PPAR-alpha ELISA Kit

Name: PPAR-alpha ELISA Kit
SKU: DEIA-XYA1499
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

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COA

SDS

Sample

nuclear lysates, cell lysates

Species Reactivity

Human, Mouse, Rat

Intended Use

The PPAR-alpha DNA-Binding ELISA Kit contains components necessary for qualitative detection of active transcription factor PPAR-alpha in eukaryotic nuclear or cell lysates.

Contents of Kit

1. 96-Well dsDNA Oligonucleotide Coated Microplate, 12 x 8-Well Microstrips.
2. 100x Primary Antibody, 100 μL, Yellow.
3. HRP-Conjugated Anti-Rabbit IgG Antibody, 2x 6 mL, Amber.
4. Nuclear Lysate Positive Control, Lyophilized, Red.
5. Wild-Type Consensus dsDNA Oligonucleotide, 20 μL, Green.
6. Mutant Consensus dsDNA Oligonucleotide, 20 μL, Purple.
7. 10x Wash Buffer, 50 mL, Clear.
8. 2x Binding Buffer, 12 mL, Clear.
9. Primary Antibody Diluent, 12 mL, Clear.
10. 100x Protease and Phosphatase Inhibitors, 100 μL, Blue.
11. Nuclear Wash Buffer, 12 mL, Clear.
12. Cytoplasmic Extraction Buffer, 6 mL, Amber.
13. Nuclear Extraction Buffer, 6 mL, Amber.
14. Ready-to-Use Substrate, 12 mL, Brown.
15. Stop Solution, 12 mL, Clear.
16. Adhesive Plate Sealers, 4 Sheets.
17. Technical Manual, 1 Manual.

Storage

4°C/6 Months

Citations

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Certificate of Analysis

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Customer Reviews

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Differential IL-4/Stat6 activities correlate with differential expression of regulatory genes SOCS-1, SHP-1, and PP2A in colon cancer cells

JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY

Authors: Yuan, Qin; Li, Pin Dong; Li, Ben Hui; Yang, Xian Zi; Xu, Shuang Bing; Liu, Xiao Hong; Zhou, Fu Xiang; Zhang, Wen Jie

Abstract

Purpose To investigate potential differences in the expression of Stat6 regulatory genes that may influence IL-4/ Stat6 activities ( phenotypes) in colon cancer cells. Methods RT-PCR method was employed to examine the constitutive mRNA expression of Stat6 negative regulators SOCS-1 and SHP-1, and positive regulator PP2A in colon cancer cell lines HT-29 and Caco-2. Stat6 protein expression and nuclear phosphorylation were detected using Western blotting. Results Caco-2 cells carrying inactive Stat6(null) phenotype showed normal constitutive expression of Stat6 but decreased phosphorylation of nuclear Stat6 compared with HT-29 cells carrying active Stat6(high) phenotype. Stat6(null) Caco-2 cells expressed increased levels of mRNA and protein of SOCS-1 and SHP-1, and decreased mRNA expression of PPP2CA and PPP2CB, encoding two critical subunits of PP2A. Conclusions Constitutively increased expression of Stat6 negative regulators SOCS-1 and SHP-1, together with decreased expression of positive regulator PP2A, may play a role in forming the inactive Stat6(null) phenotype in colon cancer cells.

Restoration of PPP2CA expression reverses epithelial-to-mesenchymal transition and suppresses prostate tumour growth and metastasis in an orthotopic mouse model

BRITISH JOURNAL OF CANCER

Authors: Bhardwaj, A.; Singh, S.; Srivastava, S. K.; Arora, S.; Hyde, S. J.; Andrews, J.; Grizzle, W. E.; Singh, A. P.

Abstract

Background: Emergence of castration-resistance in prostate cancer (PCa) is invariably associated with aggressive and metastatic disease. Previously, we reported promotion of castration-resistance upon downregulation of PPP2CA (encoding catalytic subunit of protein phosphatase 2A (PP2A), alpha-isoform); however, its role in PCa growth and metastasis remained undetermined. Methods: PPP2CA was overexpressed/silenced in PCa cells by stable transfection. Gene expression was examined by reverse transcription polymerase chain reaction, immunoblot and immunofluorescence analyses, and transcriptional activity measured by luciferase-based promoter-reporter assay. Effect on PCa phenotype was studied in vitro and in orthotopic mouse model, and immunohistochemical/histological analyses performed to assess proliferation/apoptosis and confirm metastatic lesions. Results: An inverse association of PPP2CA expression was observed with epithelial-to-mesenchymal transition (EMT) and aggressive PCa phenotype. PPP2CA restoration resulted in decreased nuclear accumulation and transcriptional activity of beta-catenin/NF-kappa B, and restitution of their activity abrogated PPP2CA-induced EMT reversal and suppression of PCa invasiveness. Akt mediated PPP2CA loss-induced nuclear accumulation of beta-catenin/NF-kappa B through inactivation of Gsk3-beta and I kappa B-alpha, respectively. Animal studies revealed a suppressive effect of PPP2CA expression on PCa growth and metastasis. Conclusions: Our findings suggest that PPP2CA downregulation serves as a molecular link between gain of castration-resistance and aggressive PCa phenotype, and its restoration could be an effective preventive/therapeutic approach against the advanced disease.