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Cow (Bovine) Monoclonal PPARA Primary Antibody for ChIP, FACS - ABIN152696
Sumanasekera, Tien, Turpey, Vanden Heuvel, Perdew: Evidence that peroxisome proliferator-activated receptor alpha is complexed with the 90-kDa heat shock protein and the hepatitis virus B X-associated protein 2. in The Journal of biological chemistry 2003
Show all 9 Pubmed References
Human Polyclonal PPARA Primary Antibody for ICC, IHC (fro) - ABIN3044397
Zhou, Zhang, Xu, Wang: Curcumin ameliorates renal fibrosis by inhibiting local fibroblast proliferation and extracellular matrix deposition. in Journal of pharmacological sciences 2015
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Cow (Bovine) Polyclonal PPARA Primary Antibody for ChIP, ELISA - ABIN153509
Selwyn, Cheng, Klaassen, Cui: Regulation of Hepatic Drug-Metabolizing Enzymes in Germ-Free Mice by Conventionalization and Probiotics. in Drug metabolism and disposition: the biological fate of chemicals 2016
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Human Monoclonal PPARA Primary Antibody for WB - ABIN1944858
Mukherjee, Jow, Noonan, McDonnell: Human and rat peroxisome proliferator activated receptors (PPARs) demonstrate similar tissue distribution but different responsiveness to PPAR activators. in The Journal of steroid biochemistry and molecular biology 1995
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Polyclonal PPARA Primary Antibody for ELISA, WB - ABIN539548
Lazar: Progress in cardiovascular biology: PPAR for the course. in Nature medicine 2001
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Mouse (Murine) Polyclonal PPARA Primary Antibody for IF, IP - ABIN285918
Suardíaz, Estivill-Torrús, Goicoechea, Bilbao, Rodríguez de Fonseca: Analgesic properties of oleoylethanolamide (OEA) in visceral and inflammatory pain. in Pain 2007
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Mouse (Murine) Polyclonal PPARA Primary Antibody for IHC, ELISA - ABIN105798
Plutzky: Medicine. PPARs as therapeutic targets: reverse cardiology? in Science (New York, N.Y.) 2003
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Mouse (Murine) Monoclonal PPARA Primary Antibody for GS, IP - ABIN284693
Longuet, Sinclair, Maida, Baggio, Maziarz, Charron, Drucker: The glucagon receptor is required for the adaptive metabolic response to fasting. in Cell metabolism 2008
Human Polyclonal PPARA Primary Antibody for ELISA, WB - ABIN2476186
Yoneda, Lyall, Alsina, Persons, Spada, Levitzki, Zilberstein, Mundy: The antiproliferative effects of tyrosine kinase inhibitors tyrphostins on a human squamous cell carcinoma in vitro and in nude mice. in Cancer research 1991
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Mouse (Murine) Polyclonal PPARA Primary Antibody for FACS, WB - ABIN656834
Spruiell, Richardson, Cullen, Awumey, Gonzalez, Gyamfi: Role of pregnane X receptor in obesity and glucose homeostasis in male mice. in The Journal of biological chemistry 2014
Circulated eosinophilic expression of PPARalpha protein is reduced in metabolic syndrome.
TNFalpha differently regulated the levels of PPARalpha, LXRalpha, and LXRbeta binding to the apoA-I gene promoter in THP-1 cells. Obtained results suggest a novel tissue-specific mechanism of the TNFalpha-mediated regulation of apoA-I gene in monocytes and macrophages and show that endogenous ApoA-I might be positively regulated in macrophage during inflammation.
MAR1 ameliorates LPS-induced atherosclerotic reactions via PPARalpha-mediated suppression of inflammation and ER stress.
Data suggest that, in hepatocytes, MIRN34A plays roles in regulation of mitochondrial remodeling and lipid metabolism including development/prevention of non-alcoholic fatty liver disease; MIRN34A appears to act via AMPK/PPARalpha signal transduction. (MIRN34A = microRNA 34a; AMPK = AMP-activated protein kinase; PPARalpha = peroxisome proliferator activated receptor alpha)
miR-214 overexpression inhibits glioma cell growth in vitro and in vivo by inducing cell cycle arrest in G0/G1. Collectively, these data uncover a novel role for a PPARalpha-miR-214-E2F2 pathway in controlling glioma cell proliferation.
Improvements in metabolic and neurodegenerative diseases are often attributed to anti-inflammatory effects of PPAR activation. (Review)
circRNA_0046366, which demonstrated expression loss in HepG2-based hepatocellular steatosis, exerts antagonistic effect on miR-34a activity. miR-34a inactivation abrogates its inhibitory role against PPARalpha.
We first reported that the FOMX1 pathway is the most upregulated and the PPARalpha pathway is the most downregulated pathway in Triple Negative Breast Cancers (TNBCs). These two pathways could be simultaneously targeted in further studies. Also the pathway classifier we performed in this study provided insight into the TNBC heterogeneity.
