Search

Your search keyword '"Wren, J. D."' showing total 23 results
Start Over Author "Wren, J. D."
23 results on '"Wren, J. D."'

4. The long noncoding RNA neuroLNC regulates presynaptic activity by interacting with the neurodegeneration-associated protein TDP-43

Author

Keihani, S., primary, Kluever, V., additional, Mandad, S., additional, Bansal, V., additional, Rahman, R., additional, Fritsch, E., additional, Gomes, L. Caldi, additional, Gärtner, A., additional, Kügler, S., additional, Urlaub, H., additional, Wren, J. D., additional, Bonn, S., additional, Rizzoli, S. O., additional, and Fornasiero, E. F., additional

Published
2019
Full Text
View/download PDF

6. Activation of the JAK/STAT pathway in Behcet’s disease

Author

Tulunay, A, primary, Dozmorov, M G, additional, Ture-Ozdemir, F, additional, Yilmaz, V, additional, Eksioglu-Demiralp, E, additional, Alibaz-Oner, F, additional, Ozen, G, additional, Wren, J D, additional, Saruhan-Direskeneli, G, additional, Sawalha, A H, additional, and Direskeneli, H, additional

Published
2014
Full Text
View/download PDF

8. Aging Exacerbates Obesity-induced Cerebromicrovascular Rarefaction, Neurovascular Uncoupling, and Cognitive Decline in Mice

Author

Tucsek, Z., primary, Toth, P., additional, Tarantini, S., additional, Sosnowska, D., additional, Gautam, T., additional, Warrington, J. P., additional, Giles, C. B., additional, Wren, J. D., additional, Koller, A., additional, Ballabh, P., additional, Sonntag, W. E., additional, Ungvari, Z., additional, and Csiszar, A., additional

Published
2014
Full Text
View/download PDF

19. Identification of susceptibility loci for Takayasu arteritis through a large multi-ancestral genome-wide association study

