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

A high frequency restriction fragment length polymorphism (RFLP) at the 3'-end of the pigeon pro alpha 2(1) collagen gene was detected using the restriction endonuclease EcoR1. The distribution of this allelic variant was analyzed in DNA isolated from White Carneau pigeons genetically susceptible to the development of spontaneous atherosclerosis. The atherogenic phenotype in individual pigeons was measured by the determination of total cholesterol and cholesterol ester levels in the celiac focus of the thoracic aorta of adult White Carneau pigeons. Aortic wall cholesterol levels correlated with an increase in lesion size. No correlation, however, was observed between allelic variants of the pigeon pro alpha 2(1) collagen gene and the atherogenic phenotype in White Carneau pigeons suggesting lack of linkage between this allelic marker and the genetic susceptibility to spontaneous atherogenesis. This is the first study of its kind in this animal model and serves to provide a basis for the further analysis of co-segregation of RFLPS in candidate genes to this polygenic phenotype.
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PMID:A restriction fragment length polymorphism in the pigeon pro alpha 2(1) collagen gene: lack of an allelic association with an atherogenic phenotype in pigeons genetically susceptible to the development of spontaneous atherosclerosis. 168 10

This study is the first to describe a molecular marker that distinguishes the celiac disease HLA-D region haplotype from a serologically identical haplotype in unaffected controls. Using a DQ beta chain cDNA probe and the restriction endonuclease Rsa I, we have detected a polymorphic 4.0 kb fragment which, in DQw2 individuals, is associated with a 40-fold increased relative risk of developing celiac disease. This finding should permit the identification of the celiac disease susceptibility gene(s) in the HLA-D region and facilitate a more precise dissection of the molecular and immunogenetic mechanisms involved in the pathogenesis of that disease.
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PMID:An HLA-D region restriction fragment length polymorphism associated with celiac disease. 301 38

The soybean SAUR (Small Auxin-Up RNA) genes are transcriptionally induced by exogenous auxins within a few minutes after hormone application. This response is specifically induced by auxins primarily in epidermal and cortical cells within elongation zones of hypocotyls and epicotyls. We have previously shown that an 832-bp soybean SAUR promoter/beta-glucuronidase (GUS) reporter gene fusion is responsive to auxin in transgenic tobacco plants (Y. Li, G. Hagen, T.J. Guilfoyle [1991] Plant Cell 3: 1167-1175). Similar results were obtained with an 868-bp SAUR 15A promoter-GUS reporter gene in transgenic tobacco (Y. Li, unpublished results). We have now analyzed a soybean SAUR 15A promoter in transgenic tobacco plants using 5' unidirectional deletions, internal deletions and mutations, and gain-of-function assays with a minimal cauliflower mosaic virus 35S promoter. Our results indicate that the distal upstream element/NdeI restriction endonuclease site element (NDE) (B.A. McClure, G. Hagen, C.S. Brown, M.A. Gee, T.J. Guilfoyle [1989] Plant Cell 1: 229-239) in the SAUR 15A promoter is necessary and sufficient for auxin induction. Our results also show that the 30-bp NDE portion of this element is responsible for most, if not all, of the auxin inducibility of the SAUR 15A promoter. The NDE contains two adjacent sequences, TGTCTC and GGTCCCAT, which have been previously identified as putative auxin-responsive elements. We propose that these elements might function independently or together, possibly with an additional element(s), to confer auxin inducibility to the SAUR promoters.
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PMID:An auxin-inducible element in soybean SAUR promoters. 797 20