Project description:pBIC-1a is a IncFIIk-IncFI blaKPC-2-producing plasmid. Transcriptomic analysis was performed to dive deeper into the biology of this prototypical successful plasmid. The transcriptional landscape of pBIC-1a was assessed without antibiotic, and differential analysis after imipenem exposure was performed on E. coli TOP10(pBIC-1a) whole transcriptome.
Project description:The purpose of the present study was to investigate the impact of heat stress for increasing imipenem susceptibility in imipenem resistant nontypeable Haemophilus influenzae (NTHi).
Project description:To study the gene expression profile in the mesendoderm differerntiation of control and Hif-1a overexpression, we performed RNA-seq on the total RNA samples collected from the differentiation of control and Hif-1a overexpression AB2.2 mESCs at differentiation day 4.In addition, to study the gene expression profile in the mesendoderm differerntiation of Hif-1a knockdown under normoxia and hypoxia, we performed RNA-seq on the total RNA samples collected from the differentiation of Hif-1a knockdown AB2.2 mESCs under normoxia or hypoxia at differentiation day 4. Cell lines were built by infecting AB2.2 cells with lentiviruses. Each group contained three biological replicates. The expression matrix was obtained by Hisat2 followed by Stringtie.
Project description:HIF-1a works as a stress-induced transcription factor to induce target genes mediating cell proliferation, meabolism and inflammation. To gain new insights into HIF-1a biology, we used high-throughput sequencing to analyze global HIF-1a transcriptional networks in WT or HIF-1a deficient bone marrow B cells under hypoxia or normoxia.
Project description:Based on the results of numerous clinical and preclinical analyses, the transcription factor HIF-1a has been identified as an important tumor-promoting factor and is considered to be an attractive target for cancer therapy. To further deconstruct the molecular nature of HIF-1a’s role in tumorigenesis, we have applied lentiviral shRNA transduction to establish HIF-1a-deficient gastric cancer cells. Interestingly, functional analyses failed to show a significant growth defect of HIF-1a-deficient gastric cancer cells in vitro and in vivo. These observations led us to propose that stable inactivation of HIF-1a resulted in efficient compensation enabling cell growth and, ultimately, tumor progression in a HIF-1a-independent manner. To better understand the mechanisms that control this compensation, we performed transcriptomics of control (“scrambled” (SCR)) and HIF-1a-deficient (HIF) gastric cancer cells. Analysis of hypoxia-inducible factor-1alpha (HIF-1a)-deficient gastric cancer cells under normoxia. The transcription factor HIF-1a is a key regulator of oxygen homeostasis and has been identified as an important tumor-promoting factor. Results provide insight into the role of HIF-1a in gastric carcinogenesis.
Project description:To know the role of PGC-1a in the change of mRNA expression during desidualization, we compared the mRNA expression profiles between cAMP-stimulation and cAMP-stimulation under PGC-1a-knockdown.
Project description:Previous synthesized Pt NPs were selected to evaluate the influences on bacterial resistance, and a typical pathogenic microbe P. aeruginosa was chosen as model bacteria. After 60-day PtNPs exposure, we found under 12.5 μg/mL of platinum nanoparticles (PtNPs) exposure for ~7200 generations, the IC50 of evolved Pseudomonas aeruginosa PAO1 to imipenem (IPM) and ciprofloxacin (CIP) reduced 77.0% and 87.8%, respectively. Interestingly, long-term of PtNPs exposure arose the bacterial susceptibility on antibiotics. We then performed gene expression profiling analysis using data obtained from RNA-seq.
Project description:Recently, we have reported on a highly drug-resistant carbapenemase-producing isolate of Enterobacter cloacae (Nepal et al., Virulence. 2018; 9: 1377-1389). In the present study, we asked the question whether and, if so, how this isolate responds to a sub-inhibitory challenge with the antibiotic imipenem. To answer this question, we applied a SILAC proteomics approach that allowed the quantification of changes in the relative abundance of bacterial protein in response to imipenem. The results show that the investigated E. cloacae isolate mounts a highly specific response to counteract the detrimental effects of imipenem.