Antibodies) 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.
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 Antibodies) induced atrophy.
mechanical vibration strongly down-regulates atrophy genes myostatin (show MSTN Antibodies) and atrogin-1 both in vivo and in vitro.
mTORC1 promotes denervation-induced muscle atrophy through a mechanism involving the activation of FoxO and E3 ubiquitin ligases.
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
Smad3 (show SMAD3 Antibodies) expression is sufficient to stimulate atrogin-1 promoter activity, inhibit Akt (show AKT1 Antibodies)/mTOR (show FRAP1 Antibodies) signaling and protein synthesis, and induce muscle fiber atrophy.
Loss of SPARC (show SPARC Antibodies) not only upregulates atrogin 1 expression but also enhances transforming growth factor (TGF)beta (show TGFB1 Antibodies) signaling, which may in turn cause muscle atrophy.
The muscle wasting effects of the myostatin (show MSTN Antibodies)-atrogin-1 axis are not only limited to the degradation of MyoD (show MYOD1 Antibodies) and eukaryotic translation initiation factor 3 subunit f (show EIF3F Antibodies), but also encompass several other muscle proteins.
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