Search

Your search keyword '"Ellerson, Debra"' showing total 25 results
Start Over Author "Ellerson, Debra"
25 results on '"Ellerson, Debra"'

10. The molecular mechanism of induction of unfolded protein response by Chlamydia

Author

George, Zenas, primary, Omosun, Yusuf, additional, Azenabor, Anthony A., additional, Goldstein, Jason, additional, Partin, James, additional, Joseph, Kahaliah, additional, Ellerson, Debra, additional, He, Qing, additional, Eko, Francis, additional, McDonald, Melissa A., additional, Reed, Matthew, additional, Svoboda, Pavel, additional, Stuchlik, Olga, additional, Pohl, Jan, additional, Lutter, Erika, additional, Bandea, Claudiu, additional, Black, Carolyn M., additional, and Igietseme, Joseph U., additional

Published
2019
Full Text
View/download PDF

11. Molecular Pathogenesis of Chlamydia Disease Complications: Epithelial-Mesenchymal Transition and Fibrosis

Author

Igietseme, Joseph U., primary, Omosun, Yusuf, additional, Nagy, Tamas, additional, Stuchlik, Olga, additional, Reed, Matthew S., additional, He, Qing, additional, Partin, James, additional, Joseph, Kahaliah, additional, Ellerson, Debra, additional, George, Zenas, additional, Goldstein, Jason, additional, Eko, Francis O., additional, Bandea, Claudiu, additional, Pohl, Jan, additional, and Black, Carolyn M., additional

Published
2018
Full Text
View/download PDF

12. The roles of unfolded protein response pathways in Chlamydia pathogenesis

Author

George, Zenas, primary, Omosun, Yusuf, additional, Azenabor, Anthony A., additional, Partin, James, additional, Joseph, Kahaliah, additional, Ellerson, Debra, additional, He, Qing, additional, Eko, Francis, additional, Bandea, Claudiu, additional, Svoboda, Pavel, additional, Pohl, Jan, additional, Black, Carolyn M., additional, and Igietseme, Joseph U., additional

Published
2016
Full Text
View/download PDF

13. Role of Epithelial-Mesenchyme Transition in Chlamydia Pathogenesis

Author

Igietseme, Joseph U., primary, Omosun, Yusuf, additional, Stuchlik, Olga, additional, Reed, Matthew S., additional, Partin, James, additional, He, Qing, additional, Joseph, Kahaliah, additional, Ellerson, Debra, additional, Bollweg, Brigid, additional, George, Zenas, additional, Eko, Francis O., additional, Bandea, Claudiu, additional, Liu, Hsi, additional, Yang, Genyan, additional, Shieh, Wun-Ju, additional, Pohl, Jan, additional, Karem, Kevin, additional, and Black, Carolyn M., additional

Published
2015
Full Text
View/download PDF

16. Use of Retroviral Markers to Identify Efficacy of Purging and Origin of Relapse Following Autologous Bone Marrow and Peripheral Blood Cell Transplantation in Indolent B Cell Neoplasms (Follicular Non-Hodgkin's Lymphoma or Chronic Lymphocytic Leukemia (CLL) Patients). The University of Texas M.D. Anderson Cancer Center

Author

Deisseroth, Albert, primary, Kantarjian, Hagop, additional, Champlin, Richard, additional, Cabanillas, Fernando, additional, Keating, Michael, additional, Reading, Chris, additional, Andersson, Borje, additional, Claxton, David, additional, Robertson, Bud, additional, Escudier, Susan, additional, Andreeff, Michael, additional, O'Brien, Susan, additional, Kornblau, Steven, additional, Ellerson, Debra, additional, Hanania, Elie, additional, and Fu, Siqing, additional

Published
1993
Full Text
View/download PDF

17. Use of Cell-Free Retroviral Vector Preparations for Transduction of Cells from the Marrow of Chronic Phase and Blast Crisis Chronic Myelogenous Leukemia Patients and from Normal Individuals

Author

Etkin, Marc, primary, Filaccio, Marylynne, additional, Ellerson, Debra, additional, Suh, Soon-Pal, additional, Claxton, David, additional, Gaozza, Eugenia, additional, Brenner, Malcolm, additional, Moen, Robert, additional, Belmont, John, additional, Moore, Kateri A., additional, Moseley, A. M., additional, Reading, Christopher, additional, Khouri, Issa, additional, Talpaz, Moshe, additional, Kantarjian, Hagop, additional, and Deisseroth, Albert, additional

