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Na Wei

Researcher at Peking University

Publications -  6
Citations -  239

Na Wei is an academic researcher from Peking University. The author has contributed to research in topics: Small interfering RNA & Trans-acting siRNA. The author has an hindex of 5, co-authored 6 publications receiving 227 citations.

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An estrogen receptor α suppressor, microRNA-22, is downregulated in estrogen receptor α-positive human breast cancer cell lines and clinical samples

TL;DR: It is found that reduction of endogenous ERα protein levels and suppression of cancer cell growth could be achieved in MCF‐7 cells by miR‐22 overexpression in a way that can be recapitulated by the introduction of specific small interfering RNA against ERα.
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Comprehensive analysis of sequence-specific stability of siRNA

TL;DR: A comprehensive picture of serum processing of siRNA as well as a starting point for a rational siRNA modification strategy are provided, both of which are of great importance to in vivo and therapeutic applications of siRNAs.
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Focusing on RISC assembly in mammalian cells.

TL;DR: The data demonstrate that there is no definite correlation between siRNA stability and gene silencing in mammalian cells, which suggests that instead of thermodynamic stability, other features of the siRNA duplex contribute to RISC assembly in RNAi.
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Site-Specific RNase A Activity Was Dramatically Reduced in Serum from Multiple Types of Cancer Patients

TL;DR: Serum RNase activities visualized with this site-specific double stranded probe were found to be significantly reduced in patients with gastric cancer, liver cancer, pancreatic cancer, esophageal cancer, ovary cancer, cervical cancer, bladder cancer, kidney cancer and lung cancer, while only minor changes were found in breast and colon cancer patients.
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siRNA has greatly elevated mismatch tolerance at 3'-UTR sites.

TL;DR: The discovery is revealed that the specificity of an siRNA can be affected by the location of its target site, and siRNA had greatly elevated tolerance towards mismatches in target sites in the 3′-UTR of the mRNA compared with the same target sites cloned in the coding region.