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73 results on '"Dickins, Ross A."'

51. Combined Targeting of JAK2 and Bcl-2/Bcl-xL to Cure Mutant JAK2-Driven Malignancies and Overcome Acquired Resistance to JAK2 Inhibitors

Author

Waibel, Michaela, primary, Solomon, Vanessa S., additional, Knight, Deborah A., additional, Ralli, Rachael A., additional, Kim, Sang-Kyu, additional, Banks, Kellie-Marie, additional, Vidacs, Eva, additional, Virely, Clemence, additional, Sia, Keith C.S., additional, Bracken, Lauryn S., additional, Collins-Underwood, Racquel, additional, Drenberg, Christina, additional, Ramsey, Laura B., additional, Meyer, Sara C., additional, Takiguchi, Megumi, additional, Dickins, Ross A., additional, Levine, Ross, additional, Ghysdael, Jacques, additional, Dawson, Mark A., additional, Lock, Richard B., additional, Mullighan, Charles G., additional, and Johnstone, Ricky W., additional

Published
2013
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53. The genomic landscape of hypodiploid acute lymphoblastic leukemia

Author

Holmfeldt, Linda, primary, Wei, Lei, additional, Diaz-Flores, Ernesto, additional, Walsh, Michael, additional, Zhang, Jinghui, additional, Ding, Li, additional, Payne-Turner, Debbie, additional, Churchman, Michelle, additional, Andersson, Anna, additional, Chen, Shann-Ching, additional, McCastlain, Kelly, additional, Becksfort, Jared, additional, Ma, Jing, additional, Wu, Gang, additional, Patel, Samir N, additional, Heatley, Susan L, additional, Phillips, Letha A, additional, Song, Guangchun, additional, Easton, John, additional, Parker, Matthew, additional, Chen, Xiang, additional, Rusch, Michael, additional, Boggs, Kristy, additional, Vadodaria, Bhavin, additional, Hedlund, Erin, additional, Drenberg, Christina, additional, Baker, Sharyn, additional, Pei, Deqing, additional, Cheng, Cheng, additional, Huether, Robert, additional, Lu, Charles, additional, Fulton, Robert S, additional, Fulton, Lucinda L, additional, Tabib, Yashodhan, additional, Dooling, David J, additional, Ochoa, Kerri, additional, Minden, Mark, additional, Lewis, Ian D, additional, To, L Bik, additional, Marlton, Paula, additional, Roberts, Andrew W, additional, Raca, Gordana, additional, Stock, Wendy, additional, Neale, Geoffrey, additional, Drexler, Hans G, additional, Dickins, Ross A, additional, Ellison, David W, additional, Shurtleff, Sheila A, additional, Pui, Ching-Hon, additional, Ribeiro, Raul C, additional, Devidas, Meenakshi, additional, Carroll, Andrew J, additional, Heerema, Nyla A, additional, Wood, Brent, additional, Borowitz, Michael J, additional, Gastier-Foster, Julie M, additional, Raimondi, Susana C, additional, Mardis, Elaine R, additional, Wilson, Richard K, additional, Downing, James R, additional, Hunger, Stephen P, additional, Loh, Mignon L, additional, and Mullighan, Charles G, additional

Published
2013
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55. RNAi Screening Identifies A Novel Role for A-Kinase Anchoring Protein 12 (AKAP12) in B Cell Development and Function

Author

Kartal-Kaess, Mutlu, primary, Cimmino, Luisa, additional, Infantino, Simona, additional, Yabas, Mehmet, additional, Zhang, Jian-Guo, additional, Tuohey, Laura, additional, Gelman, Irwin H., additional, Scott, John D., additional, Nutt, Stephen L., additional, Enders, Anselm, additional, Tarlinton, David, additional, and Dickins, Ross A, additional

Published
2012
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57. A pipeline for the generation of shRNA transgenic mice

