[Objective]To clone araC gene of Vibrio alginolyticus HY9901 strain,and analyze bioinformatics.[Methods]the whole genome sequence of Vibrio alginolyticus on GenBank was used to design specific primers.According to the...[Objective]To clone araC gene of Vibrio alginolyticus HY9901 strain,and analyze bioinformatics.[Methods]the whole genome sequence of Vibrio alginolyticus on GenBank was used to design specific primers.According to the principle of PCR amplification sequence,the target gene araC was amplified,and then the sequence was further analyzed by bioinformatics method to establish the phylogenetic tree of araC gene and its corresponding subunit three-dimensional structure model.[Results]Sequence analysis revealed araC gene is 711 bp and encodes a putative protein of 236 amino acids.The predicted molecular mass of AraC was 26.92 ku.Using Signal P 4.0 and TMHMM Server 2.0 software for analysis,it was predicted that the AraC protein did not contain a signal peptide or a transmembranous region.The AraC protein had two cAMP and cGMP dependent protein kinase phosphorylation site,five protein kinase C phosphorylation sites,three casein kinase II phosphorylation sites,one prenyl group binding site(CAAX box)and five microbodies C-terminal targeting signal.The predicted results of protein subcellular localization showed that AraC was located in the mitochondria,nucleus and cytoplasm.Its protein is unstable and hydrophilic.The AraC protein is a transcriptional regulatory protein which belongs to HTH_18 superfamily.According to the prediction,secondary structure:a-helix(Alpha helix)accounted for 52.12%,random coil(31.78%),extended strand(11.02%),b-fold(Beta turn)accounted for 5.08%.V.alginolyticus,Vibrio parahaemolyticus and Vibrio palustris were clustered together,which implies that the genetic relationship between these three species was the closest.展开更多
This study aims to identify the inflammatory factor-related genes which help to predict the prognosis of patients with colorectal cancer.GSEA(Gene Set Enrichment Analysis)was used to acquire inflammation-related genes...This study aims to identify the inflammatory factor-related genes which help to predict the prognosis of patients with colorectal cancer.GSEA(Gene Set Enrichment Analysis)was used to acquire inflammation-related genes and the corresponding expression information was collected from TCGA database to determine the DEGs(differentially-expressed genes)in CRC patients.We conducted enrichment analysis and PPI(protein–protein interaction)of these DEGs.Besides,key genes that are both differentially-expressed and prognosis-related were screened out,which were used to establish the prognostic model.We obtained 79 DEGs and 19 prognostic genes,10 prognostic-related differential genes were eventually screened.These genes were used to construct the prognostic model.We also identified that the immune infiltration score of macrophages between different risk groups was significantly different and similar distinction was witnessed in immune function score of APC(antigen-presenting cell)co-stimulation and type I IFN(interferon)response.展开更多
Biofilm formation has been implicated to be tightly regulated in bacteria. Mycobacterial species possess a unique cell-wall structure; however, the underlying regulation mechanism for their biofilm formation remains l...Biofilm formation has been implicated to be tightly regulated in bacteria. Mycobacterial species possess a unique cell-wall structure; however, the underlying regulation mechanism for their biofilm formation remains largely unclear. In this study, we characterized a hypothetical mannitol metabolism and transportation gene cluster(Ms5571-Ms5576), designated as mmt operon, whose expression significantly contributes to the biofilm formation in Mycobacterium smegmatis. We showed that in the operon the Ms5575 gene encodes a GntR-like transcriptional repressor and the Ms5576 gene encodes a mannitol2-dehydrogenase which can produce D-mannitol from D-mannose. Strikingly, the D-mannitol molecule can derepress the negative regulation of Ms5575 on the mmt operon to stimulate the operon's expression. Consistently, addition of D-mannitol into the medium can obviously induce mycobacterial biofilm formation. Furthermore, we found that Ms0179 positively regulates the mmt operon through its downstream regulator Ms0180. Ms0180 directly binds the mmt operon to positively regulate its expression. Both Ms0179 and Ms0180 significantly affect the mycobacterial biofilm formation. Taken together, we explored a regulatory pathway for the mannitol metabolism and its coordination with the biofilm formation in M. smegmatis. This finding provides novel insights into the unique mechanism of biofilm formation regulation in mycobacteria.展开更多
Metastasis remains the primary cause for mortality of breast cancer.Despite advances in current therapeutic agents,patients with metastatic breast cancer still have poor prognoses.Tumor hypoxia,a key microenvironment ...Metastasis remains the primary cause for mortality of breast cancer.Despite advances in current therapeutic agents,patients with metastatic breast cancer still have poor prognoses.Tumor hypoxia,a key microenvironment factor,is emerging as an attractive target to prevent metastasis and is also involved with resistance to phototherapy.Here,we show an effective nanotherapeutic approach based on manganese dioxide-coated polydopamine nanocarriers to trigger robust anti-tumor and anti-metastasis responses against metastatic breast cancer by supplemental oxygenation and multimodal imaging-guided phototherapies.In cancer cells,the produced oxygen by the developed nanoplatform decreases the expression of hypoxia-inducible factors 1 a to inhibit tumor metastasis,and enhances the efficacy of photodynamic therapy.This nanotherapeutic approach enables the combined photodynamic/photothermal treatments with great inhibition on cell migration and invasion in vitro.Moreover,the nanotherapeutics effectively suppresses primary tumor progress and inhibits lung metastasis in v ivo in a breast cancer mouse model with satisfying biosafety.This study suggests that the tumor hypoxia-targeting nanotherapeutics have great potential for preventing and treating metastatic cancers.展开更多
基金National Natural Science Foundation of China(32073015).
