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The primers for dsRNA synthesis are presented in Table S3

The company has all the internationally leading core technologies of siRNA chemical synthesis, which include the RNA monomer synthesis technology, the custom and chemically-modified siRNA oligo synthesis technology, the nucleic acid fluorescent labeling technology, and many nucleotide chemical modification technologies.

Metabolic Circuit Involving Free Fatty Acids, microRNA 122, and Triglyceride Synthesis in Liver ..

N2 - The last decade witnessed exponential growth in our understanding of the role of microRNAs (miRNAs) in cancer. In addition to a clearly defined role in cancer initiation and progression, miRNAs are now believed to determine sensitivity to therapy. The post-genomic era has seen rapid growth in our understanding of drug resistance mechanisms at the genomic level including genomic aberrations involving miRNA clusters and in the development of targeted therapies. Aberrant activity of a single miRNA can influence multiple signaling pathways associated with therapeutic response because it can target multiple proteins. Although it is difficult to pinpoint a single downstream effector of a miRNA, studies focusing on known oncogenes and tumor suppressors targeted by miRNA as well as advanced bioinformatics capabilities have enabled the discovery of integrated mRNA-miRNA-protein circuitry in cancer cells that govern multiple aspects of cancer including drug sensitivity. These studies have provided evidence for specific miRNAs targeting signaling molecules involved in drug transport, drug metabolism, synthesis of ligands for receptors, drug-induced DNA damage response and apoptotic pathways, and growth factor receptors/kinases/phosphatases that form the backbone of targeted therapies. Extensive knowledge of miRNA expression pattern and targets has allowed clinical translation of miRNAs as prognostic and predictive markers of therapies. miRNAs expressed in cancer cells govern signaling not only in cancer cells but also in neighboring cells and distant organs because they are incorporated into secretory microvesicles, remain stable in body fluids, and cross plasma membrane or cell-cell junctions. These properties of miRNAs have generated considerable interest in developing means to restore normal miRNA patterns in cancer through therapeutic approaches. Indeed, miRNA-based therapies are already in phase II clinical trial for hepatitis C infection, confirming feasibility of this approach. Therefore, miRNA or miRNA antagomir-based therapies are likely the next-revolutionary therapeutic approach to combat cancer.

Peer Review Examples - F1000Research

Antagomir synthesis is essentially the same as synthesis of modified RNA oligonucleotides

The rabbits were randomly assigned to either theintervention group or the control group (n=4 in each group).Chemically synthesized antagomir or antagomir control (RiboBio Co.,Ltd.) were used to inhibit miR-21 expression. Experimental woundswere injected, under the new epithelium, with 100 µl solutioncontaining 10 nM miR-21 antagomir or antagomir control. Theinjections were carried out on days 15 and 25 after wounding. Onday 65 post-wounding, rabbits in each group were anaesthetized withintramuscular ketamine (40 mg/kg) and xylazine (4 mg/kg) and thenscars were harvested. One half of each scar was fixed in 4%paraformaldehyde for 24 h, embedded in paraffin, cut in 4-mmsections, and stained with hematoxylin and eosin. The thickness ofthe epidermis in uninjured skin and of the epidermis of the scarwas measured at ×400 magnification under optical microscope(Olympus Corporation, Tokyo, Japan). The other half was frozen forRT-qPCR analysis, which was performed according to theaforementioned description. The degree of dermal hypertrophy ofeach scar was expressed as the scar elevation index (SEI). Thisindex is the ratio of the area of newly formed dermis of the scarto the area of surrounding normal dermis. An SEI value greater than1 was considered to indicate a hypertrophic dermis.

For the mRNA, synthesis of cDNA was performed using TransScript® All-in-One First-Strand cDNA Synthesis SuperMix for qPCR (Transgen Biotech, Beijing, China). Real-time qPCR was performed using TransStart® Top Green qPCR SuperMix (Transgen Biotech), and β-actin was used for normalization of the results. The primer sequences are provided in Supplementary Methods.

Research news archive - Royal College Surgeons in Ireland

An antagomir is a small synthetic RNA that is perfectly complementary to the specific miRNA target with ..

For miRNA, synthesis of cDNA and qRT-PCR was performed using a human microRNA qRT-PCR detection kit specifically for hsa-miR-140-5p and RNU6B (BioTNT, Shanghai, China). RNU6B was used for normalization of the results. The sequences are provided in Supplementary Methods.

