Pub Date : 2022-12-01DOI: 10.1136/lupus-2022-lupus21century.113
E. Lilly, Vincent Chan, Jimmie Ye, Andy Gross, Max Krummel, Jeroen M. Roose
{"title":"2105 UCSF AutoImmunoProfiler – Understanding the Immunomes of Autoimmune diseases","authors":"E. Lilly, Vincent Chan, Jimmie Ye, Andy Gross, Max Krummel, Jeroen M. Roose","doi":"10.1136/lupus-2022-lupus21century.113","DOIUrl":"https://doi.org/10.1136/lupus-2022-lupus21century.113","url":null,"abstract":"","PeriodicalId":90374,"journal":{"name":"Transcriptomics: open access","volume":"39 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83924895","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}
Pub Date : 2022-12-01DOI: 10.1136/lupus-2022-lupus21century.110
Ann E. Wells, John J. Wilson, D. Roopenian, Chih-Hao Chang, G. Carter
{"title":"2102 Inhibition of glycolysis modifies distinctive wound and immune pathways across multiple tissue compartments associated with activated autoreactive B Cells","authors":"Ann E. Wells, John J. Wilson, D. Roopenian, Chih-Hao Chang, G. Carter","doi":"10.1136/lupus-2022-lupus21century.110","DOIUrl":"https://doi.org/10.1136/lupus-2022-lupus21century.110","url":null,"abstract":"","PeriodicalId":90374,"journal":{"name":"Transcriptomics: open access","volume":"116 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73104332","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}
Pub Date : 2022-12-01DOI: 10.1136/lupus-2022-lupus21century.111
K. Kingsmore, S. Shrotri, P. Bachali, N. Shen, A. Grammer, P. Lipsky
{"title":"2103 Molecular characterization of lupus nephritis kidneys and blood","authors":"K. Kingsmore, S. Shrotri, P. Bachali, N. Shen, A. Grammer, P. Lipsky","doi":"10.1136/lupus-2022-lupus21century.111","DOIUrl":"https://doi.org/10.1136/lupus-2022-lupus21century.111","url":null,"abstract":"","PeriodicalId":90374,"journal":{"name":"Transcriptomics: open access","volume":"75 5","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72484267","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}
Pub Date : 2022-12-01DOI: 10.1136/lupus-2022-lupus21century.112
M. Olferiev, D. Greenman, Jeffrey Zhang-Sun, David Fernandez, K. Kirou, M. Crow
{"title":"2104 Lupus autoantibodies associated with cell cycle gene expression in peripheral blood of SLE patients","authors":"M. Olferiev, D. Greenman, Jeffrey Zhang-Sun, David Fernandez, K. Kirou, M. Crow","doi":"10.1136/lupus-2022-lupus21century.112","DOIUrl":"https://doi.org/10.1136/lupus-2022-lupus21century.112","url":null,"abstract":"","PeriodicalId":90374,"journal":{"name":"Transcriptomics: open access","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79017211","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}
Pub Date : 2022-12-01DOI: 10.1136/lupus-2022-lupus21century.109
Erika L. Hubbard, P. Bachali, K. Kingsmore, Yisha He, Michelle D Catalina, A. Grammer, P. Lipsky
{"title":"2101 Gene Expression Profiling of Key Immune/Inflammatory Pathways Reveals Molecular Endotypes of SLE with Clinical Implications","authors":"Erika L. Hubbard, P. Bachali, K. Kingsmore, Yisha He, Michelle D Catalina, A. Grammer, P. Lipsky","doi":"10.1136/lupus-2022-lupus21century.109","DOIUrl":"https://doi.org/10.1136/lupus-2022-lupus21century.109","url":null,"abstract":"","PeriodicalId":90374,"journal":{"name":"Transcriptomics: open access","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82312072","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}
Pub Date : 2015-12-28DOI: 10.4172/2329-8936.1000124
J. Crain, J. Watters
Inflammatory damage in many neurodegenerative diseases is restricted to certain regions of the CNS, and while microglia have long been implicated in the pathology of many of these disorders, information comparing their gene expression in different CNS regions is lacking. Here we tested the hypothesis that the expression of purinergic receptors, estrogen receptors and other neuroprotective and pro-inflammatory genes differed among CNS regions in healthy mice. Because neurodegenerative diseases vary in incidence by sex and age, we also examined the regional distribution of these genes in male and female mice of four different ages between 21 days and 12 months. We postulated that pro-inflammatory gene expression would be higher in older animals, and lower in young adult females. We found that microglial gene expression differed across the CNS. Estrogen receptor alpha (Esr1) mRNA levels were often lower in microglia from the brainstem/spinal cord than from the cortex, whereas tumor necrosis factor alpha (Tnfα) expression was several times higher. In addition, the regional pattern of gene expression often changed with animal age; for example, no regional differences in P2X7 mRNA levels were detected in 21 day-old animals, but at 7 weeks and older, expression was highest in cerebellar microglia. Lastly, the expression of some genes was sexually dimorphic. In microglia from 12 month-old animals, mRNA levels of inducible nitric oxide synthase, but not Tnfα, were higher in females than males. These data suggest that microglial gene expression is not uniformly more pro-inflammatory in males or older animals. Moreover, microglia from CNS regions in which neuronal damage predominates in neurodegenerative disease do not generally express more pro-inflammatory genes than microglia from regions less frequently affected. This study provides an in-depth assessment of regional-, sex- and age-dependent differences in key microglial transcripts from the healthy mouse CNS.