Published
1992
Full Text
View/download PDF

18. New Directions in the Biology and Therapy of Chronic Myeloid Leukemia

Author

Deisseroth, Albert B., primary, Zhang, Wei, additional, Cha, Ying, additional, Yuan, Tianying, additional, Chen, Hanchun, additional, Sims, Simon, additional, Wedrychowski, Andrzej, additional, Gao, Pei-Qing, additional, Huston, Laurel, additional, Filaccio, Marylynne, additional, Claxton, David, additional, Kornblau, Steven, additional, Johnson, Elizabeth, additional, Zack Howard, O. M., additional, Andersson, Borje, additional, Giglio, Auro Del, additional, Gressot, Laurent, additional, Kantarjian, Hagop, additional, Talpaz, Moshe, additional, Khouri, Issa, additional, Champlin, Richard, additional, Andreeff, Michael, additional, Gaozza, Eugenia, additional, Seong, David, additional, Suh, Soon-Pal, additional, Ellerson, Debra, additional, Hu, Guiying, additional, and Chou, Marian, additional

Published
1992
Full Text
View/download PDF

19. Molecular Analysis of Retroviral Transduction in Chronic Myelogenous Leukemia

Author

Claxton, David, primary, Suh, Soon-Pal, additional, Filaccio, Marylynńe, additional, Ellerson, Debra, additional, Gaozza, Eugenia, additional, Andersson, Borje, additional, Brenner, Malcolm, additional, Reading, Christopher, additional, Feinberg, Andrew, additional, Moen, Robert, additional, Belmont, John, additional, Moore, Kateri, additional, Talpaz, Moshe, additional, Kantarjian, Hagop, additional, and Deisseroth, Albert, additional

Published
1991
Full Text
View/download PDF

20. Epidermal Growth Factor Receptor and Transforming Growth Factor ß Signaling Pathways Cooperate To Mediate ChlamydiaPathogenesis

Author

Igietseme, Joseph U., Partin, James, George, Zenas, Omosun, Yusuf, Goldstein, Jason, Joseph, Kahaliah, Ellerson, Debra, Eko, Francis O., Pohl, Jan, Bandea, Claudiu, and Black, Carolyn M.

Abstract

Human genital Chlamydiainfection is a major public health concern due to the serious reproductive system complications. Chlamydiabinds several receptor tyrosine kinases (RTKs) on host cells, including the epidermal growth factor receptor (EGFR), and activates cellular signaling cascades for host invasion, cytoskeletal remodeling, optimal inclusion development, and induction of pathogenic epithelial-mesenchyme transition (EMT). Chlamydiaalso upregulates transforming growth factor beta (TGF-ß) expression, whose signaling pathway synergizes with the EGFR cascade, but its role in infectivity, inclusions, and EMT induction is unknown.

Published
2020
Full Text
View/download PDF

21. Additional file 1: of A unique insight into the MiRNA profile during genital chlamydial infection

Author

Ifeyinwa Benyeogor, Tankya Simoneaux, Yuehao Wu, Lundy, Stephanie, Zenas George, Khamia Ryans, McKeithen, Danielle, Pais, Roshan, Ellerson, Debra, W. Lorenz, Tolulope Omosun, Thompson, Winston, Eko, Francis, Black, Carolyn, Blas-Machado, Uriel, Igietseme, Joseph, He, Qing, and Omosun, Yusuf

Subjects
3. Good health
Abstract

Figure S1. Venn diagram of differentially expressed miRNAs after chlamydia infection. Figure S2. Venn diagram of differentially expressed miRNAs after chlamydia reinfection. Figure S3. Pathways predicted to be regulated by miRNAs differentially expressed in mice after chlamydia infection. Figure S4. Pathways predicted to be regulated by miRNAs differentially expressed in mice after chlamydia reinfection. Figure S5. A: Network One for Chlamydia infection shows CEBPA a transcription regulator as the focus molecule with associated miRNAs. B: Network Two for Chlam ydia infection shows CREB1 a transcription regulator as the focus molecule with associated miRNAs. C: Network One for Chlamydia reinfection shows RHOA, an enzyme, as the focus molecule with associated miRNAs and other molecules D: Network Two for Chlamydia reinfection shows mir-423-5p as the focus molecule with associated miRNAs and other molecules. E: Network Three for Chlamydia reinfection shows TNFSF10 as the focus molecule with associated miRNAs and other molecules. F: Network Four for Chlamydia reinfection shows the kinase SRC as the focus molecule with associated miRNAs and other molecules. G: Network Five for Chlamydia reinfection shows the transporter BCL2 as the focus molecule with associated miRNAs and other molecules. Table S1. Summary Analysis of Top Diseases and Biological Functions of miRNA expressed in the Chlamydia Infection and Re-Infection. Table S2. Networks for the Top Diseases and Biological Function Category of miRNA expressed in the Chlamydia Reinfection. Figure S6. Example of quality scoring for miRNA sequencing in this study. Figure S7. (A) Validation of miRNA 378b expression after single infection using qPCR, (B) Validation of miRNA 142-5p expression after single infection using qPCR. Figure S8. Comprehensive Analysis Pipeline for miRNA-seq data (CAP-miRSeq), adapted from Sun et al., 2014 [35]. (PDF 1710 kb)

