PA1-822A

antibody from Invitrogen Antibodies

Targeting: PPARA hPPAR, NR1C1, PPAR

Provider product page for PA1-822A

Western blot

Immunoprecipitation

Flow cytometry

Other assay

Antibody data

Antibody Data
Antigen structure
References [43]
Comments [0]
Validations
Flow cytometry [1]
Other assay [28]

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Product number: PA1-822A - Provider product page
Provider: Invitrogen Antibodies
Product name: PPAR alpha Polyclonal Antibody
Antibody type: Polyclonal
Antigen: Synthetic peptide
Description: PA1-822A detects peroxisome proliferator activated receptor (PPAR) alpha from mouse samples. PA1-822A has been successfully used in Western blot, immunoprecipitation and immunofluoresence procedures. By Western blot, this antibody detects an ~52 kDa protein representing PPAR alpha from 3T3-L1 cell lysate. Immunofluoresence staining is observed predominantly in the nucleus as well as the cytoplasm. PA1-822A immunogen is a synthetic peptide corresponding to residues M(1) V D T E S P I C P L S P L E A D D(18) C of mouse PPAR alpha. A single amino acid substitution (I8 to L8) exists between the mouse and human protein. This immunizing peptide (Cat.# PEP-025) is available for use in neutralization and control experiments.
Reactivity: Human, Mouse
Host: Rabbit
Isotype: IgG
Vial size: 100 µL
Concentration: 1 mg/mL
Storage: -20°C, Avoid Freeze/Thaw Cycles

PPARA protein structure - PA1-822A shown in red.

Supportive validation

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Supportive validation

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Supportive validation

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Supportive validation

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

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Supportive validation

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Supportive validation

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Experimental details: Figure 11 Expression of key nuclear receptors involved in fatty acid and glucose metabolism as a function of time. Primary hepatocytes were isolated from mouse livers and maintained in culture for up to four days as described in Methods. Representative western blots relative to a housekeeping protein (COX-1) are shown in the inserts. Quantitative analysis of multiple western blots relative to housekeeping protein was shown as black bars for PPAR alpha (Panel a), LXR alpha (Panel b), SREBP1 (Panel c), and ChREBP (Panel d) as described in Methods. Time 0 = concentration in liver while time of 1-4 days indicates time in culture. Mean +- SEM, n = 3-6.

Supportive validation

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Experimental details: Figure 4 Immunocytochemical analyses of NAPE-PLD, FAAH, NAAA, CB 1 and PPAR alpha in dentate gyrus 24hpl. Left column: DG in overview after DAB staining. Middle column; Triple staining of eCB system related proteins with NeuN and IB 4 . Right column; Triple staining of OHSC with eCB system related proteins in combination with NeuN and GFAP. The granular cell layer of the DG and interneurons in the hilus region showed a strong immunoreaction for NAPE-PLD. No overlap was observed with GFAP or IB 4 . The granular cell layer of the DG and especially interneurons in the hilus region were strongly immunoreactive for FAAH. No overlap was observed with GFAP or IB 4 . Please note the similarity of staining pattern of NAPE-PLD and FAAH immunoreactions. NAAA was found in perikarya and nuclei of neurons. In addition to granular cell layer of the DG and hilar neurons CA3 region was strongly labeled. Astrocytes and microglia seem free of NAAA. The entire molecular layer of the dentate gyrus showed a positive CB 1 immunoreaction. CB 1 was present in Microglia and to a lesser extent in astrocytes. PPAR alpha was observed in perikarya and nuclei of neurons. Microglia and Astrocytes showed a positive immunoreaction for PPAR alpha (n = 3, bars: left column = 100 um, middle and right columns = 50 um).

Supportive validation

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Experimental details: Figure 5 Immunocytochemical analyses of NAPE-PLD, FAAH, NAAA, CB 1 and PPAR alpha in primary neuronal (left column), microglia (middle column) and astrocyte (left column) cell cultures. In neurons, NAPE-PLD was distributed in the perikarya but not in neuronal processes. In microglia NAPE-PLD immunoreactions was detectable in small vesicles closely located to the nucleus. NAPE-PLD was not found in protoplasmic astrocytes whereas fibrillary astrocytes showed an immunosignal comparable to microglia. The immunosignal for FAAH in primary neurons was localized in the cell bodies as well as in the primary branches of the neurites. In microglia and astrocytes, FAAH was localized within the nucleus, respectively. In fibrillary astrocytes a FAAH immunoreaction was additionally observed in vesicles. NAAA was clearly found in neurons but was barely found in microglia and astrocytes. In microglia NAAA showed a vesicular staining pattern close to the nucleus. Protoplasmic astrocytes were immunoreactive for NAAA whereas fibrillary astrocytes did not show any NAAA immunosignal. A robust CB 1 immunoreaction was found in neurons. To a lower extent, CB 1 immunosignals were detectable in microglia and astrocytes. Primary neurons showed a strong PPAR alpha immunoreaction in their Perikarya and nuclei. Microglia and astrocytes were positive for PPAR alpha immunoreaction in a vesicular pattern. (n = 3, bar = 20 um).