Author

Dow, Lukas E, primary, Premsrirut, Prem K, additional, Zuber, Johannes, additional, Fellmann, Christof, additional, McJunkin, Katherine, additional, Miething, Cornelius, additional, Park, Youngkyu, additional, Dickins, Ross A, additional, Hannon, Gregory J, additional, and Lowe, Scott W, additional

Published
2012
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59. A Rapid and Scalable System for Studying Gene Function in Mice Using Conditional RNA Interference

Author

Premsrirut, Prem K., primary, Dow, Lukas E., additional, Kim, Sang Yong, additional, Camiolo, Matthew, additional, Malone, Colin D., additional, Miething, Cornelius, additional, Scuoppo, Claudio, additional, Zuber, Johannes, additional, Dickins, Ross A., additional, Kogan, Scott C., additional, Shroyer, Kenneth R., additional, Sordella, Raffaella, additional, Hannon, Gregory J., additional, and Lowe, Scott W., additional

Published
2011
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63. Tissue-specific and reversible RNA interference in transgenic mice

Author

Dickins, Ross A, primary, McJunkin, Katherine, additional, Hernando, Eva, additional, Premsrirut, Prem K, additional, Krizhanovsky, Valery, additional, Burgess, Darren J, additional, Kim, Sang Yong, additional, Cordon-Cardo, Carlos, additional, Zender, Lars, additional, Hannon, Gregory J, additional, and Lowe, Scott W, additional

Published
2007
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67. Generation and Analysis of Siah2 Mutant Mice

Author

Frew, Ian J., primary, Hammond, Vicki E., additional, Dickins, Ross A., additional, Quinn, Julian M. W., additional, Walkley, Carl R., additional, Sims, Natalie A., additional, Schnall, Ralf, additional, Della, Neil G., additional, Holloway, Andrew J., additional, Digby, Matthew R., additional, Janes, Peter W., additional, Tarlinton, David M., additional, Purton, Louise E., additional, Gillespie, Matthew T., additional, and Bowtell, David D. L., additional

Published
2003
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70. Drosophila Hfp negatively regulates dmyc and stg to inhibit cell proliferation.

Author

Quinn, Leonie M., Dickins, Ross A., Coombe, Michelle, Hime, Gary R., Bowtelll, David D. L., and Richardson, Helena

Subjects
*CELL proliferation, *DROSOPHILA, *CELL cycle, *CELL growth, *PROTEINS
Abstract

Mammalian FIR has dual roles in pre-mRNA splicing and in negative transcriptional control of Myc. Here we show that Half pint (Hfp), the Drosophila orthologue of FIR, inhibits cell proliferation in Drosophila. We find that Hfp overexpression potently inhibits G1/S progression, while hfp mutants display ectopic cell cycles. Hfp negatively regulates dmyc expression and function, as reducing the dose of hfp increases levels of dmyc mRNA and rescues defective oogenesis in dmyc hypomorphic flies. The G2delay in dmyc-overexpressing cells is suppressed by halving the dosage of hfp, indicating that Hfp is also rate-limiting for G2-M progression. Consistent with this, the cycle 14 G2-arrest of stg mutant embryos is rescued by the hfp mutant. Analysis of hfp mutant clones revealed elevated levels of Stg protein, but no change in the level of stg mRNA, suggesting that hfp negatively regulates Stg via a post-transcriptional mechanism. Finally, ectopic activation of the wingless pathway, which is known to negatively regulate dmyc expression in the wing, results in an accumulation of Hfp protein. Our findings indicate that Hfp provides a critical molecular link between the developmental patterning signals induced by the wingless pathway and dMyc-regulated cell growth and proliferation. [ABSTRACT FROM AUTHOR]

Published
2004
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71. Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas.

Author

Wen Xue, Zender, Lars, Miething, Cornelius, Dickins, Ross A., Hernando, Eva, Krizhanovsky, Valery, Cordon-Cardo, Carlos, and Lowe, Scott W.

