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Anti-PPAR gamma Picoband Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB |
|---|---|
| Primary Accession | P37231 |
| Host | Rabbit |
| Reactivity | Human, Mouse, Rat |
| Clonality | Polyclonal |
| Format | Lyophilized |
| Description | Rabbit IgG polyclonal antibody for Peroxisome proliferator-activated receptor gamma(PPARG) detection. Tested with WB in Human;Mouse;Rat. |
| Reconstitution | Add 0.2ml of distilled water will yield a concentration of 500ug/ml. |
| Gene ID | 5468 |
|---|---|
| Other Names | Peroxisome proliferator-activated receptor gamma, PPAR-gamma, Nuclear receptor subfamily 1 group C member 3, PPARG, NR1C3 |
| Calculated MW | 57620 MW KDa |
| Application Details | Western blot, 0.1-0.5 µg/ml, Human, Mouse, Rat |
| Subcellular Localization | Nucleus. Cytoplasm. Redistributed from the nucleus to the cytosol through a MAP2K1/MEK1-dependent manner. CCRN4L/NOC enhances its nuclear translocation. |
| Tissue Specificity | Highest expression in adipose tissue. Lower in skeletal muscle, spleen, heart and liver. Also detectable in placenta, lung and ovary. . |
| Contents | Each vial contains 5mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg NaN3. |
| Immunogen | A synthetic peptide corresponding to a sequence in the middle region of human PPAR gamma (207-248aa AIRFGRMPQAEKEKLLAEISSDIDQLNPESADLRALAKHLYD), identical to the related mouse and rat sequences. |
| Purification | Immunogen affinity purified. |
| Cross Reactivity | No cross reactivity with other proteins. |
| Storage | At -20˚C for one year. After r˚Constitution, at 4˚C for one month. It˚Can also be aliquotted and stored frozen at -20˚C for a longer time. Avoid repeated freezing and thawing. |
| Name | PPARG |
|---|---|
| Synonyms | NR1C3 |
| Function | Nuclear receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand, the nuclear receptor binds to DNA specific PPAR response elements (PPRE) and modulates the transcription of its target genes, such as acyl-CoA oxidase. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids. Key regulator of adipocyte differentiation and glucose homeostasis. ARF6 acts as a key regulator of the tissue-specific adipocyte P2 (aP2) enhancer. Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated pro-inflammatory responses. Plays a role in the regulation of cardiovascular circadian rhythms by regulating the transcription of BMAL1 in the blood vessels (By similarity). |
| Cellular Location | Nucleus. Cytoplasm. Note=Redistributed from the nucleus to the cytosol through a MAP2K1/MEK1-dependent manner. NOCT enhances its nuclear translocation |
| Tissue Location | Highest expression in adipose tissue. Lower in skeletal muscle, spleen, heart and liver. Also detectable in placenta, lung and ovary. |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Background
The peroxisome proliferator-activated receptors (PPARs) are a group of three nuclear receptor isoforms, PPAR gamma, PPAR alpha, and PPAR delta, encoded by different genes. PPARs are ligand-regulated transcription factors that control gene expression by binding to specific response elements (PPREs) within promoters. PPAR gamma is a transcription factor that has a pivotal role in adipocyte differentiation and expression of adipocyte-specific genes. The PPAR gamma1 and gamma2 isoforms result from alternative splicing and have ligand-dependent and -independent activation domains. PPAR gamma is a member of a family of nuclear receptors/ligand-dependent transcription factors, which bind to hormone response elements on target gene promoters. PPAR gamma is abundantly expressed in normal lung tissues, especially in endothelial cells, but that its expression is reduced or absent in the angiogenic plexiform lesions of pulmonary hypertensive lungs and in the vascular lesions of a rat model of severe pulmonary hypertension. And it is concluded that fluid shear stress decreases the expression of PPARgamma in endothelial cells and that loss of PPARgamma expression characterizes an abnormal, proliferating, apoptosis-resistant endothelial cell phenotype.
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