{"title":"Microglial P2 Purinergic Receptor and Immunomodulatory Gene Transcripts Vary By Region, Sex, and Age in the Healthy Mouse CNS.","authors":"J. Crain, J. Watters","doi":"10.4172/2329-8936.1000124","DOIUrl":"https://doi.org/10.4172/2329-8936.1000124","url":null,"abstract":"Inflammatory damage in many neurodegenerative diseases is restricted to certain regions of the CNS, and while microglia have long been implicated in the pathology of many of these disorders, information comparing their gene expression in different CNS regions is lacking. Here we tested the hypothesis that the expression of purinergic receptors, estrogen receptors and other neuroprotective and pro-inflammatory genes differed among CNS regions in healthy mice. Because neurodegenerative diseases vary in incidence by sex and age, we also examined the regional distribution of these genes in male and female mice of four different ages between 21 days and 12 months. We postulated that pro-inflammatory gene expression would be higher in older animals, and lower in young adult females. We found that microglial gene expression differed across the CNS. Estrogen receptor alpha (Esr1) mRNA levels were often lower in microglia from the brainstem/spinal cord than from the cortex, whereas tumor necrosis factor alpha (Tnfα) expression was several times higher. In addition, the regional pattern of gene expression often changed with animal age; for example, no regional differences in P2X7 mRNA levels were detected in 21 day-old animals, but at 7 weeks and older, expression was highest in cerebellar microglia. Lastly, the expression of some genes was sexually dimorphic. In microglia from 12 month-old animals, mRNA levels of inducible nitric oxide synthase, but not Tnfα, were higher in females than males. These data suggest that microglial gene expression is not uniformly more pro-inflammatory in males or older animals. Moreover, microglia from CNS regions in which neuronal damage predominates in neurodegenerative disease do not generally express more pro-inflammatory genes than microglia from regions less frequently affected. This study provides an in-depth assessment of regional-, sex- and age-dependent differences in key microglial transcripts from the healthy mouse CNS.","PeriodicalId":90374,"journal":{"name":"Transcriptomics: open access","volume":"103 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79525081","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}
Pub Date : 2015-01-01Epub Date: 2015-01-31DOI: 10.4172/2329-8936.1000e108
Jing Hao, Wenge Zhu
Maintenance of genomic stability is critical for living organisms because it is crucial for cell survival and development, and it prevents the development of deleterious mutations. Overriding this control will cause genomic instability, a hallmark of cancer. The genome is highly vulnerable to damage, especially during DNA replication because chromosome is decondensed and the replication forks are extremely sensitive to DNA damage agents. The eukaryotic replisome, which consists of a large number of replication fork-associated proteins, is essential for the elongation of replication forks during DNA replication. This complex contains DNA polymerases, MCM helicase, single stranded DNA (ssDNA) binding protein RPA, sliding clamp PCNA, Tipin, Timeless, Claspin, And-1, etc. In cells with DNA damage such as replication stress, replication forks are stalled Figure 1. At stalled replication forks, some of replisome components switch their role from facilitating DNA synthesis to inducing activation of DNA replication checkpoint, a signaling transduction pathway that is critical to maintain fork stability and triggers cell cycle arrest.