Author

Sharon A. Chung, Gökhan Keser, Ayten Yazici, Zeynep Ozbalkan, R. Maughan, Servet Akar, Fatma Alibaz-Oner, Nurullah Akkoc, Kathleen McKinnon-Maksimowicz, Patrick Coit, Güher Saruhan-Direskeneli, Chris Wallace, Omer Karadag, Muge Bicakcigil, Antoine G. Sreih, Ahmet Mesut Onat, Paul A. Monach, Ying Sun, Kenan Aksu, Carol A. Langford, Mehmet Akif Ozturk, Izzet Fresko, Eren Erken, Lindsay Lally, Lindsy J. Forbess, Christian Pagnoux, Ayse Cefle, Ediz Dalkilic, Timothy J. Vyse, Veli Cobankara, Peter C. Grayson, Guillermo Reales, David Cuthbertson, Philip Seo, Gozde Yildirim Cetin, Curry L. Koening, Sibel P. Yentür, Yaşar Karaaslan, Lourdes Ortiz-Fernández, Nilufer Alpay-Kanitez, Bunyamin Kisacik, Xiufang Kong, Sibel Zehra Aydin, Enrico Tombetti, Sule Yavuz, Lindi Jiang, Fatos Onen, Allan P. Kiprianos, Nurşen Düzgün, Nader Khalidi, Justin C. Mason, Huiyong Chen, Aşkın Ateş, Angelo A. Manfredi, Murat Inanc, Sevil Kamali, Sema Kaymaz-Tahra, Steven R. Ytterberg, Timuçin Kaşifoğlu, Emire Seyahi, Elena Baldissera, Deborah S. Cunninghame-Graham, Sedat Kiraz, Jason M. Springer, Peter A. Merkel, Haner Direskeneli, Jonathan D. Wren, Kenneth J. Warrington, Carol A. McAlear, Amr H. Sawalha, Huseyin T. E. Ozer, Wallace, Chris [0000-0001-9755-1703], Apollo - University of Cambridge Repository, Ortiz-Fernandez, Lourdes, Saruhan-Direskeneli, Guher, Alibaz-Oner, Fatma, Kaymaz-Tahra, Sema, Coit, Patrick, Kong, Xiufang, Kiprianos, Allan P., Maughan, Robert T., Aydin, Sibel Z., Aksu, Kenan, Keser, Gokhan, Kamali, Sevil, Inanc, Murat, Springer, Jason, Akar, Servet, Onen, Fatos, Akkoc, Nurullah, Khalidi, Nader A., Koening, Curry, Karadag, Omer, Kiraz, Sedat, Forbess, Lindsy, Langford, Carol A., McAlear, Carol A., Ozbalkan, Zeynep, Yavuz, Sule, Cetin, Gozde Yildirim, Alpay-Kanitez, Nilufer, Chung, Sharon, Ates, Askin, Karaaslan, Yasar, McKinnon-Maksimowicz, Kathleen, Monach, Paul A., Ozer, Huseyin T. E., Seyahi, Emire, Fresko, Izzet, Cefle, Ayse, Seo, Philip, Warrington, Kenneth J., Ozturk, Mehmet A., Ytterberg, Steven R., Cobankara, Veli, Onat, Ahmet Mesut, Duzgun, Nursen, Bicakcigil, Muge, Yentur, Sibel P., Lally, Lindsay, Manfredi, Angelo A., Baldissera, Elena, Erken, Eren, Yazici, Ayten, Kisacik, Bunyamin, Kasifoglu, Timucin, Dalkilic, Ediz, Cuthbertson, David, Pagnoux, Christian, Sreih, Antoine, Reales, Guillermo, Wallace, Chris, Wren, Jonathan D., Cunninghame-Graham, Deborah S., Vyse, Timothy J., Sun, Ying, Chen, Huiyong, Grayson, Peter C., Tombetti, Enrico, Jiang, Lindi, Mason, Justin C., Merkel, Peter A., Direskeneli, Haner, Sawalha, Amr H., Ortiz-Fernandez, L., Saruhan-Direskeneli, G., Alibaz-Oner, F., Kaymaz-Tahra, S., Coit, P., Kong, X., Kiprianos, A. P., Maughan, R. T., Aydin, S. Z., Aksu, K., Keser, G., Kamali, S., Inanc, M., Springer, J., Akar, S., Onen, F., Akkoc, N., Khalidi, N. A., Koening, C., Karadag, O., Kiraz, S., Forbess, L., Langford, C. A., Mcalear, C. A., Ozbalkan, Z., Yavuz, S., Cetin, G. Y., Alpay-Kanitez, N., Chung, S., Ates, A., Karaaslan, Y., McKinnon-Maksimowicz, K., Monach, P. A., Ozer, H. T. E., Seyahi, E., Fresko, I., Cefle, A., Seo, P., Warrington, K. J., Ozturk, M. A., Ytterberg, S. R., Cobankara, V., Onat, A. M., Duzgun, N., Bicakcigil, M., Yentur, S. P., Lally, L., Manfredi, A. A., Baldissera, E., Erken, E., Yazici, A., Kisacik, B., Kasifoglu, T., Dalkilic, E., Cuthbertson, D., Pagnoux, C., Sreih, A., Reales, G., Wallace, C., Wren, J. D., Cunninghame-Graham, D. S., Vyse, T. J., Sun, Y., Chen, H., Grayson, P. C., Tombetti, E., Jiang, L., Mason, J. C., Merkel, P. A., Direskeneli, H., Sawalha, A. H., Ege Üniversitesi, [Belirlenecek], Imperial College Healthcare NHS Trust- BRC Funding, and İç Hastalıkları