Supportive validation

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Experimental details: Fig. 7 Activation of PPARalpha in SGC promotes axon regeneration in neuron-SGC cocultures. a t-SNE overlay for expression of the genes Pparalpha , Ppargamma , and Pparalpha target genes Ppargc1a , Fads2 , and Pex11a . b Heat map of PPARalpha target genes expression after nerve injury in SGC and neurons. c Representative images of DRG sections immunostained for PPARalpha (green) and TUJ1 (magenta). n = 3 biologically independent animals. Scale bar: 100 um. d Neuronal and axonal area in embryonic DRG spot co-cultures at DIV7, immunostained for FABP7 (green) and TUJ1 (magenta). n = 3 biologically independent experiments. Scale Bar: 100 um (neuronal) and 50 um (axonal). e Embryonic DRG spot co-cultures axotomized at DIV7 after a 24 h pre-treatment with the indicated PPARalpha agonists at the indicated concentration. Cultures were fixed after 24 h and stained with SCG10. Scale Bar: 50 um. f Distance of regenerating axons was measured from the injury site from images shown in ( e ). g Embryonic DRG spot culture was supplement with FDU (5-deoxyfluoruridine) to eliminate dividing cells in the culture. Axotomy was performed at DIV7 after a 24 h pre-treatment with the indicated PPARalpha agonists. Distance of regenerating axons was measured from injury site after 24 h. ns-non significant. n = 4 biologically independent animals examined over 2 independent experiments for ( f and g ). P values determined by One way ANOVA followed by Dunnett's multiple comparisons test are presented in (

Supportive validation

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Experimental details: Fig. 8 ACOX2 inhibits tumor through the PPARalpha signaling pathway. A The GSEA showed that PPAR ( P = 0.004) and FATTY_ACID_METABOLISM ( P = 0.006) were significantly changed. B The PPI network of ACOX2, PPARA, PPARD, and PPARG was constructed by the String database. C The expression of PPARA, PPARD, and PPARG genes in liver cancer tissues and adjacent noncancerou tissues by using RT-qPCR. D The mRNA expression of PPARA, PPARD, and PPARG was detected by RT-qPCR in HepG2 and SMCC-7721 (NC, the normal HCC cell lines; ACOX2-Ov, overexpression of ACOX2; Sh- ACOX2, knockdown ACOX2). E The protein levels of PPARA, PPARD, and PPARG were detected by Western blot in HepG2 and SMCC-7721 (NC, the normal HCC cell lines; ACOX2-Ov, overexpression of ACOX2; Sh- ACOX2, knockdown ACOX2, * P < 0.05; ** P < 0.01; n.s. not significant). F The Pearson correlation analysis between ACOX2 and PPARA, PPARD, and PPARG by the GEPIA database.

Supportive validation

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Experimental details: Fig. 7 Validation of predictions for the ISMARA-inferred activity of transcription factors (TFs) during muscle aging. a Representative western blot analysis of the abundance of TFs ERRalpha, YY1, and PPARalpha in the gastrocnemius muscle (tissue lysate) of 8 and 28-months-old mice, respectively. b Quantification of western blots showing the relative abundance of TFs ERRalpha, YY1, and PPARalpha normalized to the nuclear protein histone H3, respectively. *Denotes a significant difference based on two-sided Mann-Whitney U test between 8 and 28 months-old mice with p -value < 0.05. c Representative images of tibialis anterior cross sections of 8 and 28-months-old mice with magnification stained for ERRalpha (red), Laminin alpha2 (white), and DAPI (blue). d Quantification of the percentage of ERRalpha-positive nuclei in tibialis anterior fibers of 8 and 28-months-old mice, respectively. ***Denotes a significant difference based on two-sided Student's t -test between 8 and 28-months-old mice with p -value < 0.001. All values were visualized as mean +- standard error of the mean (SE).

