PPARgamma EMSA Probe Set
- Known as:
- PPARgamma EMSA Probe Set
- Catalog number:
- AY1141P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- PPARgamma EMSA Probe Set
Related genes to: PPARgamma EMSA Probe Set
- Gene:
- PPARG NIH gene
- Name:
- peroxisome proliferator activated receptor gamma
- Previous symbol:
- -
- Synonyms:
- PPARG1, PPARG2, NR1C3, PPARgamma
- Chromosome:
- 3p25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-03-12
- Date modifiied:
- 2016-10-05
Related products to: PPARgamma EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: PPARgamma EMSA Probe Set
- Ferroptosis and lipid metabolism disturbances are increasingly recognized as critical factors in cancer biology, yet their specific mechanisms in cutaneous squamous cell carcinoma (CSCC) remain unclear. In this study, we integrated bioinformatics analyses and single-cell RNA sequencing analyses to identify ferroptosis- and lipid-related biomarkers in CSCC. ACSL1, PPARD, and PPARG emerged as key genes enriched in pathways such as cell cycle regulation and Toll-like receptor signaling. Immune infiltration analyses revealed a strong positive correlation between PPARD and CD56^dim natural killer cells, and a negative correlation between PPARG and activated dendritic cells. Single-cell transcriptomic profiling pinpointed keratinocytes as central players, with ACSL1 and PPARD exhibiting dynamic expression patterns during differentiation. RT-qPCR validation in clinical CSCC tissues confirmed elevated PPARD expression and reduced ACSL1 expression. These findings suggest an association between ACSL1/PPARD and the lipid-ferroptosis interplay via keratinocyte remodeling, rather than establishing causality. Accordingly, we frame ACSL1 and PPARD as candidate markers pending protein-level and functional validation. - Source: PubMed
Publication date: 2026/05/19
Shi Xiao-XiaoLi Gai-YingYang Xiao-YanZeng Zi-XunZhou Ting-TingZhang Yuan-JinHuang Meng-TingTang YangXu Ning - Obesity is associated with metabolic disorders due to unhealthy white adipose tissue (WAT) failing to sustain energy homeostasis, highlighting the importance of adipose development. The lactation period is critical for epididymal WAT (eWAT) development and metabolic programming. However, the role of lactoferrin (LF) in the early development of adipose remains unclear. Using a mouse model of lactational LF deficiency and single-nucleus RNA sequencing, we assessed the long-term impact of LF deficiency on eWAT plasticity and metabolic homeostasis at weaning, adulthood, and under a high-fat diet (HFD). LF deficiency persistently impaired eWAT development, causing restricted adipocyte hyperplasia, exacerbated hypertrophy, diminished lipid uptake, and sustained adiponectin decline with resistin elevation. These defects led to long-term metabolic disorders, worsening HFD-induced eWAT remodeling, glucose intolerance, dyslipidemia, and chronic inflammation. Mechanistically, LF could bind CSK and PRMT5. LF promoted CSK degradation, activating SRC to drive preadipocyte proliferation. Additionally, LF stabilized PRMT5 to enhance PPARg-mediated differentiation and lipid uptake. Rescue experiments confirmed that CSK overexpression reversed LF-induced proliferation, while PRMT5 knockdown blocked LF-enhanced differentiation. This study reveals lactational LF as a key nutritional signal that programs adipose development and long-term metabolic health via CSK-SRC and PRMT5-PPARg pathways, offering an early-life intervention strategy against obesity-related metabolic diseases. - Source: PubMed
Publication date: 2026/05/19
An QinZou YunxiaWang WenliCheng ZhimeiZhang ZhuoxingLiu RuweiWang XiongHuang KunlunDing FangrongDai YunpingMeng QingyongZhang Yali - By employing network pharmacology and molecular docking techniques, this study seeks to elucidate the targets and molecular mechanisms of Bu-Zhong-Yi-Qi decoction (BZYQD) in the management of pelvic organ prolapse (POP). Active components of BZYQD were identified via liquid chromatography-tandem mass spectrometry analysis and matched with potential targets in POP utilizing databases like Swiss Target Prediction, Gene Expression Omnibus, and "Disease" + "Gene" + "NETwork" (DisGeNET). The overlapping genes underwent Gene Ontology and pathway analyses, followed by visualization of protein-protein interactions using Search