Subjects
Male, 0301 basic medicine, genetic association, PROTEIN, Integrin, Genome-wide association study, Disease, DISEASE, vasculitis, Genetic Risk, ACTIVATION, 0302 clinical medicine, LEFLUNOMIDE, Polymorphism (computer science), CRITERIA, GWAS, skin and connective tissue diseases, 11 Medical and Health Sciences, Genetics (clinical), Genetics & Heredity, Genetics, PSORIASIS, genetic risk scroe, Classification, HLA, Polydom, Female, Vasculitis, Leflunomide, epigenetic, vasculitis genetic association, POLYDOM, Activation, GENETIC RISK, Human leukocyte antigen, Biology, eQTL, Polymorphism, Single Nucleotide, Article, CLASSIFICATION, 03 medical and health sciences, medicine, Psoriasis, Humans, Genetic Predisposition to Disease, cardiovascular diseases, Tıp uygulaması, Genetic association, 030203 arthritis & rheumatology, Protein, [No Keywords], Case-control study, 06 Biological Sciences, Inflammatory Bowel Diseases, medicine.disease, Criteria, Takayasu Arteritis, 030104 developmental biology, [No Keyword], Case-Control Studies, Expression quantitative trait loci, chromatin interaction, INTEGRIN, Genome-Wide Association Study
Abstract

Takayasu arteritis is a rare inflammatory disease of large arteries. We performed a genetic study in Takayasu arteritis comprising 6,670 individuals (1,226 affected individuals) from five different populations. We discovered HLA risk factors and four non-HLA susceptibility loci in VPS8, SVEP1, CFL2, and chr13q21 and reinforced IL12B, PTK2B, and chr21q22 as robust susceptibility loci shared across ancestries. Functional analysis proposed plausible underlying disease mechanisms and pinpointed ETS2 as a potential causal gene for chr21q22 association. We also identified >60 candidate loci with suggestive association (p < 5 x 10(-s)) and devised a genetic risk score for Takayasu arteritis. Takayasu arteritis was compared to hundreds of other traits, revealing the closest genetic relatedness to inflammatory bowel disease. Epigenetic patterns within risk loci suggest roles for monocytes and B cells in Takayasu arteritis. This work enhances understanding of the genetic basis and pathophysiology of Takayasu arteritis and provides clues for potential new therapeutic targets., National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of HealthUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Arthritis & Musculoskeletal & Skin Diseases (NIAMS) [R01 AR070148]; National Institute of Arthritis and Musculoskeletal and Skin DiseasesUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Arthritis & Musculoskeletal & Skin Diseases (NIAMS) [U54 AR057319, U01 AR51874 04]; National Center for Research ResourcesUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Center for Research Resources (NCRR) [U54 RR019497]; Office of Rare Diseases Research of the National Center for Advancing Translational Sciences; Imperial College, National Institute for Health Research, Biomedical Research Centre; Wellcome TrustWellcome TrustEuropean Commission [WT107881]; Medical Research CouncilUK Research & Innovation (UKRI)Medical Research Council UK (MRC)European Commission [MC_UU_00002/4], This work was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health grant R01 AR070148 to A.H.S. The Vasculitis Clinical Research Consortium has received support from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (U54 AR057319 and U01 AR51874 04), the National Center for Research Resources (U54 RR019497), and the Office of Rare Diseases Research of the National Center for Advancing Translational Sciences. J.C.M., A.P.K., and R.M.M. acknowledge support from the Imperial College, National Institute for Health Research, Biomedical Research Centre. C.W. and G.R. acknowledge support from The Wellcome Trust (WT107881) and the Medical Research Council (MC_UU_00002/4). This work was supported by the use of study data downloaded from the dbGaP website, under dbGaP: phs000272.v1.p1, phs000431.v2.p1, phs000583.v1.p1, and phs000444.v1.p1.

Published
2021

20. Activation of the JAK/STAT pathway in Behcet's disease

Author

Gulsen Ozen, Amr H. Sawalha, Filiz Ture-Ozdemir, Jonathan D. Wren, Haner Direskeneli, Fatma Alibaz-Oner, Emel Eksioglu-Demiralp, Mikhail G. Dozmorov, Vuslat Yilmaz, Güher Saruhan-Direskeneli, Aysin Tulunay, Tulunay, A., Dozmorov, M. G., Ture-Ozdemir, F., Yilmaz, V., Eksioglu-Demiralp, E., Alibaz-Oner, F., Ozen, G., Wren, J. D., Saruhan-Direskeneli, G., Sawalha, A. H., and Direskeneli, H.

