結(jié)核分枝桿菌調(diào)節(jié)蛋白R(shí)elA結(jié)構(gòu)和功能的生物信息學(xué)分析
發(fā)布時(shí)間:2018-12-14 06:01
【摘要】:目的應(yīng)用生物信息學(xué)方法分析預(yù)測(cè)結(jié)核分枝桿菌調(diào)節(jié)蛋白R(shí)elA的結(jié)構(gòu)及功能。方法從NCBI數(shù)據(jù)庫(kù)獲取結(jié)核分枝桿菌RelA蛋白的氨基酸序列,采用ProtParam工具預(yù)測(cè)蛋白質(zhì)理化性質(zhì),采用Predict-Protein工具預(yù)測(cè)二級(jí)結(jié)構(gòu)和疏水性,采用TMHMM軟件包和TMpred程序?qū)缒^(qū)預(yù)測(cè),采用SignalP 4.1Server,用神經(jīng)網(wǎng)絡(luò)模型對(duì)信號(hào)肽預(yù)測(cè),分析亞細(xì)胞定位、結(jié)構(gòu)域和功能,運(yùn)用SWISS-MODEL工具在線預(yù)測(cè)三維結(jié)構(gòu)等。結(jié)果結(jié)核分枝桿菌RelA蛋白含有894個(gè)氨基酸,為不穩(wěn)定性疏水性分泌蛋白,二級(jí)結(jié)構(gòu)以螺旋結(jié)構(gòu)和環(huán)狀結(jié)構(gòu)為主,無(wú)跨膜區(qū),包含5個(gè)保守域,在胞漿中發(fā)揮生物學(xué)效應(yīng),調(diào)節(jié)(p)ppGpp合成。結(jié)論結(jié)核分枝桿菌RelA基因編碼蛋白為不穩(wěn)定性疏水性分泌蛋白,作為調(diào)節(jié)蛋白,主要參與細(xì)菌在生存壓力下引起的嚴(yán)緊反應(yīng),調(diào)節(jié)(p)ppGpp的合成,因此可作為抗結(jié)核潛伏、持續(xù)感染治療靶點(diǎn)。
[Abstract]:Objective to analyze and predict the structure and function of Mycobacterium tuberculosis regulatory protein RelA by bioinformatics. Methods the amino acid sequence of RelA protein of Mycobacterium tuberculosis was obtained from NCBI database. The physicochemical properties of the protein were predicted by ProtParam, the secondary structure and hydrophobicity were predicted by Predict-Protein, and the transmembrane region was predicted by TMHMM software package and TMpred program. SignalP 4.1 Server was used to predict the signal peptide with neural network model, to analyze subcellular localization, domain and function, and to use SWISS-MODEL tools to predict 3D structure online. Results the RelA protein of Mycobacterium tuberculosis contained 894 amino acids and was an unstable hydrophobic secretory protein. The secondary structure was mainly helical structure and annular structure with no transmembrane region and five conserved domains, which played a biological role in the cytoplasm. Regulate (p) ppGpp synthesis. Conclusion the RelA gene encoding protein of Mycobacterium tuberculosis is an unstable hydrophobic secretory protein, which is mainly involved in the severe response of bacteria under survival pressure and regulates the synthesis of (p) ppGpp, so it can be used as an antituberculous latent protein. Persistent infection is a therapeutic target.
【作者單位】: 濰坊醫(yī)學(xué)院醫(yī)學(xué)檢驗(yàn)學(xué)系;濰坊醫(yī)學(xué)院病原生物學(xué)教研室;
【基金】:國(guó)家自然科學(xué)基金項(xiàng)目(No.30972639) 山東省自然科學(xué)基金項(xiàng)目(No.ZR2016HM09)
【分類號(hào)】:R378.911
,
本文編號(hào):2378056
[Abstract]:Objective to analyze and predict the structure and function of Mycobacterium tuberculosis regulatory protein RelA by bioinformatics. Methods the amino acid sequence of RelA protein of Mycobacterium tuberculosis was obtained from NCBI database. The physicochemical properties of the protein were predicted by ProtParam, the secondary structure and hydrophobicity were predicted by Predict-Protein, and the transmembrane region was predicted by TMHMM software package and TMpred program. SignalP 4.1 Server was used to predict the signal peptide with neural network model, to analyze subcellular localization, domain and function, and to use SWISS-MODEL tools to predict 3D structure online. Results the RelA protein of Mycobacterium tuberculosis contained 894 amino acids and was an unstable hydrophobic secretory protein. The secondary structure was mainly helical structure and annular structure with no transmembrane region and five conserved domains, which played a biological role in the cytoplasm. Regulate (p) ppGpp synthesis. Conclusion the RelA gene encoding protein of Mycobacterium tuberculosis is an unstable hydrophobic secretory protein, which is mainly involved in the severe response of bacteria under survival pressure and regulates the synthesis of (p) ppGpp, so it can be used as an antituberculous latent protein. Persistent infection is a therapeutic target.
【作者單位】: 濰坊醫(yī)學(xué)院醫(yī)學(xué)檢驗(yàn)學(xué)系;濰坊醫(yī)學(xué)院病原生物學(xué)教研室;
【基金】:國(guó)家自然科學(xué)基金項(xiàng)目(No.30972639) 山東省自然科學(xué)基金項(xiàng)目(No.ZR2016HM09)
【分類號(hào)】:R378.911
,
本文編號(hào):2378056
本文鏈接:http://sikaile.net/xiyixuelunwen/2378056.html
最近更新
教材專著