Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A method is described whereby rubella virus RNA was reverse transcribed and the resulting cDNA enzymatically amplified using Taq polymerase. The reactions were carried out in a single reaction vessel, with only minor modifications to the buffer conditions between the reverse transcription and the subsequent amplification step. Using an oligonucleotide probe to the E1 glycoprotein region and limited restriction endonuclease mapping, the resulting amplified products were shown to be specific for rubella virus. This method was also successfully applied to crude cell lysates, without the need for RNA purification. The possible applications of the polymerase chain reaction as applied to RNA sequences are discussed.
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PMID:Reverse transcription and subsequent DNA amplification of rubella virus RNA. 247 57

Type 1 diabetes results from the destruction of insulin-producing pancreatic beta cells. Genetic and environmental factors are implicated in the beta cell destruction. As environmental factors affecting the induction of type 1 diabetes, diabetogenic viruses, chemicals, toxins, and diet are likely candidates as either primary injurious agents of beta cells or triggering agents for the induction of autoimmunity. Regarding viruses as a triggering factor of type 1 diabetes, there are at least two different pathogenic mechanisms in virus-induced diabetes: cytolytic infection of beta cells, leading to their destruction, and triggering of autoimmunity, leading to the autoimmune-mediated destruction of beta cells. Since there is no correlation between the induction of antibodies to Coxsackie B viruses and the presence of islet cell autoantibodies in patients with type 1 diabetes, the induction of diabetes by Coxsackie B viruses may be due to cytolytic infection of beta cells rather than an autoimmune response. In contrast, rubella virus and cytomegalovirus (CMV) do appear to be somehow associated with autoimmune type 1 diabetes since there is a strong correlation between the presence of islet cell autoantibodies and persistent infections. Regarding genetic factors, there are distinct markers related to the susceptibility to Coxsackie B4 virus-associated type 1 diabetes and CMV-associated type 1 diabetes. Four specific DNA restriction endonuclease fragments (BamHI-DQ-beta 6.6, TaqI-DR-beta 4.3, TaqI-DR-beta 2.5 and TaqI-DR-beta 1.5 kb) are related to the susceptibility to Coxsackie B4 virus-associated type 1 diabetes while six specific DNA restriction endonuclease fragments (BamHI-DQ-alpha 12.5, -beta 3.7 and -beta 3.2 kb, TaqI-DQ-alpha 7.2, -beta 7.2 and -beta 5.4 kb) are related to the susceptibility to CMV-associated type 1 diabetes.
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PMID:Viruses as a triggering factor of type 1 diabetes and genetic markers related to the susceptibility to the virus-associated diabetes. 268 Mar 67

Restriction endonuclease digestion was used to eliminate false-positive signals caused by polymerase chain reaction (PCR) product DNA contamination in a reverse transcribed (RT) PCR for amplifying rubella virus (RV) RNA sequences. A restriction enzyme selected to cut the PCR product DNA between, but not within, the primer binding sites was used to digest reaction mixtures after reverse transcription but before PCR amplification. Because restriction enzymes generally react only with specific double-strand sequences, contaminating DNA was rendered inactive while reverse-transcribed single strand cDNA was amplified. Assays showed that restriction enzyme digestion reduced template activity of product DNA by a factor of 10(7), while leaving sensitivity of the RT-PCR unaffected.
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PMID:Restriction endonuclease digestion eliminates product contamination in reverse transcribed polymerase chain reaction. 768 88