Subjects
Adult, CD4-Positive T-Lymphocytes, Male, STAT3 Transcription Factor, INVOLVEMENT, CD14, Immunology, Lipopolysaccharide Receptors, Biology, SUSCEPTIBILITY, HAN CHINESE, Peripheral blood mononuclear cell, Article, Stat3 Signaling Pathway, MECHANISMS, Interferon, GENETIC-VARIANTS, Genetics, medicine, Humans, REGULATORY T-CELLS, TRANSCRIPTION, STAT3, TH1 CELLS, Genetics (clinical), Behcet Syndrome, Gene Expression Profiling, Interleukins, Interleukin, JAK-STAT signaling pathway, Janus Kinase 1, ASSOCIATION, STAT protein, Cancer research, biology.protein, Female, SIGNALING PATHWAY, Genome-Wide Association Study, Signal Transduction, medicine.drug
Abstract

Th1/Th17-type T-cell responses are upregulated in Behcet's disease (BD). However, signaling pathways associated with this aberrant immune response are not clarified. Whole-genome microarray profiling was performed with human U133 (Plus 2.0) chips using messenger RNA of isolated CD14(+) monocytes and CD4(+) T cells from peripheral blood mononucleated cell (PBMC) in patients with BD (n = 9) and healthy controls (HCs) (n = 9). Flow cytometric analysis of unstimulated (US) and stimulated (phytohaemagglutinin) signal transducer and activator of transcription (STAT3) and pSTAT3 expressions of PBMCs were also analyzed (BD and HC, both n = 26). Janus family of kinase (JAK1) was observed to be upregulated in both CD14(+) monocytes (1.95-fold) and CD4(+) T lymphocytes (1.40-fold) of BD patients. Using canonical pathway enrichment analysis, JAK/STAT signaling was identified as activated in both CD14(+) monocytes (P = 9.55E - 03) and in CD4(+) lymphocytes (P = 8.13E - 04) in BD. Interferon signaling was also prominent among upregulated genes in CD14(+) monocytes (P = 5.62E -05). Glucocorticoid receptor signaling and interleukin (IL-6) signaling were among the most enriched pathways in differentially expressed genes in CD14(+) monocytes (P = 2.45E - 09 and 1.00E - 06, respectively). Basal US total STAT3 expression was significantly higher in BD (1.2 vs 3.45, P < 0.05). The JAK1/STAT3 signaling pathway is activated in BD, possibly through the activation of Th1/Th17-type cytokines such as IL-2, interferon (IFN-gamma), IL-6, IL-17 and IL-23.

Published
2015

21. Prospective evaluation of protein C and factor VIII in prediction of cancer-associated thrombosis.

Author

Tafur AJ, Dale G, Cherry M, Wren JD, Mansfield AS, Comp P, Rathbun S, and Stoner JA

Subjects
Aged, Female, Humans, Male, Middle Aged, Platelet Activation, Proportional Hazards Models, Prospective Studies, Venous Thromboembolism blood, Factor VIII analysis, Neoplasms complications, Protein C analysis, Venous Thromboembolism etiology
Abstract

Venous thromboembolism (VTE) is a preventable disease, yet it is one of the leading causes of death among patients with cancer. Improving risk stratification mechanisms will allow us to personalize thrombo-prophylaxis strategies. We sought to evaluate Collagen and Thrombin Activated Platelets (COAT-platelets) as well as protein C and factor VIII as biomarkers predictive of cancer-associated thrombosis in a prospective cohort of patients with cancer. Protein C was selected as a candidate based on bioinformatics prediction. Blood samples were collected before chemotherapy. All specimen processing was blinded to clinical data. Surveillance and adjudication of the main outcome of VTE was performed for up to 1 year. We used Cox proportional hazard regression to measure the association of biomarkers and incident events using SAS 9.2 for all statistical analysis. Death was modeled as a competing event. Among 241 patients followed for an average of 10.4 months, 15% died and 13% developed a VTE. COAT-platelets were not predictive of VTE. Low levels of pre-chemotherapy protein C (<118%) (HR 2.5; 95% CI 1.1-5.5) and high baseline factor VIII (>261% I) (HR 3.0; 95% CI 1.1-8.0) were predictive of VTE after adjusting for age, Khorana prediction risk, metastatic disease and D dimer. In addition, low protein C was predictive of overall mortality independent of age, metastatic disease and functional status (HR 2.8; 95% CI 1.3-6.0). Addition of these biomarkers to cancer-VTE risk prediction models may add to risk stratification and patient selection to optimize thrombo-prophylaxis., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Published
2015
Full Text
View/download PDF