22. Additional file 1: of A unique insight into the MiRNA profile during genital chlamydial infection

Author

Ifeyinwa Benyeogor, Tankya Simoneaux, Yuehao Wu, Lundy, Stephanie, Zenas George, Khamia Ryans, McKeithen, Danielle, Pais, Roshan, Ellerson, Debra, W. Lorenz, Tolulope Omosun, Thompson, Winston, Eko, Francis, Black, Carolyn, Blas-Machado, Uriel, Igietseme, Joseph, He, Qing, and Omosun, Yusuf

Subjects
3. Good health
Abstract

Figure S1. Venn diagram of differentially expressed miRNAs after chlamydia infection. Figure S2. Venn diagram of differentially expressed miRNAs after chlamydia reinfection. Figure S3. Pathways predicted to be regulated by miRNAs differentially expressed in mice after chlamydia infection. Figure S4. Pathways predicted to be regulated by miRNAs differentially expressed in mice after chlamydia reinfection. Figure S5. A: Network One for Chlamydia infection shows CEBPA a transcription regulator as the focus molecule with associated miRNAs. B: Network Two for Chlam ydia infection shows CREB1 a transcription regulator as the focus molecule with associated miRNAs. C: Network One for Chlamydia reinfection shows RHOA, an enzyme, as the focus molecule with associated miRNAs and other molecules D: Network Two for Chlamydia reinfection shows mir-423-5p as the focus molecule with associated miRNAs and other molecules. E: Network Three for Chlamydia reinfection shows TNFSF10 as the focus molecule with associated miRNAs and other molecules. F: Network Four for Chlamydia reinfection shows the kinase SRC as the focus molecule with associated miRNAs and other molecules. G: Network Five for Chlamydia reinfection shows the transporter BCL2 as the focus molecule with associated miRNAs and other molecules. Table S1. Summary Analysis of Top Diseases and Biological Functions of miRNA expressed in the Chlamydia Infection and Re-Infection. Table S2. Networks for the Top Diseases and Biological Function Category of miRNA expressed in the Chlamydia Reinfection. Figure S6. Example of quality scoring for miRNA sequencing in this study. Figure S7. (A) Validation of miRNA 378b expression after single infection using qPCR, (B) Validation of miRNA 142-5p expression after single infection using qPCR. Figure S8. Comprehensive Analysis Pipeline for miRNA-seq data (CAP-miRSeq), adapted from Sun et al., 2014 [35]. (PDF 1710 kb)

23. Molecular Pathogenesis of ChlamydiaDisease Complications: Epithelial-Mesenchymal Transition and Fibrosis

Author

Igietseme, Joseph U., Omosun, Yusuf, Nagy, Tamas, Stuchlik, Olga, Reed, Matthew S., He, Qing, Partin, James, Joseph, Kahaliah, Ellerson, Debra, George, Zenas, Goldstein, Jason, Eko, Francis O., Bandea, Claudiu, Pohl, Jan, and Black, Carolyn M.

Abstract

ABSTRACTThe reproductive system complications of genital chlamydial infection include fallopian tube fibrosis and tubal factor infertility. However, the molecular pathogenesis of these complications remains poorly understood. The induction of pathogenic epithelial-mesenchymal transition (EMT) through microRNA (miRNA) dysregulation was recently proposed as the pathogenic basis of chlamydial complications. Focusing on fibrogenesis, we investigated the hypothesis that chlamydia-induced fibrosis is caused by EMT-driven generation of myofibroblasts, the effector cells of fibrosis that produce excessive extracellular matrix (ECM) proteins. The results revealed that the targets of a major category of altered miRNAs during chlamydial infection are key components of the pathophysiological process of fibrogenesis; these target molecules include collagen types I, III, and IV, transforming growth factor β (TGF-β), TGF-β receptor 1 (TGF-βR1), connective tissue growth factor (CTGF), E-cadherin, SRY-box 7 (SOX7), and NFAT (nuclear factor of activated T cells) kinase dual-specificity tyrosine (Y) phosphorylation-regulated kinase 1a (Dyrk1a). Chlamydial induction of EMT resulted in the generation of α-smooth muscle actin (α-SMA)-positive myofibroblasts that produced ECM proteins, including collagen types I and III and fibronectin. Furthermore, the inhibition of EMT prevented the generation of myofibroblasts and production of ECM proteins during chlamydial infection. These findings may provide useful avenues for targeting EMT or specific components of the EMT pathways as a therapeutic intervention strategy to prevent chlamydia-related complications.