Subjects
GENETICS of aging, P53 antioncogene
Abstract

A correction to the article "Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas" that was published in the 2007 issue is presented.

Published
2011
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72. IL-10 Controls Cystatin C Synthesis and Blood Concentration in Response to Inflammation through Regulation of IFN Regulatory Factor 8 Expression.

Author

Yuekang Xu, Schnorrer, Petra, Proietto, Anna, Kowalski, Greg, Febbraio, Mark A., Acha-Orbea, Hans, Dickins, Ross A., and Villadangos, Jose A.

Subjects
*INTERLEUKIN-10, *CYSTATINS, *ATHEROSCLEROSIS, *TRANSCRIPTION factors, *DENDRITIC cells, *LABORATORY mice, *GENE expression
Abstract

Cystatin C (CstC) is a cysteine protease inhibitor of major clinical importance. Low concentration of serum CstC is linked to atherosclerosis. CstC can prevent formation of amyloid β associated with Alzheimer's disease and can itself form toxic aggregates. CstC regulates NO secretion by macrophages and is a TGF-β antagonist. Finally, the serum concentration of CstC is an indicator of kidney function. Yet, little is known about the regulation of CstC expression in vivo. In this study, we demonstrate that the transcription factor IFN regulatory factor 8 (IRF-8) is critical for CstC expression in primary dendritic cells. Only those cells with IRF-8 bound to the CstC gene promoter expressed high levels of the inhibitor. Secretion of IL-10 in response to inflammatory stimuli downregulated IRF-8 expression and consequently CstC synthesis in vivo. Furthermore, the serum concentration of CstC decreased in an IL-10-dependent manner in mice treated with the TLR9 agonist CpG. CstC synthesis is therefore more tightly regulated than hitherto recognized. The mechanisms involved in this regulation might be targeted to alter CstC production, with potential therapeutic value. Our results also indicate that caution should be exerted when using the concentration of serum CstC as an indicator of kidney function in conditions in which inflammation may alter CstC production. [ABSTRACT FROM AUTHOR]

Published
2011
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73. Generation of an inducible mouse model to reversibly silence Stat3.

Author

Alorro MG, Pierce TP, Eissmann MF, Dijkstra C, Dickins RA, Ernst M, Buchert M, and Masson F

Subjects
Animals, Cell Line, Doxycycline pharmacology, Embryonic Stem Cells drug effects, Embryonic Stem Cells metabolism, Gene Dosage, Mice, Mice, Inbred C57BL, Mice, Knockout, STAT3 Transcription Factor metabolism, Stomach Neoplasms genetics, Stomach Neoplasms metabolism, Transcription, Genetic drug effects, Gene Silencing, Gene Targeting methods, STAT3 Transcription Factor genetics
Abstract

Signal transducer and activator of transcription 3 (Stat3) is a transcription factor that has many essential roles during inflammation, development and cancer. Stat3 is therefore an attractive therapeutic target in many diseases. While current Stat3 knockout mouse models led to a better understanding of the role of Stat3, the irreversible nature of Stat3 ablation does not model the effects of transient Stat3 therapeutic inhibition, and does not inform on potential dosage effects of Stat3. Using RNAi technology, we have generated a new mouse model allowing the inducible and reversible silencing of Stat3 in vivo, which mirrors the effects of specific Stat3 therapeutic interference. We showed that upon Doxycycline-mediated activation of the Stat3 short-hairpin RNA, Stat3 expression was efficiently reduced by about 80% in multiple organs and cell types. Moreover, Stat3 reduction was sufficient to reduce tumor burden in a clinically-validated mouse model of gastric cancer. Finally, we demonstrated that Stat3 silencing during embryonic development led to reduced birth rate without leading to complete embryonic lethality, in contrast to full Stat3 ablation. In conclusion, this new mouse model will be invaluable to understand the effects of Stat3 therapeutic interference and Stat3 dosage effects., (© 2017 Wiley Periodicals, Inc.)

Published
2017
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