RNA Interference RNAi | siRNA

microRNA in situ hybridization protocol: zebrafish embryos & adult tissues Lagendijk AK, Moulton JD, Bakkers J. Revealing details: whole mount microRNA in situ hybridization protocol for zebrafish embryos and adult tissues...
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Curing "incurable" cancer.

Curing "incurable" cancer.

Cancer Discov. 2011 Nov;1(6):477-80

Authors: Watson JD

Abstract
Cancer cells are preferentially killed by anticancer agents because key signals for growth and cell division are "always on" as opposed to the alternative "on" and "off" signaling of normal cells. Too much of today's anticancer drug discovery effort may go toward reversing genetically promoted "always on" signals. More effective anticancer drug targets may be found through use of RNAi technologies that pinpoint the key gene regulatory and metabolic weakness of the "always on" cancer cells. Cancer Discovery; 1(6); 477-80. ©2011 AACR.

PMID: 22586652 [PubMed - in process]

Depletion of cellular pre-replication complex factors results in increased human cytomegalovirus DNA replication.

PLoS One. 2012;7(5):e36057

Authors: Evans Braun T, Poole E, Sinclair J

Abstract
Although HCMV encodes many genes required for the replication of its DNA genome, no HCMV-encoded orthologue of the origin binding protein, which has been identified in other herpesviruses, has been identified. This has led to speculation that HCMV may use other viral proteins or possibly cellular factors for the initiation of DNA synthesis. It is also unclear whether cellular replication factors are required for efficient replication of viral DNA during or after viral replication origin recognition. Consequently, we have asked whether cellular pre-replication (pre-RC) factors that are either initially associated with cellular origin of replication (e.g. ORC2), those which recruit other replication factors (e.g. Cdt1 or Cdc6) or those which are subsequently recruited (e.g. MCMs) play any role in the HCMV DNA replication. We show that whilst RNAi-mediated knock-down of these factors in the cell affects cellular DNA replication, as predicted, it results in concomitant increases in viral DNA replication. These data show that cellular factors which initiate cellular DNA synthesis are not required for the initiation of replication of viral DNA and suggest that inhibition of cellular DNA synthesis, in itself, fosters conditions which are conducive to viral DNA replication.

PMID: 22586460 [PubMed - in process]

RNAi screen for kinases and phosphatases that play a role in antigen presentation by dendritic cells.

Eur J Immunol. 2012 May 14;

Authors: Moita CF, Chora A, Hacohen N, Moita LF

Abstract
Effective CD8(+) T-cell responses against tumor or microbial antigens that are not directly expressed in antigen presenting cells (APCs) depend on the cross-presentation of these antigens on MHC Class I in APCs. To identify signaling molecules that regulate cross-presentation, we used lentiviral-based RNA interference to test the roles of hundreds of kinases and phosphatases in this process. Our study uncovered 8 previously unknown genes, consisting of 1 positive and 7 negative regulators of antigen cross-presentation. Depletion of Acvr1c, a type I receptor for TGF? family of signaling molecules, led to an increase in CD80 and CD86 co-stimulator surface expression and secreted IL-12 in mouse bone marrow-derived DCs, as well as antigen-specific T-cell proliferation.

PMID: 22585713 [PubMed - as supplied by publisher]

Inhibition of RhoA/ROCK Signaling Pathway Promotes the Apoptosis of Gastric Cancer Cells.

Hepatogastroenterology. 2012 May 14;59(120)

Authors: Xiao-Tao X, Qi-Bin S, Yi Y, Bin X, Peng R, Ze-Zhang T

Abstract
Background/Aims: Ras homologue A (RhoA) plays a crucial role in the proliferation, apoptosis, adhesion and migration of gastric cancer cells. Rho associated kinase (ROCK) is an effector protein of RhoA. Methodology: In the present study, RhoA activity was inhibited by siRNA targeting RhoA and Y-27632, an inhibitor of ROCK, and the role of RhoA/ROCK signaling pathway in the apoptosis of gastric cancer cells was investigated. Results: RNAi of RhoA inhibited the survival and promoted the apoptotic of AGS cells. RhoA RNAi caused an obvious decrease of ROCK1 expression but an increase of caspase-3/cleaved-caspase-8. Inhibition of ROCK by Y-27632 inhibited the activity of RhoA and promoted the apoptosis. Conclusions: We speculate that RhoA/ROCK signaling pathway plays an important role in the regulation of apoptosis of gastric cancer, and to inhibit this pathway may promote the apoptosis of cancer cells. Thus, inhibition of RhoA/ROCK signaling pathway may become a novel target in the treatment of gastric cancer.

PMID: 22584506 [PubMed - as supplied by publisher]

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