Rabbit Anti-Human UVRAG (a.a. 501-600) Polyclonal antibody

Class III phosphoinositide 3-kinase (class III PI3K), which specifically phosphorylate Ptdlns to generate PtdIns3P, plays a vital role in autophagy and vacuolar sorting pathways by forming Class III PI3K (PI3KC3) complexes with a variety of regulatory proteins. Proteins that compose PI3KC3 complex, namely, PI3K, p150, Beclin 1, ATG14L, UVRAG, Bif-1 and Rubicon are conserved in evolution. In addition, neurodevelopment, situs inversus totalis and development of tumor are found to closely related to these members.

C. trachomatis is the most common sexually transmitted bacterial infection in the world. Although the infection can be easily controlled by the use of antibiotics, several reports of clinical isolates that are resistant to antibiotics have prompted us to search for alternative strategies to manage this disease. In this paper, we developed a nanoparticle formulation (PDGFR-beta siRNA-PEI-PLGA-PEG NP) that can simultaneously induce autophagy in human cells and knock down PDGFR-beta gene expression, an important surface binding protein for C. trachomatis, as a strategy to reduce vaginal infection of C. trachomatis. PDGFR-beta siRNA-PEI-PLGA-PEG NP significantly induced autophagy in human vaginal epithelial cells (VK2/E6E7) 48 hr post treatment by improving autophagic degradation activity without causing inflammation, apoptosis or any decrease in cell viability. Beclin-1, VPS34 (markers for initiation stage of autophagy), UVRAG, TECPR-1 (markers for degradation stage of autophagy) were found to be significantly upregulated after treatment with PDGFR-beta siRNA-PEI-PLGA-PEG NP. Furthermore, PDGFR-beta siRNA-PEI-PLGA-PEG NP decreased PDGFR-beta mRNA expression by 50% and protein expression by 43% in VK2/E6E7 cells 48 hr post treatment. Treatment of cells with PDGFR-beta siRNA-PEI-PLGA-PEG NP significantly decreased the intracellular C. trachomatis and extracellular release of C. trachomatis by approximately 65% and 67%, respectively, in vitro through augmenting autophagic degradation pathways and reducing bacterial binding simultaneously.