{"title":"Maintain Genomic Stability: Multitask of DNA Replication Proteins.","authors":"Jing Hao, Wenge Zhu","doi":"10.4172/2329-8936.1000e108","DOIUrl":"https://doi.org/10.4172/2329-8936.1000e108","url":null,"abstract":"Maintenance of genomic stability is critical for living organisms because it is crucial for cell survival and development, and it prevents the development of deleterious mutations. Overriding this control will cause genomic instability, a hallmark of cancer. \u0000 \u0000The genome is highly vulnerable to damage, especially during DNA replication because chromosome is decondensed and the replication forks are extremely sensitive to DNA damage agents. The eukaryotic replisome, which consists of a large number of replication fork-associated proteins, is essential for the elongation of replication forks during DNA replication. This complex contains DNA polymerases, MCM helicase, single stranded DNA (ssDNA) binding protein RPA, sliding clamp PCNA, Tipin, Timeless, Claspin, And-1, etc. In cells with DNA damage such as replication stress, replication forks are stalled Figure 1. At stalled replication forks, some of replisome components switch their role from facilitating DNA synthesis to inducing activation of DNA replication checkpoint, a signaling transduction pathway that is critical to maintain fork stability and triggers cell cycle arrest.","PeriodicalId":90374,"journal":{"name":"Transcriptomics: open access","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2329-8936.1000e108","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35915668","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}
Pub Date : 2013-06-19DOI: 10.4172/2329-8936.1000101
Ahsan Huda, Pierre R Bushel
Background: Transposable Elements (TEs) have long been regarded as selfish or junk DNA having little or no role in the regulation or functioning of the human genome. However, over the past several years this view came to be challenged as several studies provided anecdotal as well as global evidence for the contribution of TEs to the regulatory and coding needs of human genes. In this study, we explored the incorporation and epigenetic regulation of coding sequences donated by TEs using gene expression and other ancillary genomics data from two human hematopoietic cell-lines: GM12878 (a lymphoblastoid cell line) and K562 (a Chronic Myelogenous Leukemia cell line). In each cell line, we found several thousand instances of TEs donating coding sequences to human genes. We compared the transcriptome assembly of the RNA sequencing (RNA-Seq) reads with and without the aid of a reference transcriptome and found that the percentage of genes that incorporate TEs in their coding sequences is significantly greater than that obtained from the reference transcriptome assemblies using Refseq and Gencode gene models. We also used histone modifications chromatin immunoprecipitation sequencing (ChIP-Seq) data, Cap Analysis of Gene Expression (CAGE) data and DNAseI Hypersensitivity Site (DHS) data to demonstrate the epigenetic regulation of the TE derived coding sequences. Our results suggest that TEs form a significantly higher percentage of coding sequences than represented in gene annotation databases and these TE derived sequences are epigenetically regulated in accordance with their expression in the two cell types.
{"title":"Widespread Exonization of Transposable Elements in Human Coding Sequences is Associated with Epigenetic Regulation of Transcription.","authors":"Ahsan Huda, Pierre R Bushel","doi":"10.4172/2329-8936.1000101","DOIUrl":"https://doi.org/10.4172/2329-8936.1000101","url":null,"abstract":"<p><strong>Background: </strong>Transposable Elements (TEs) have long been regarded as selfish or junk DNA having little or no role in the regulation or functioning of the human genome. However, over the past several years this view came to be challenged as several studies provided anecdotal as well as global evidence for the contribution of TEs to the regulatory and coding needs of human genes. In this study, we explored the incorporation and epigenetic regulation of coding sequences donated by TEs using gene expression and other ancillary genomics data from two human hematopoietic cell-lines: GM12878 (a lymphoblastoid cell line) and K562 (a Chronic Myelogenous Leukemia cell line). In each cell line, we found several thousand instances of TEs donating coding sequences to human genes. We compared the transcriptome assembly of the RNA sequencing (RNA-Seq) reads with and without the aid of a reference transcriptome and found that the percentage of genes that incorporate TEs in their coding sequences is significantly greater than that obtained from the reference transcriptome assemblies using Refseq and Gencode gene models. We also used histone modifications chromatin immunoprecipitation sequencing (ChIP-Seq) data, Cap Analysis of Gene Expression (CAGE) data and DNAseI Hypersensitivity Site (DHS) data to demonstrate the epigenetic regulation of the TE derived coding sequences. Our results suggest that TEs form a significantly higher percentage of coding sequences than represented in gene annotation databases and these TE derived sequences are epigenetically regulated in accordance with their expression in the two cell types.</p>","PeriodicalId":90374,"journal":{"name":"Transcriptomics: open access","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2013-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4028971/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32369654","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}
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