RNA Interference RNAi | siRNA

siRNA gene silencing? What is siRNA gene silencing and what does it do? Thanks, Ikie
RNA interference :: Discovery of mechanism??? PLEASE HELP!!!? i know that andrew fire and craig mello discovered that dsRNA cause RNA interference but they could not deduce RNAi Pathway.( involving Dicer, RISC...
RNA interference :: Discovery of mechanism??? PLEASE HELP!!!? i know that andrew fire and craig mello discovered that dsRNA cause RNA interference but they could not deduce RNAi Pathway.( involving Dicer, RISC...
Multiple copy number of a transgene vs RNAi? Is RNAi related with the presence of multiple copy number of T-DNA in transgenic plants? can a single stranded RNA induce RNAi? anwers are much...
You must REGISTER NOW to post a question in the RNAi SiRNA Forum. Login now if you have already registered.

The synthesis of therapeutic locked nucleos(t)ides. Related Articles

The synthesis of therapeutic locked nucleos(t)ides.

Curr Opin Drug Discov Devel. 2009 Nov;12(6):876-98

Authors: Zhou C, Chattopadhyaya J

This review highlights progress made during the past 2 to 3 years in the field of therapeutic locked nucleos(t)ides. Synthetic strategies to construct the conformationally locked nucleos(t)ides, their properties and potential therapeutic applications as antiviral compounds, and modified oligonucleotides to modulate antisense and RNAi properties are described.

PMID: 19894196 [PubMed - in process]

A Quantitative RNAi Screen for JNK Modifiers Identifies Pvr as a Novel Regulator of Drosophila Immune Signaling.

PLoS Pathog. 2009 Nov;5(11):e1000655

Authors: Bond D, Foley E

Drosophila melanogaster responds to gram-negative bacterial challenges through the IMD pathway, a signal transduction cassette that is driven by the coordinated activities of JNK, NF-kappaB and caspase modules. While many modifiers of NF-kappaB activity were identified in cell culture and in vivo assays, the regulatory apparatus that determines JNK inputs into the IMD pathway is relatively unexplored. In this manuscript, we present the first quantitative screen of the entire genome of Drosophila for novel regulators of JNK activity in the IMD pathway. We identified a large number of gene products that negatively or positively impact on JNK activation in the IMD pathway. In particular, we identified the Pvr receptor tyrosine kinase as a potent inhibitor of JNK activation. In a series of in vivo and cell culture assays, we demonstrated that activation of the IMD pathway drives JNK-dependent expression of the Pvr ligands, Pvf2 and Pvf3, which in turn act through the Pvr/ERK MAP kinase pathway to attenuate the JNK and NF-kappaB arms of the IMD pathway. Our data illuminate a poorly understood arm of a critical and evolutionarily conserved innate immune response. Furthermore, given the pleiotropic involvement of JNK in eukaryotic cell biology, we believe that many of the novel regulators identified in this screen are of interest beyond immune signaling.

PMID: 19893628 [PubMed - in process]

Polycomb protein EZH2 regulates E2F1-dependent apoptosis through epigenetically modulating Bim expression.

Cell Death Differ. 2009 Nov 6;

Authors: Wu ZL, Zheng SS, Li ZM, Qiao YY, Aau MY, Yu Q

Deregulation of the pRB/E2F pathway, which occurs frequently in human malignancy, is often associated with inappropriate proliferation and/or apoptosis. While the role of E2F1 in apoptosis induction has been well-established, it remains unclear how this pro-apoptotic activity is regulated in cancer. Here we describe EZH2, an oncogenic polycomb histone methyltransferase and an E2F1 target, as an important regulator of E2F1-dependent apoptosis. We show that E2F1 induces EZH2 expression, which in turn antagonizes the induction of E2F1 pro-apoptotic target Bim expression. RNAi-mediated gene depletion of EZH2 enhances E2F1-dependent Bim expression, thereby promoting the pro-apoptotic activity of E2F1. Hence, the concomitant induction of EZH2 and Bim by E2F1 constitutes a fail-safe mechanism to allow tumor cells with aberrant E2F1 activity to evade apoptosis. These findings reveal a novel mechanism by which the apoptotic activity of E2F1 is restrained in human cancer and also provide the first evidence that EZH2 directly regulates apoptotic process in cancer cells.Cell Death and Differentiation advance online publication, 6 November 2009; doi:10.1038/cdd.2009.162.

PMID: 19893569 [PubMed - as supplied by publisher]

[Construction and identification of RNAi lentiviral vector targeting at triggering receptors expressed on myeloid cells-1.]

Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2009 Oct;34(10):970-7

Authors: Song D, Huang X, Yang X, Xiao M, Wang S

Objective To construct a lentiviral vector of RNA interference (RNAi) of murine triggering receptor expressed on myeloid cells-1(TREM-1) gene and to explore the effect of TREM-1 on the inflammatory response caused by Bacteroides fragilis.Methods Four target sequences were selected according to murine TREM-1 mRNA sequence, and then 4 pairs of double-strand DNA oligo according to these target sequences and one pair of negative control double-strand DNA oligo were designed and synthesized. These fragments were subcloned into pGCSIL-GFP/Lenti plasmid. After being identified by PCR and sequencing, these plasmids were cotransfected into 293T cells to package lentiviral particles. The lentiviral vector particles were transfected into Raw 264.7 cells and TREM-1 expression in the transfected cells was assayed by real-time PCR and ELISA. Different concentrations of Bacteroides fragilis lipopolysaccaride (LPS) were administered in the Raw264.7 cells, and the cells were stimulated with LPS for 12 h. TREM-1 expression was determined by real-time PCR and ELISA at the time points.Results PCR and sequencing confirmed that lentiviral vectors had the correct structure and could express high titer of virus. After being transfected into Raw264.7 cells, TREM-1 expression was knocked down significantly by all of these lentiviral vectors at both protein and mRNA levels, and the pGCSIL-GFP/Lenti-1 had the most efficient interference. TREM-1 was upregulated in the presence of Bacteroides fragilis LPS, and this increase was partly abrogated in the TREM-1 siRNA-treated cell models of endotoxemia, depending on the sequence. Conclusion The lentivirus RNAi vector of TREM-1 was constructed successfully. The lentivirus RNAi vector of TREM-1 can inhibit the expression of TREM-1 in the murine endotoxemia model caused by Bacteroides fragilis LPS.

PMID: 19893247 [PubMed - in process]