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Articles by Kui Li
Total Records ( 3 ) for Kui Li
  Qiang Zhong , Xin-Yun Li , Jia-Hua Cao , Shu-Hong Zhao and Kui Li
  Using CaMK2B gene cds of human and mouse to blast Sus scrofa 9 genome, the porcine CaMK2B gene sequence was obtained. Homologous protein sequence between four isoforms in 9 species was analyzed. The results indicate that some key residues differences are responsible for different enzymatic properties of different isoforms.
  Huiming Ju , Lijing Bai , Yuefei Yang , Xing Jiang , Anzhi Sheng and Kui Li
  It has been widely acknowledged that introns can influence the efficiency of gene expression. Most transcriptional regulatory elements are located within non-coding DNA. The aim of the study was to study introns affecting porcine Growth Hormone (pGH) expression levels. A program was developed for mammalian cells (PK15 cells) by measuring the enhancement effect on GH expression of different introns inserted with otherwise identical plasmids. After selection with G418, quantitative Polymerase Chain Reaction (qRT-PCR) assays was performed to determine pGH mRNA expression levels. Western blotting was used to analyze pGH protein expression. The qPCR and Western blot results revealed that various introns have different effects on pGH expression efficiency. The recombinant pGH gene with introns 3 and 4 had the highest expression activity. In this study, researchers have provided the first insights into the function of pGH introns, establishing a foundation for the recognition and better utilization of these introns.
  Ping Liu , Kui Li , Roberto P. Garofalo and Allan R. Brasier
  Respiratory syncytial virus (RSV) is a primary cause of severe lower respiratory tract infection in children worldwide. RSV infects airway epithelial cells, where it activates inflammatory genes via the NF-κB pathway. NF-κB is controlled by two pathways, a canonical pathway that releases sequestered RelA complexes from the IκBα inhibitor, and a second, the noncanonical pathway, that releases RelB from the 100-kDa NF-κB2 complex. Recently we found that the retinoic acid-inducible gene I (RIG-I) is a major intracellular RSV sensor upstream of the canonical pathway. In this study, we surprisingly found that RIG-I silencing also inhibited p100 processing to 52-kDa NF-κB2 ("p52"), suggesting that RIG-I was functionally upstream of the noncanonical regulatory kinase complex composed of NIK·IKKα subunits. Co-immunoprecipitation experiments not only demonstrated that NIK associated with RIG-I and its downstream adaptor, mitochondrial antiviral signaling (MAVS), but also showed the association between IKKα and MAVS. To further understand the role of the NIK·IKKα pathway, we compared RSV-induced NF-κB activation using wild type, Ikkγ-/-, Nik-/-, and Ikkα-/--deficient MEF cells. Interestingly, we found that in canonical pathway-defective Ikkγ-/- cells, RSV induced RelA by liberation from p100 complexes. RSV was still able to activate IP10, Rantes, and Groβ gene expression in Ikkγ-/- cells, and this induction was inhibited by small interfering RNA-mediated RelA knockdown but not RelB silencing. These data suggest that part of the RelA activation in response to RSV infection was induced by a "cross-talk" pathway involving the noncanonical NIK·IKKα complex downstream of RIG-I·MAVS. This pathway may be a potential target for RSV treatment.
 
 
 
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