AB - The last decade witnessed exponential growth in our understanding of the role of microRNAs (miRNAs) in cancer. In addition to a clearly defined role in cancer initiation and progression, miRNAs are now believed to determine sensitivity to therapy. The post-genomic era has seen rapid growth in our understanding of drug resistance mechanisms at the genomic level including genomic aberrations involving miRNA clusters and in the development of targeted therapies. Aberrant activity of a single miRNA can influence multiple signaling pathways associated with therapeutic response because it can target multiple proteins. Although it is difficult to pinpoint a single downstream effector of a miRNA, studies focusing on known oncogenes and tumor suppressors targeted by miRNA as well as advanced bioinformatics capabilities have enabled the discovery of integrated mRNA-miRNA-protein circuitry in cancer cells that govern multiple aspects of cancer including drug sensitivity. These studies have provided evidence for specific miRNAs targeting signaling molecules involved in drug transport, drug metabolism, synthesis of ligands for receptors, drug-induced DNA damage response and apoptotic pathways, and growth factor receptors/kinases/phosphatases that form the backbone of targeted therapies. Extensive knowledge of miRNA expression pattern and targets has allowed clinical translation of miRNAs as prognostic and predictive markers of therapies. miRNAs expressed in cancer cells govern signaling not only in cancer cells but also in neighboring cells and distant organs because they are incorporated into secretory microvesicles, remain stable in body fluids, and cross plasma membrane or cell-cell junctions. These properties of miRNAs have generated considerable interest in developing means to restore normal miRNA patterns in cancer through therapeutic approaches. Indeed, miRNA-based therapies are already in phase II clinical trial for hepatitis C infection, confirming feasibility of this approach. Therefore, miRNA or miRNA antagomir-based therapies are likely the next-revolutionary therapeutic approach to combat cancer.

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Treatment of HCV Infection by Targeting MicroRNA — NEJM

Expression of fibrosis-associatedgenes is decreased following inhibition of miR-21 by miR-21antagomir in HSFBs. (A) NSFBs and HSFBs were treated with miR-21antagomir or miR-21 antagomir control for 48 h. Messenger RNAlevels of COL1A1, COL1A2 and Fn were determined by reversetranscription-quantitative polymerase chain reaction. (B)Inhibition of collagen synthesis was measured by H3-prolineincorporation assay. **P

antagomir 132 MicroRNA Analysis products

The last decade witnessed exponential growth in our understanding of the role of microRNAs (miRNAs) in cancer. In addition to a clearly defined role in cancer initiation and progression, miRNAs are now believed to determine sensitivity to therapy. The post-genomic era has seen rapid growth in our understanding of drug resistance mechanisms at the genomic level including genomic aberrations involving miRNA clusters and in the development of targeted therapies. Aberrant activity of a single miRNA can influence multiple signaling pathways associated with therapeutic response because it can target multiple proteins. Although it is difficult to pinpoint a single downstream effector of a miRNA, studies focusing on known oncogenes and tumor suppressors targeted by miRNA as well as advanced bioinformatics capabilities have enabled the discovery of integrated mRNA-miRNA-protein circuitry in cancer cells that govern multiple aspects of cancer including drug sensitivity. These studies have provided evidence for specific miRNAs targeting signaling molecules involved in drug transport, drug metabolism, synthesis of ligands for receptors, drug-induced DNA damage response and apoptotic pathways, and growth factor receptors/kinases/phosphatases that form the backbone of targeted therapies. Extensive knowledge of miRNA expression pattern and targets has allowed clinical translation of miRNAs as prognostic and predictive markers of therapies. miRNAs expressed in cancer cells govern signaling not only in cancer cells but also in neighboring cells and distant organs because they are incorporated into secretory microvesicles, remain stable in body fluids, and cross plasma membrane or cell-cell junctions. These properties of miRNAs have generated considerable interest in developing means to restore normal miRNA patterns in cancer through therapeutic approaches. Indeed, miRNA-based therapies are already in phase II clinical trial for hepatitis C infection, confirming feasibility of this approach. Therefore, miRNA or miRNA antagomir-based therapies are likely the next-revolutionary therapeutic approach to combat cancer.

Metabolic Circuit Involving Free Fatty Acids, microRNA …

Recent studies have shown that paracrine mechanisms including exosomes are responsible for stem cell- or progenitor cell-mediated tissue regeneration [, ]. We found that exosomes derived from SMSCs (SMSC-Exos) clearly promoted chondrocyte proliferation and migration. However, they had one crucial shortcoming: the inhibition of ECM protein synthesis including aggrecan and collagen II. To establish the reason for this, we measured the mRNA expression levels of Wnt family members in SMSCs and found that Wnt5a and Wnt5b were highly expressed in SMSCs. Furthermore, we found that Wnt5a and Wnt5b promoted chondrocyte proliferation and migration by activating YAP through alternative Wnt signalling pathways. The activation of YAP clearly suppressed the expression of SOX9 and led to the suppression of ECM formation.

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