Published
2017
Full Text
View/download PDF

24. Genetic Marking Shows That Ph+ Cells Present in Autologous Transplants of Chronic Myelogenous Leukemia (CML) Contribute to Relapse After Autologous Bone Marrow in CML

Author

Deisseroth, Albert B., Zu, Zhifei, Claxton, David, Hanania, Elie G., Fu, Siqing, Ellerson, Debra, Goldberg, Leah, Thomas, Michael, Janicek, Karen, Anderson, W. French, Hester, Jeane, Korbling, Martin, Durett, April, Moen, Robert, Berenson, Ronald, Heimfeld, Shelly, Hamer, Joy, Calvert, Leslie, Tibbits, Patricia, Talpaz, Moshe, Kantarjian, Hagop, Champlin, Richard, and Reading, Christopher

Published
1994
Full Text
View/download PDF

25. Molecular Pathogenesis of Chlamydia Disease Complications: Epithelial-Mesenchymal Transition and Fibrosis.

Author

Igietseme JU, Omosun Y, Nagy T, Stuchlik O, Reed MS, He Q, Partin J, Joseph K, Ellerson D, George Z, Goldstein J, Eko FO, Bandea C, Pohl J, and Black CM

Subjects
Actins metabolism, Animals, Cadherins metabolism, Cell Line, Chlamydia Infections microbiology, Collagen metabolism, Connective Tissue Growth Factor metabolism, Extracellular Matrix Proteins metabolism, Fibronectins metabolism, Fibrosis microbiology, Mice, MicroRNAs metabolism, Myofibroblasts microbiology, Myofibroblasts pathology, NFATC Transcription Factors metabolism, Protein Serine-Threonine Kinases metabolism, Protein-Tyrosine Kinases metabolism, Receptor, Transforming Growth Factor-beta Type I, Receptors, Transforming Growth Factor beta metabolism, SOXF Transcription Factors metabolism, Transforming Growth Factor beta metabolism, Chlamydia pathogenicity, Chlamydia Infections complications, Chlamydia Infections pathology, Epithelial-Mesenchymal Transition physiology, Fibrosis etiology, Fibrosis pathology
Abstract

The reproductive system complications of genital chlamydial infection include fallopian tube fibrosis and tubal factor infertility. However, the molecular pathogenesis of these complications remains poorly understood. The induction of pathogenic epithelial-mesenchymal transition (EMT) through microRNA (miRNA) dysregulation was recently proposed as the pathogenic basis of chlamydial complications. Focusing on fibrogenesis, we investigated the hypothesis that chlamydia-induced fibrosis is caused by EMT-driven generation of myofibroblasts, the effector cells of fibrosis that produce excessive extracellular matrix (ECM) proteins. The results revealed that the targets of a major category of altered miRNAs during chlamydial infection are key components of the pathophysiological process of fibrogenesis; these target molecules include collagen types I, III, and IV, transforming growth factor β (TGF-β), TGF-β receptor 1 (TGF-βR1), connective tissue growth factor (CTGF), E-cadherin, SRY-box 7 (SOX7), and NFAT (nuclear factor of activated T cells) kinase dual-specificity tyrosine (Y) phosphorylation-regulated kinase 1a (Dyrk1a). Chlamydial induction of EMT resulted in the generation of α-smooth muscle actin (α-SMA)-positive myofibroblasts that produced ECM proteins, including collagen types I and III and fibronectin. Furthermore, the inhibition of EMT prevented the generation of myofibroblasts and production of ECM proteins during chlamydial infection. These findings may provide useful avenues for targeting EMT or specific components of the EMT pathways as a therapeutic intervention strategy to prevent chlamydia-related complications., (Copyright © 2017 American Society for Microbiology.)

Published
2017
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results