Journal of proteomics and genomics research最新文献

{"title":"The Evolution of the Enzyme Immunoassay/Enzyme-Linked Immunosorbent Assay","authors":"L. Tarassishin","doi":"10.14302/issn.2326-0793.jpgr-21-3917","DOIUrl":"https://doi.org/10.14302/issn.2326-0793.jpgr-21-3917","url":null,"abstract":"50 years ago the Enzyme Immunoassay Enzyme-Linked Immunosorbent Assay, mostly known as ELISA was developed. This is a powerful but simple method that is very widely used in the diagnostic practice, as well as in biomedical research. During this time a number of ELISA modification were developed that significantly increased its properties, especially the senstivity, such as avidin-biotin assay, immuno-PCR, nano-ELISA and finally, the digital ELISA. This short review describes the principles of ELISA and the evolution from a conventional assay to the modern ultra-sensitive method.\u0000\u0000Most of the immunological methods have two components: antigen and antibody. The high specificity of their interaction gives a possibility to detect one of them if other one is included in the reaction as a specific partner. The simplest method for antigen detection in the presence of the antibody is immune diffusion (radial immune diffusion in that case), which practically the formation of precipitate of the “antigen-antibody” complex, when the target antigen diffuses from well into agarose containing the specific antibody. Unfortunately, this assay, as well as other traditional methods, like hemagglutination or complement fixation, have a low sensitivity and are unwieldy.","PeriodicalId":90235,"journal":{"name":"Journal of proteomics and genomics research","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41583654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor Development in p53 Knockout Mice: A Review of Mice Deficient for p53","authors":"S. Patra","doi":"10.14302/ISSN.2326-0793.JPGR-18-2422","DOIUrl":"https://doi.org/10.14302/ISSN.2326-0793.JPGR-18-2422","url":null,"abstract":"","PeriodicalId":90235,"journal":{"name":"Journal of proteomics and genomics research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49095767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Biomarkers: A Brief Review","authors":"L. Tarassishin","doi":"10.14302/ISSN.2326-0793.JPGR-18-2418","DOIUrl":"https://doi.org/10.14302/ISSN.2326-0793.JPGR-18-2418","url":null,"abstract":"","PeriodicalId":90235,"journal":{"name":"Journal of proteomics and genomics research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49418875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological Networks: An Introductory Review","authors":"Mohammad Saad Zaghloul Salem","doi":"10.14302/ISSN.2326-0793.JPGR-18-2312","DOIUrl":"https://doi.org/10.14302/ISSN.2326-0793.JPGR-18-2312","url":null,"abstract":"All aspects of life activities in living cells are mediated/executed and regulated by a vast number of networks, comprising a wide spectrum of components, starting with simple biomolecules and ending with the whole organism, and functioning within a precisely organized tight framework. Proper mediation of cellular activities necessitates their inclusion within the context of structured and organized network systems capable of regulating/coordinating and synchronizing the countless numbers of biological processes occurring within living cells. The number of biological networks and pathways within the living cell is considerably huge, being dependent on the structural complexity and functional capabilities of the cell. Pathogenesis and progression of human diseases result from functional disturbances of biological networks within the cell as disturbed network function leads to deleterious effects on physiological processes dependent on, and mediated by, affected network(s). Ensuing pathological processes, defined by the nature of disturbed networks and the specific organs or tissues affected, pave the way for the development of pathognomonic and characteristic disease entities. As most network functions are dependent on relatively small number of key regulatory biomolecules, i.e. enzymes/proteins and signal transducing factors, it follows that functional disturbances of biological networks and pathogenesis of disease states can be attributed, in most instances, to quantitative and/or qualitative abnormalities of these key regulatory molecules. Study and analysis of the structural designs and the functional mechanisms of biological networks would have crucial and important impacts on many theoretical and applied aspects of biology, in general, and of medical sciences in particular. Meticulous study of biological networks represents an important and integral aspect in study of biology. Interpretation and analysis of key information deduced from observing and analyzing structural designs and functional characteristics and dynamics of biological networks discloses and defines the basic framework within which life activities in living cells are initiated, adapted to physiological requirements, maintained, and terminated upon completion of their aims. More important, however, is the contribution of this information to proper understanding of the different mechanisms responsible for regulating and synchronizing the functions and performances of the vast spectrum of different network categories within the cell. In addition to its vital scientific significance, discovering and defining the key pivotal structural and regulatory molecules within life-mediating networks, and along different pathways responsible for controlling functional dynamics of the network, represent an indispensable diagnostic approach insistent for designing proper therapeutic approaches to diseases caused by network defects.","PeriodicalId":90235,"journal":{"name":"Journal of proteomics and genomics research","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46725950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioinformatic Analysis of Coronary Disease Associated SNPs and Genes to Identify Proteins Potentially Involved in the Pathogenesis of Atherosclerosis.","authors":"Chunhong Mao,&nbsp;Timothy D Howard,&nbsp;Dan Sullivan,&nbsp;Zongming Fu,&nbsp;Guoqiang