Polymorphism of PPARA is associated with late onset of type 2 diabetes mellitus.
results demonstrated that OEA exerts anti-inflammatory effects by enhancing PPARalpha signaling, inhibiting the TLR4-mediated NF-kappaB signaling pathway, and interfering with the ERK1/2-dependent signaling cascade (TLR4/ERK1/2/AP-1/STAT3), which suggests that OEA may be a therapeutic agent for inflammatory diseases.
data suggested that miR-19a negatively controlled the autophagy of hepatocytes attenuated in D-GalN/LPS-stimulated hepatocytes via regulating NBR2 and AMPK/PPARalpha signaling.
The minor allele of rs1800206 and rs1805192 from PPAR A and PPAR G and its interaction were associated with increased Breast Cancer risk.
High concentrations of DINCH urinary metabolites activate human PPAR-alpha.
PPARalpha is overexpressed in primary glioblastoma
these results suggest that the E2F1/miR19a/PPARalpha feedback loop is critical for glioma progression
Data conclude that the ER-stress mediated reduction in apoA-I transcription could be partly mediated via the inhibition of PPARalpha mRNA expression and activity. In addition, BET inhibition increased apoA-I transcription, even if PPARalpha production and activity were decreased. Both BET inhibition and PPARalpha activation ameliorate the apoA-I lowering effect of ER-stress and are therefore interesting targets to elev...
Results demonstrated that PPARa directly inhibited Glut1 mRNA expression resulting in influx of glucose in cancer cells.
PPARalpha and LXRalpha may be mediators by which omega3PUFA attenuate bile acid-induced hepatocellular injury
Our results support an important association between rs1800206 minor allele of PPAR alpha and diabetic retinopathy, and the interaction analysis also shown a combined effect of Leu162 allele-abdominal obesity interaction on diabetic retinopathy.
Taken together, our data suggest that eupatilin inhibits TNFalpha-induced MMP-2/-9 expression by suppressing NF-kappaB and MAPKAP-1 pathways via PPARalpha. Our findings suggest the usefulness of eupatilin for preventing skin aging.
This study investigated FA composition in yaks and cattle, in order to ascertain whether a correlation between PPARalpha signal pathway genes as candidate genes and meat FA composition in yaks and cattle exists.
OCTN2 expression and carnitine transport in cattle, as in rodents, are regulated by PPARalpha.
In conclusion, H8H8 haplotype combination of the PPARalpha may be advantageous for heat resistance traits in Chinese Holstein cattle.
Data suggest that PPARalpha (but not PPARgamma) is involved in vasorelaxation of ophthalmic artery in response to endocannabinoids (i.e., anandamide, palmitoylethanolamide); endothelium removal slightly decreases the response to endocannabinoids.
Data from gene profiling experiments in bovine cell line support hypothesis that saturated long-chain fatty acids modulate ruminant lipid metabolism and expression of inflammation mediators with major effects induced via activation of PPARalpha.
Dietary trans fatty acids may affect liver lipid metabolism in post-partum dairy cows through alterations in PPARalpha gene expression.
Oxidized fataprevent an alcohol-induced triacylglycerol accumulation in rats possibly by upregulation of hepatic PPARalpha-responsive genes, whwereas conjugated linoleic acid does not.
The results are consistent with the hypothesis that arachidonic acid acts via PPARalpha to increase PTGS2 levels in bovine endometrial stromal cells.
Our results provide novel insights into regulation of PPAR expression in ovarian follicles. We observed that FSH increased mRNA and protein expression of all PPARs isoforms, while LH only increased PPAR alpha and gamma. Steroids like progesterone and estradiol increased expression of PPAR alpha and gamma without affecting the beta isoform, while testosterone had no effect on all PPARs expression.
The c.*636A>G SNP in the PPARA gene can be considered in Polish Landrace breed as a useful genetic marker for adipose tissue accumulation.
The results indicate that the endometrial expression of PPARalpha genes fluctuates during the estrous cycle and pregnancy.
PPARalpha is likely to play a central role in adaptation to fasting in pig liver
Despite expression of PPAR-alpha in porcine myocardium and effects of fenofibrate on systemic metabolism, treatment with this PPAR-alpha activator does not alter myocardial metabolic or contractile responses to I/R in pigs.
FISH localization of 4 BAC clones harbouring potential candidate genes for fatness traits: DGAT1 (SSC4p15), PPARA (SSC5p15), ADIPOR1 (SSC10p13) and CREB (SSC15q24)
PPAR profiles in bladder smooth muscle (BSM) may contribute to the susceptibility of BSM to lipotoxicity in the metabolic syndrome.
Peroxisome proliferation could lead to increased susceptibility to bacterial pathogens in tobacco by altering the redox balance of the plant and the expression pattern of key defense signaling pathway genes.
