Slicing and Dicing RNA with Dicer

Wed, 03/12/2014 - 11:33

Dicer is an RNaseIII-like enzyme capable of cleaving double-stranded RNA (dsRNA) into smaller 21-23 nt RNA fragments known as short interfering RNA (siRNAs). It targets the selective degradation of complementary RNAs in a posttranscriptional gene silencing (PTGS) manner and is key for cell differentiation and development. Unlike long-dsRNA-dependent PTGS which is limited to certain cell types, siRNA can act in a wide variety of cells. Mutations in Dicer are found in blastoma, breast cancer, adenocarcinoma, and pancreatitis. Dicer also appears to be involved in myelination and nervous system protection, as well as miRNA-induced pathologies found in vision and hearing sensory cells and cardiovascular diseases. The Dicer antibody allowed Doi’s group to determine that Dicer and eIF2 family transcription factors mediate PTGS synergistically by directly associating through the PIWI domain1. To follow Dicer’s role in cardiomyopathy, Chen et al employed the Dicer antibody in their knockout mouse studies to demonstrate that Dicer plays an essential role in cardiac contraction, normal profiles of contractile protein expression, and heart muscle architecture2. Grelier’s group assessed both the prognostic and biological value of Dicer in breast cancer through use of comparative profiles developed from microarray and RT-PCR assays that employed Dicer antibody3.  Their data suggests that Dicer is a strong predictor for distant metastases.

Western Blot: Dicer Antibody Western Blot: Dicer Antibody

Immunoblotting studies with Dicer antibody in a Washington University lab found that lower Dicer activity enhances cell migration and soft agar growth, but not cell proliferation, in endometrial cancer cells4. Furthermore, the Dicer antibody allowed researchers at Duke’s Translational Research Center to publish interesting results in Nature Biotechnology detailing their development of an aptamer-siRNA chimerical RNA system for targeted and specific manner delivery into cells5.

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