Yu,&nbsp;Sarah J Parker,&nbsp;Rebecca Will,&nbsp;Richard S Vander Heide,&nbsp;Yue Wang,&nbsp;James Hixson,&nbsp;Jennifer Van Eyk,&nbsp;David M Herrington","doi":"10.14302/issn.2326-0793.jpgr-17-1447","DOIUrl":"https://doi.org/10.14302/issn.2326-0793.jpgr-17-1447","url":null,"abstract":"<p><p>Factors that contribute to the onset of atherosclerosis may be elucidated by bioinformatic techniques applied to multiple sources of genomic and proteomic data. The results of genome wide association studies, such as the CardioGramPlusC4D study, expression data, such as that available from expression quantitative trait loci (eQTL) databases, along with protein interaction and pathway data available in Ingenuity Pathway Analysis (IPA), constitute a substantial set of data amenable to bioinformatics analysis. This study used bioinformatic analyses of recent genome wide association data to identify a seed set of genes likely associated with atherosclerosis. The set was expanded to include protein interaction candidates to create a network of proteins possibly influencing the onset and progression of atherosclerosis. Local average connectivity (LAC), eigenvector centrality, and betweenness metrics were calculated for the interaction network to identify top gene and protein candidates for a better understanding of the atherosclerotic disease process. The top ranking genes included some known to be involved with cardiovascular disease (<i>APOA1, APOA5, APOB, APOC1, APOC2, APOE, CDKN1A, CXCL12, SCARB1, SMARCA4</i> and <i>TERT</i>), and others that are less obvious and require further investigation (<i>TP53, MYC, PPARG, YWHAQ, RB1, AR, ESR1, EGFR, UBC</i> and <i>YWHAZ</i>). Collectively these data help define a more focused set of genes that likely play a pivotal role in the pathogenesis of atherosclerosis and are therefore natural targets for novel therapeutic interventions.</p>","PeriodicalId":90235,"journal":{"name":"Journal of proteomics and genomics research","volume":"2 1","pages":"1-12"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.14302/issn.2326-0793.jpgr-17-1447","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35764221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differences in the alveolar macrophage proteome in transgenic mice expressing human SP-A1 and SP-A2.","authors":"David S Phelps,&nbsp;Todd M Umstead,&nbsp;Patricia Silveyra,&nbsp;Sanmei Hu,&nbsp;Guirong Wang,&nbsp;Joanna Floros","doi":"10.14302/issn.2326-0793.jpgr-12-207","DOIUrl":"https://doi.org/10.14302/issn.2326-0793.jpgr-12-207","url":null,"abstract":"<p><p>Surfactant protein A (SP-A) plays a number of roles in lung host defense and innate immunity. There are two human genes, <i>SFTPA1</i> and <i>SFTPA2</i>, and evidence indicates that the function of SP-A1 and SP-A2 proteins differ in several respects. To investigate the impact of SP-A1 and SP-A2 on the alveolar macrophage (AM) phenotype, we generated humanized transgenic (hTG) mice on the SP-A knockout (KO) background, each expressing human SP-A1 or SP-A2. Using two-dimensional difference gel electrophoresis (2D-DIGE) we studied the AM cellular proteome. We compared mouse lines expressing high levels of SPA1, high levels of SP-A2, low levels of SP-A1, and low levels of SP-A2, with wild type (WT) and SP-A KO mice. AM from mice expressing high levels of SP-A2 were the most similar to WT mice, particularly for proteins related to actin and the cytoskeleton, as well as proteins regulated by Nrf2. The expression patterns from mouse lines expressing higher levels of the transgenes were almost the inverse of one another - the most highly expressed proteins in SP-A2 exhibited the lowest levels in the SP-A1 mice and vice versa. The mouse lines where each expressed low levels of SP-A1 or SP-A2 transgene had very similar protein expression patterns suggesting that responses to low levels of SP-A are independent of SP-A genotype, whereas the responses to higher amounts of SP-A are genotype-dependent. Together these observations indicate that in vivo exposure to SP-A1 or SP-A2 differentially affects the proteomic expression of AMs, with SP-A2 being more similar to WT.</p>","PeriodicalId":90235,"journal":{"name":"Journal of proteomics and genomics research","volume":"1 2","pages":"2-26"},"PeriodicalIF":0.0,"publicationDate":"2013-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3981560/pdf/nihms-548595.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32260327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Determination of the Proteomic Response to Lapatinib Treatment using a comprehensive and reproducible ion-current-based proteomics strategy.","authors":"Kathleen O'Connell,&nbsp;Jun Li,&nbsp;Frank Engler,&nbsp;Kim Hennessy,&nbsp;Fiona O'Neill,&nbsp;Robert M Straubinger,&nbsp;Jun Qu,&nbsp;Robert O'Connor","doi":"10.14302/issn.2326-0793.jpgr-13-257","DOIUrl":"https://doi.org/10.14302/issn.2326-0793.jpgr-13-257","url":null,"abstract":"<p><p>Lapatinib, a small molecule tyrosine kinase inhibitor is currently used in the treatment of HER2-positive breast cancer. The aim of this study was to further understanding of lapatinib response for the development of novel treatment lapatinib-focussed treatment strategies. HER2-overexpressing SKBR3 breast cancer cells were treated with lapatinib for 12 hours and the resultant proteome analyzed by a comprehensive ion-current-based LC-MS strategy. Among the 1224 unique protein identified from SKBR3 cell lysates, 67 showed a significant change in protein abundance in response to lapatinib. Of these, CENPE a centromeric protein with increased abundance, was chosen for further validation. Knockdown and inhibition of CENPE demonstrated that CENPE enhances SKBR3 cell survival in the presence of lapatinib. Based on this study, CENPE inhibitors may warrant further investigation for use in combination with lapatinib.</p>","PeriodicalId":90235,"journal":{"name":"Journal of proteomics and genomics research","volume":"1 3","pages":"27-42"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5642974/pdf/nihms908409.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35527955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}