22. Searching for microsatellite mutations in coding regions in lung, breast, ovarian and colorectal cancers.

Author

Forgacs E, Wren JD, Kamibayashi C, Kondo M, Xu XL, Markowitz S, Tomlinson GE, Muller CY, Gazdar AF, Garner HR, and Minna JD

Subjects
Base Pair Mismatch, Databases, Factual, Female, Humans, Polymorphism, Single-Stranded Conformational, Software, Breast Neoplasms genetics, Colorectal Neoplasms genetics, Lung Neoplasms genetics, Microsatellite Repeats genetics, Mutation, Ovarian Neoplasms genetics
Abstract

RepX represents a new informatics approach to probe the UniGene database for potentially polymorphic repeat sequences in the open reading frame (ORF) of genes, 56% of which were found to be actually polymorphic. We now have performed mutational analysis of 17 such sites in genes not found to be polymorphic (<0.03 frequency) in a large panel of human cancer genomic DNAs derived from 31 lung, 21 breast, seven ovarian, 21 (13 microsatellite instability (MSI)+ and eight MSI-) colorectal cancer cell lines. In the lung, breast and ovarian tumor DNAs we found no mutations (<0.03-0.04 rate of tumor associated open reading frame mutations) in these sequences. By contrast, 18 MSI+ colorectal cancers (13 cancer cell lines and five primary tumors) with mismatch repair defects exhibited six mutations in three of the 17 genes (SREBP-2, TAN-1, GR6) (P<0.000003 compared to all other cancers tested). We conclude that coding region microsatellite alterations are rare in lung, breast, ovarian carcinomas and MSI (-) colorectal cancers, but are relatively frequent in MSI (+) colorectal cancers with mismatch repair deficits.

Published
2001
Full Text
View/download PDF

23. Repeat polymorphisms within gene regions: phenotypic and evolutionary implications.

Author

Wren JD, Forgacs E, Fondon JW 3rd, Pertsemlidis A, Cheng SY, Gallardo T, Williams RS, Shohet RV, Minna JD, and Garner HR

Subjects
Algorithms, Alleles, Genome, Human, Genotype, Humans, Molecular Sequence Data, Phenotype, Sensitivity and Specificity, Software, Evolution, Molecular, Genes, Polymorphism, Genetic genetics, Repetitive Sequences, Amino Acid genetics, Repetitive Sequences, Nucleic Acid genetics
Abstract

We have developed an algorithm that predicted 11,265 potentially polymorphic tandem repeats within transcribed sequences. We estimate that 22% (2,207/9,717) of the annotated clusters within UniGene contain at least one potentially polymorphic locus. Our predictions were tested by allelotyping a panel of approximately 30 individuals for 5% of these regions, confirming polymorphism for more than half the loci tested. Our study indicates that tandem-repeat polymorphisms in genes are more common than is generally believed. Approximately 8% of these loci are within coding sequences and, if polymorphic, would result in frameshifts. Our catalogue of putative polymorphic repeats within transcribed sequences comprises a large set of potentially phenotypic or disease-causing loci. In addition, from the anomalous character of the repetitive sequences within unannotated clusters, we also conclude that the UniGene cluster count substantially overestimates the number of genes in the human genome. We hypothesize that polymorphisms in repeated sequences occur with some baseline distribution, on the basis of repeat homogeneity, size, and sequence composition, and that deviations from that distribution are indicative of the nature of selection pressure at that locus. We find evidence of selective maintenance of the ability of some genes to respond very rapidly, perhaps even on intragenerational timescales, to fluctuating selective pressures.

Published
2000
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results