For the first time, we report here the importance of GPER-PPARalpha and -PPARgamma 'neopartnership' in maintenance of Leydig cell morpho-functional status.
Integrated transcriptomics and proteomics data predicted the activation of TGF beta and inactivation of PPAR alpha signaling pathways in mouse heart tissue 40 weeks after local radiation exposure (16 Gy). This study strongly suggests a crosstalk between the two pathways via MAPK signaling.
The study suggests that persistent alteration of cardiac metabolism due to impaired PPAR alpha activity contributes to the heart pathology after radiation.Ionizing radiation markedly changed the phosphorylation and ubiquitination status of PPAR alpha. This was reflected as decreased expression of its target genes involved in energy metabolism and mitochondrial respiratory chain.
These results indicate that wistin could suppress lipid accumulation through PPARalpha activation. The action of wistin on PPARalpha could be of interest for the amelioration of lipid metabolic disorders.
These data may indicate that insulin resistance in Adp(-/-) mice is likely caused by an increase in concentrations of TNFalpha and FFA via downregulation of PPARalpha.
Results from transcriptional and epigenomic analyses in the livers of mice fed either a high-fat diet or nutrition-restricted diet, found extensive binding of PPARalpha near genes involved in glycolysis/gluconeogenesis and uncovered a role for this factor in regulating anaerobic glycolysis.
Peroxisome proliferator-activated receptor alpha (PPARalpha) target gene expression was almost absent in contrast to increased lipid synthesis in the TIS21 protein (TIS21) knockout (TIS21-KO) mice compared to WT mice.
Clofibrate treatment revealed an essential role of PPARalpha in regulating hepatic bile acid synthesis, transport and signaling.
IL-6 and aging are involved in regulation of PPARalpha and PGC-1alpha expression and may influence the mitochondrial function.
The authors identify an endogenous role for PPARalpha in retinal neuronal survival and lipid metabolism, and furthermore underscore the importance of fatty acid oxidation in photoreceptor survival. They also suggest PPARalpha as a putative therapeutic target for age-related macular degeneration, which may be due in part to decreased mitochondrial efficiency and subsequent energetic deficits
p21 plays a relevant role in fasting adaptation through the positive regulation of PPARalpha.
PPARalpha is required for the ChREBP-induced glucose response of FGF21. Loss of PPARalpha impairs Fgf21 promoter accessibility at the carbohydrate-responsive element .
Data, including data from studies in knockout mice, suggest that hepatic induction of cytochrome P450s (Cyp3a, Cyp2b, and Cyp2c) by hypolipidemic agent gemfibrozil is suppressed by Ppara activation.
We demonstrated that PPARalpha activation contributes to liver protection and decreases liver inflammation in acute liver failue (ALF), particularly through regulating CHOP. Our findings may provide a rationale for targeting PPARalpha as a potential therapeutic strategy to ameliorate ALF.
These findings indicate that PPARalpha promotes osteogenic differentiation via the Sirt1-dependent signaling pathway.
CD36 is essential for endurance improvement, changes in whole-body metabolism, and efficient peroxisome-proliferator activated receptors (PPAR)-related transcriptional responses in the muscle with exercise training.
In mice, the oral administration of linalool for 3 weeks reduced plasma TG concentrations in Western-diet-fed C57BL/6J mice (31%, P < 0.05) and human apo E2 mice (50%, P < 0.05) and regulated hepatic PPARalpha target genes.
a novel PPARalpha-dependent gene
fenofibrate upregulated VLDLR transcriptional activity through PPAR response element binding to the VLDLR promoter.
PPARalpha activation contributes to liver protection and decreases hepatocyte apoptosis in acute liver failure, particularly through regulating endoplasmic reticulum stress.
Peroxisome proliferators include hypolipidemic drugs, herbicides, leukotriene antagonists, and plasticizers\; this term arises because they induce an increase in the size and number of peroxisomes. Peroxisomes are subcellular organelles found in plants and animals that contain enzymes for respiration and for cholesterol and lipid metabolism. The action of peroxisome proliferators is thought to be mediated via specific receptors, called PPARs, which belong to the steroid hormone receptor superfamily. PPARs affect the expression of target genes involved in cell proliferation, cell differentiation and in immune and inflammation responses. Three closely related subtypes (alpha, beta/delta, and gamma) have been identified. This gene encodes the subtype PPAR-alpha, which is a nuclear transcription factor. Multiple alternatively spliced transcript variants have been described for this gene, although the full-length nature of only two has been determined.
, nuclear receptor subfamily 1 group C member 1
, peroxisome proliferative activated receptor, alpha
, peroxisome proliferator-activated nuclear receptor alpha variant 3
, PPAR alpha
, peroxisome proliferator activated receptor alpha
, peroxisome proliferator-activated receptor alpha
, ppar alpha
, xPPAR alpha
, peroxisome proliferator-activated receptor-alpha