Tool for the Retrieval of Interacting Genes/Proteins and Cytoscape. Binding affinities between the active compounds and target proteins were assessed through molecular docking simulations employing AutoDock (The Scripps Research Institute [TSRI]) software. A total of 504 compounds were detected, with 13 identified as active ingredients, including benzenepropanoic acid and narirutin. Analysis revealed 96 shared targets with POP-related genes, of which 28 key targets displayed significant interactions impacting biological processes associated with mechanistic pathways like oxidative stress, inflammatory responses, and extracellular matrix remodeling. Network analysis identified benzenepropanoic acid, narirutin, pinostrobin 5-glucoside, and scopoletin as significant regulators. Key genes with high network degrees included PTGS2, ESR2, ESR1, MMP3, CASP3, MAPK1, MMP2, MMP9, PPARG, and CTNNB1. Molecular docking simulations demonstrated favorable binding properties of these compounds to core targets, with benzenepropanoic acid showing the lowest binding free energy with MMP2. The research emphasizes the complex and multi-target characteristics of BZYQD, indicating its potential efficacy in the management of POP. It offers insights into the pharmacological mechanisms of the decoction, advocating for the investigation of traditional Chinese medicine in the treatment of pelvic disorders. Further clinical research is needed to confirm. - Source: PubMed
Wu HuayeYang LuZhang LingYuan JiakunTao QinYu XiaLin Yonghong - Tissue whole mounts have long been used to assess morphological changes following genetic perturbation in mice. Traditional methods for preparing dorsal skin whole mounts, however, often lead to breakage of hair follicle structures, such as sebaceous glands, making it difficult to perform unbiased quantitation. Here, we describe a modified technique for preparing whole mounts harvested from mouse dorsal skin. This protocol incorporates adhesives to stiffen the tissue and facilitate the separation of intact epidermis from the dermis. Critically, this method is compatible with downstream applications such as lipid staining of sebaceous glands and immunofluorescence, and we provide protocols for both approaches. Overall, the use of this modified "glue technique" for preparing skin whole mounts will help preserve tissue integrity for morphological analysis. - Source: PubMed
Veniaminova Natalia AGrachtchouk MarinaDlugosz Andrzej AWong Sunny Y - Osteocytes and adipocytes represent cells with disparate functions. Osteocytes regulate bone metabolism (remodeling) and bone homeostasis, while adipocytes regulate energy metabolism and energy storage. Here, we demonstrate that osteocyte phenotype consists of adipocytic features which are under control of peroxisome proliferator-activated receptor gamma (PPARG), a master regulator of adipocyte differentiation and function. Using a mouse model with osteocyte-specific deletion of PPARG (OT ) and osteocyte cellular model of MLO-Y4 cells edited with CRISPR/Cas9 for PPARG deficiency, we are demonstrating that under PPARG control osteocytes produce and secrete adiponectin (ADIPOQ), and they are equipped in adipocyte-specific mechanisms for lipid-storage and their metabolism. Under PPARG, osteocytes accumulate lipid droplets which correlate with their capability to cover up to 20% of energy requirements from fatty acids metabolism. Although osteocytes like osteoblasts mainly express ( ), however similarly to adipocytes, lipid droplets accumulation is associated with expression of ( ) under PPARG control. Similarly, lipids accumulation and metabolism involve adipocyte-specific activities including ( ), ( ) and ( ), which expression are under PPARG control. These studies provide a new understanding of osteocyte biology which include adipocyte-like endocrine and lipid metabolism features probably reflecting an adaptation to their unique localization and a need for a maintenance of functional fitness in these conditions. They deepen our comprehension of the crossroads of osteocyte and adipocyte function and underscore the therapeutic potential of targeting common molecular pathways in both cell types for managing metabolic disorders and skeletal diseases. - Source: PubMed
Publication date: 2026/05/06
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