文摘[Objective]To clone araC gene of Vibrio alginolyticus HY9901 strain,and analyze bioinformatics.[Methods]the whole genome sequence of Vibrio alginolyticus on GenBank was used to design specific primers.According to the principle of PCR amplification sequence,the target gene araC was amplified,and then the sequence was further analyzed by bioinformatics method to establish the phylogenetic tree of araC gene and its corresponding subunit three-dimensional structure model.[Results]Sequence analysis revealed araC gene is 711 bp and encodes a putative protein of 236 amino acids.The predicted molecular mass of AraC was 26.92 ku.Using Signal P 4.0 and TMHMM Server 2.0 software for analysis,it was predicted that the AraC protein did not contain a signal peptide or a transmembranous region.The AraC protein had two cAMP and cGMP dependent protein kinase phosphorylation site,five protein kinase C phosphorylation sites,three casein kinase II phosphorylation sites,one prenyl group binding site(CAAX box)and five microbodies C-terminal targeting signal.The predicted results of protein subcellular localization showed that AraC was located in the mitochondria,nucleus and cytoplasm.Its protein is unstable and hydrophilic.The AraC protein is a transcriptional regulatory protein which belongs to HTH_18 superfamily.According to the prediction,secondary structure:a-helix(Alpha helix)accounted for 52.12%,random coil(31.78%),extended strand(11.02%),b-fold(Beta turn)accounted for 5.08%.V.alginolyticus,Vibrio parahaemolyticus and Vibrio palustris were clustered together,which implies that the genetic relationship between these three species was the closest.
基金funded by the Natural Science Foundation of China(No.81860034 to WXZ).
文摘This study aims to identify the inflammatory factor-related genes which help to predict the prognosis of patients with colorectal cancer.GSEA(Gene Set Enrichment Analysis)was used to acquire inflammation-related genes and the corresponding expression information was collected from TCGA database to determine the DEGs(differentially-expressed genes)in CRC patients.We conducted enrichment analysis and PPI(protein–protein interaction)of these DEGs.Besides,key genes that are both differentially-expressed and prognosis-related were screened out,which were used to establish the prognostic model.We obtained 79 DEGs and 19 prognostic genes,10 prognostic-related differential genes were eventually screened.These genes were used to construct the prognostic model.We also identified that the immune infiltration score of macrophages between different risk groups was significantly different and similar distinction was witnessed in immune function score of APC(antigen-presenting cell)co-stimulation and type I IFN(interferon)response.
基金supported by the National Key R&D Program of China (2017YFD0500300)the National Natural Science Foundation of China (Nos.31730005,31401108,and 31670075)+1 种基金the Fundamental Research Funds for the Central Universities (2662016PY090)Chang Jiang Scholars Program (to Z.-G. He)
文摘Biofilm formation has been implicated to be tightly regulated in bacteria. Mycobacterial species possess a unique cell-wall structure; however, the underlying regulation mechanism for their biofilm formation remains largely unclear. In this study, we characterized a hypothetical mannitol metabolism and transportation gene cluster(Ms5571-Ms5576), designated as mmt operon, whose expression significantly contributes to the biofilm formation in Mycobacterium smegmatis. We showed that in the operon the Ms5575 gene encodes a GntR-like transcriptional repressor and the Ms5576 gene encodes a mannitol2-dehydrogenase which can produce D-mannitol from D-mannose. Strikingly, the D-mannitol molecule can derepress the negative regulation of Ms5575 on the mmt operon to stimulate the operon's expression. Consistently, addition of D-mannitol into the medium can obviously induce mycobacterial biofilm formation. Furthermore, we found that Ms0179 positively regulates the mmt operon through its downstream regulator Ms0180. Ms0180 directly binds the mmt operon to positively regulate its expression. Both Ms0179 and Ms0180 significantly affect the mycobacterial biofilm formation. Taken together, we explored a regulatory pathway for the mannitol metabolism and its coordination with the biofilm formation in M. smegmatis. This finding provides novel insights into the unique mechanism of biofilm formation regulation in mycobacteria.
基金This work is supported by the National Natural Science Foundation of China(Nos.81602610,21874103)Fundam ental Research Funds for the Central Universities(Nos.2042018kf1006,2042018kf0210).
文摘Metastasis remains the primary cause for mortality of breast cancer.Despite advances in current therapeutic agents,patients with metastatic breast cancer still have poor prognoses.Tumor hypoxia,a key microenvironment factor,is emerging as an attractive target to prevent metastasis and is also involved with resistance to phototherapy.Here,we show an effective nanotherapeutic approach based on manganese dioxide-coated polydopamine nanocarriers to trigger robust anti-tumor and anti-metastasis responses against metastatic breast cancer by supplemental oxygenation and multimodal imaging-guided phototherapies.In cancer cells,the produced oxygen by the developed nanoplatform decreases the expression of hypoxia-inducible factors 1 a to inhibit tumor metastasis,and enhances the efficacy of photodynamic therapy.This nanotherapeutic approach enables the combined photodynamic/photothermal treatments with great inhibition on cell migration and invasion in vitro.Moreover,the nanotherapeutics effectively suppresses primary tumor progress and inhibits lung metastasis in v ivo in a breast cancer mouse model with satisfying biosafety.This study suggests that the tumor hypoxia-targeting nanotherapeutics have great potential for preventing and treating metastatic cancers.
