PLIN3抗体—艾普蒂

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     Western blot analysis using PLIN3 mouse mAb against THP-1 (1), HepG2 (2), K562 (3) and Hela (4) cell lysate.    

  
  

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     Immunofluorescence analysis of Hela cells using PLIN3 mouse mAb (green). Blue: DRAQ5 fluorescent DNA dye. Red: Actin filaments have been labeled with Alexa Fluor- 555 phalloidin. Secondary antibody from Fisher (Cat#: 35503)    

  
  

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     Flow cytometric analysis of Hela cells using PLIN3 mouse mAb (green) and negative control (red).    

  
  

PLIN3 (Perilipin 3), also known as TIP47 (Tail-Interacting Protein 47 kDa), is a member of the perilipin family of lipid droplet-associated proteins. It plays a critical role in lipid metabolism by regulating the formation, stabilization, and intracellular trafficking of lipid droplets (LDs), which are dynamic organelles involved in lipid storage and mobilization. PLIN3 is ubiquitously expressed and interacts with LDs during their biogenesis, facilitating neutral lipid deposition and protecting LDs from premature hydrolysis by lipases. Its expression is modulated by metabolic cues, such as nutritional status and hormonal signals, linking it to energy homeostasis.

PLIN3 antibodies are essential tools for studying LD biology and metabolic disorders. These antibodies enable the detection, localization, and quantification of PLIN3 in cells and tissues through techniques like Western blotting, immunofluorescence, and immunohistochemistry. Researchers use PLIN3-specific antibodies to investigate its role in pathologies such as obesity, non-alcoholic fatty liver disease (NAFLD), and atherosclerosis, where aberrant LD accumulation is a hallmark. Additionally, PLIN3 antibodies help explore its interaction with other LD-associated proteins (e.g., PLIN2. ATGL) and membrane trafficking machinery. Validated antibodies are critical for distinguishing PLIN3 from structurally related perilipin family members, ensuring specificity in experimental models. As interest in metabolic diseases grows, PLIN3 antibodies remain pivotal in elucidating molecular mechanisms underlying lipid dysregulation and identifying therapeutic targets.