Supportive validation

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Experimental details: Figure 7 Fatty acid metabolism-related protein expression in the peritumor liver tissue. Protein expression of CD36 (a), FABP1 (b), PPAR alpha (c), and PGC1 alpha (d) in the peritumor liver tissue of male mice was detected, and alpha -tubulin was used as a loading control for western blot assay. Quantitative data were normalized to the control and expressed as mean +- SEM ( n = 7). * p < 0.05 and *** p < 0.01, Con-Can vs. control; # p < 0.05, Cd-Can vs. Con-Can. CD36: cluster of differentiation 36; FABP1: fatty acid-binding protein 1; PPAR alpha : peroxisome proliferator-activated receptor alpha; PGC1 alpha : peroxisome co-activator-1 alpha; SEM: standard error of the mean.

Supportive validation

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Experimental details: Immunoblot analysis of markers of glucose and lipid metabolism in the hearts of CoV2 infected, T. cruzi infected, and coinfected huACE2 mice. Immunoblot images of (A) markers of glucose metabolism (pAMPK and hexokinase II) and (B) markers of lipid metabolism (PPARalpha and PPARgamma). beta-Actin was used as loading control. Fold changes in the protein levels normalized to beta-Actin are shown as bar graphs (A dot plot displaying individual data points is presented in Supplementary Figure 4 ). The error bars represent standard error of the mean. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 compared to uninfected sex matched mice ( n = 4/sex/group) ( ### p

Supportive validation

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Experimental details: Immunoblot analysis of beta-Adrenergic Receptor and markers of mitochondrial beta-oxidation in the hearts of CoV2 infected, T. cruzi infected, and coinfected huACE2 mice. Western blot images (A) of beta-Adrenergic Receptor (beta-AR), cytochrome C (Cyto C), and superoxide dismutase (SOD). beta-Actin was used as loading control. Fold changes in the protein levels of beta-AR (B) , Cyto C (C) and SOD (D) were normalized to beta-Actin expression and are shown as bar graphs (A dot plot displaying individual data points is presented in Supplementary Figure 4 ). The error bars represent standard error of the mean. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 compared to uninfected sex matched mice ( n = 4/sex/group) ( # p

Supportive validation

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Experimental details: Figure 5 Effect of Rb1 on browning in mature 3T3-L1 adipocytes. (A) Western blot assays were performed to measure the changes of PPARalpha, PGC1alpha, and UCP1. Relative expression levels of (B) PPARalpha, (C) PGC1alpha, and (D) UCP1 were quantified. Expressions of PPARalpha, PGC1alpha, and UCP1 were normalized against GAPDH. (E) mRNA levels of beige-specific genes ( Prdm16, Tmem26, Tbx1 and Cd137 ) and (F) mitochondrial beta oxidation-related genes ( Cpt1a and Cpt1b ) were analyzed by RT-PCR. Relative mRNA level of each gene was normalized against Gapdh . (G) Effect of Rb1 (20 muM) on OCR in mature adipocytes. DMSO was used as vehicle. Data are expressed as mean +- S.E.M. of three or more experiments. * p < 0.05 vs. vehicle-treated 3T3-L1 adipocytes.

Supportive validation

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Experimental details: Fig. 8 FN increases PPARalpha expression and regulates beta-oxidation in human chondrocytes. a. Relative expression of PPARalpha in T/C28a2 human chondrocytes untreated or treated with FN (10, 50 muM) for 24 h. Values are mean +- SEM of 3 independent observations, *p < .05 vs. Ctrl , two-tailed unpaired Student's t-test. b. Western blot and densitometric analysis of PPARalpha expression in human OA primary chondrocytes treated with FN (10, 50 muM) for 24 h. Values are mean +- SEM of 3 human donors, *p < .05 vs. Ctrl , two-tailed unpaired Student's t-test. alpha-tubulin was employed as a loading control. c. Relative expression of ACOX1 in T/C28a2 human chondrocytes untreated or treated with PPARalpha agonists FN, CP and GW (10, 50 muM) for 8 and 24 h. Values are mean +- SEM of 3 independent observations (8 h: *p < .05 vs. Ctrl , two-tailed unpaired Student's t-test; 24 h: *p < .001 vs. Ctrl , two-tailed unpaired Student's t-test). d. Relative expression of CPT1A in T/C28a2 human chondrocytes untreated or treated with PPARalpha agonists FN, CP and GW (10, 50 muM) for 8 and 24 h. Values are mean +- SEM of 3 independent observations (8 h: *p < .05 vs. Ctrl , two-tailed unpaired Student's t-test; 24 h: *p < .01, **p < 0,01, ***p < .001 vs. Ctrl , two-tailed unpaired Student's t-test). Fig. 8