mProX™ Human PTAFR Stable Cell Line

Jianfeng Zheng et al. "PAIP1 regulates expression of immune and inflammatory response associated genes at transcript level in liver cancer cell." PeerJ, 2023
In this study, the authors examined the functions and molecular mechanisms of Poly(A) binding protein interacting protein 1 (PAIP1) in liver cancer. Prior studies have shown that PAIP1 is involved in both translation regulation and mRNA decay, and high levels of PAIP1 have been linked to increased invasive potential of liver cancer. However, the specific roles of PAIP1 in liver cancer are not well understood. Using HepG2 cells, the researchers compared cell viability and gene expression profiles after transfecting with PAIP1 siRNA or non-targeting control siRNA. They found that PAIP1 knockdown not only inhibited cell viability, but also affected the expression of 893 genes at the transcriptional level. Functional analysis revealed that the up-regulated genes were enriched in DNA-dependent transcription, while the down-regulated genes were enriched in pathways related to immune and inflammatory response. Further confirmation through quantitative PCR (qPCR) showed that PAIP1 knockdown positively regulated the expression of certain immune and inflammatory factor genes in HepG2 cells. Additionally, analysis of the TCGA database showed that PAIP1 expression was positively correlated with two immune-related genes, IL1R2 and PTAFR, in liver tumor tissue. Overall, the results suggest that PAIP1 plays a crucial role in both translation and transcription regulation in liver cancer, and may also function as a regulatory factor for immune and inflammatory genes in this cancer. This study provides important insights for future research on the role of PAIP1 in liver cancer.
Jianfeng Zheng et al. "PAIP1 regulates expression of immune and inflammatory response associated genes at transcript level in liver cancer cell." PeerJ, 2023
Pubmed: 37101794   DOI: 10.7717/peerj.15070

Yee AJ, et al. "Platelet Activating Factor Activity Modulates Hyperoxic Neonatal Lung Injury ." bioRxiv : the preprint server for biology, 2023.
The role of hyperoxia-induced inflammation in causing developmental lung injury and bronchopulmonary dysplasia (BPD) in preterm infants is significant. The platelet activating factor (PAF) has been identified as a major driver of inflammation in lung diseases like asthma and pulmonary fibrosis, but its involvement in BPD has not been investigated before. To determine whether PAF signaling independently affects neonatal hyperoxic lung injury and BPD development, the lung structure of 14-day-old C57BL/6 wild-type (WT) and PAF receptor knockout (PAFR KO) mice exposed to 21% (normoxia) or 85% O (2) (hyperoxia) was evaluated. The results showed that PAFR KO mice experienced less alveolar simplification compared to WT mice under hyperoxic conditions. Gene expression analysis revealed that the most highly activated pathways in response to hyperoxia were hypercytokinemia/hyperchemokinemia in WT mice, NAD signaling pathway in PAFR KO mice, and agranulocyte adhesion and diapedesis, as well as other pro-fibrotic pathways like tumor microenvironment and oncostatin-M signaling in both strains of mice. This suggests that while PAF signaling may play a role in inflammation, it is not a significant mediator of fibrotic processes during hyperoxic neonatal lung injury. Further analysis also showed increased expression of pro-inflammatory genes like CXCL1, CCL2, and IL-6 in the lungs of hyperoxia-exposed WT mice, and metabolic regulators like HMGCS2 and SIRT3 in the lungs of PAFR KO mice, indicating that PAF signaling may impact BPD risk through changes in pulmonary inflammation and/or metabolic reprogramming in preterm infants.
Yee AJ, et al. "Platelet Activating Factor Activity Modulates Hyperoxic Neonatal Lung Injury ." bioRxiv : the preprint server for biology, 2023.
Pubmed: 36993203   DOI: 10.1101/2023.03.14.532697