Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 1110-base-pair cDNA clone for human cathepsin D was obtained by screening a lambda gt10 human hepatoma G2 cDNA library with a human renin exon 3 genomic fragment. Poly(A)+ RNA blot analysis with this cathepsin D clone demonstrated a message length of about 2.2 kilobases. The partial clone was used to screen a size-selected human kidney cDNA library, from which two cathepsin D recombinant plasmids with inserts of about 2200 and 2150 base pairs were obtained. The nucleotide sequences of these clones and of the lambda gt10 clone were determined. The amino acid sequence predicted from the cDNA sequence shows that human cathepsin D consists of 412 amino acids with 20 and 44 amino acids in a pre- and a prosegment, respectively. The mature protein region shows 87% amino acid identity with porcine cathepsin D but differs in having nine additional amino acids. Two of these are at the COOH terminus; the other seven are positioned between the previously determined junction for the light and heavy chains of porcine cathepsin D. A high degree of sequence homology was observed between human cathepsin D and other aspartyl proteases, suggesting a conservation of three-dimensional structure in this family of proteins.
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PMID:Cloning and sequence analysis of cDNA for human cathepsin D. 392 92

Using 32P-labeled DNA complementary to mouse submaxillary gland renin mRNA, we probed mRNA gel blots from mouse testis and kidney tissues. Poly(A)-RNA from testis contained a hybridizable RNA species which was blotted onto nitrocellulose paper. The molecular size of testicular renin mRNA (approximately 1600 nucleotides in length) was not significantly different from tht of kidney renin mRNA. Densitometric scan revealed that the content of renin mRNA in mouse testis was approximately 5-fold lower than that in mouse kidney. These results support the proposal that mouse testicular cells synthesize renin.
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PMID:Detection of renin mRNA in mouse testis by hybridization with renin cDNA probe. 608 88

The molecular weight of human renin precursor (preprorenin) was determined to be 43,000 by cell-free translation of its mRNA. Poly(A)+-containing RNA from human infarcted kidney was translated in a cell-free reticulocyte lysate system containing [35S] methionine. Immunoprecipitation with anti-renin antibody gave one major band with an apparent Mr = 43,000, as determined by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis and fluorography. The specific band, which represents the prepro-form of human renal renin, was very similar to mouse submandibular gland preprorenin in its electrophoretic mobility.
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PMID:Cell-free translation of human renin mRNA. 635 67

1. Poly(A)+ mRNA from mouse submaxillary gland encodes a polypeptide of molecular weight 48 000 (48K polypeptide) which is abundant in the male. 2. This polypeptide is selectively absent in the translation products of mRNA from a strain of genetically renin-deficient mice C57 BL/10J. 3. The 48K polypeptide binds and co-elutes in identical fashion with pure authentic renin on pepstatin affinity chromatography. 4. Immunoprecipitation of translation products of male glandular mRNA with renin-specific antibody yielded this 48K band upon analysis by SDS/polyacrylamide gel electrophoresis and fluorography. Pure renin of molecular weight 37 000 blocked the binding of this polypeptide to antirenin antibody. 5. Mouse submaxillary gland synthesizes a renin precursor. The renin mRNA is androgenically regulated.
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PMID:Studies of the biosynthesis of renin with a cell-free translation system. 703 13

Non-steroidal anti-inflammatory drugs (NSAIDs) represent a clinically important class of agents. NSAIDs are commonly used in treatment of conditions such as headache, fever, inflammation and joint pain. Complications often arise from chronic use of NSAIDs. Gastrointestinal (GI) toxicity in the form of gastritis, peptic erosions and ulcerations and GI bleeds limit usage of NSAIDs. These toxicities are thought to be due to cyclooxygenase (COX)-1 blockade. COX-1 generates cytoprotective prostanoids such as prostaglandin (PG) E2 and prostacyclin (PGI2). COX-2 inhibitors, commonly referred to as coxibs, were developed to inhibit inflammatory prostanoids without interfering with production of COX-1 prostanoids. Concerns over cardiovascular safety, however, have evolved based on the concept of inhibition of COX-2-derived endothelial prostanoids without inhibition of platelet thromboxane A2, leading to increased cardiovascular risk. The Celecoxib Long-Term Arthritis Safety Study (CLASS) trial did not show a significant increase in cardiovascular risk for celecoxib (Celebrex), but results of the Vioxx Gastrointestinal Outcomes Research (VIGOR) study showed an increased cardiovascular risk with long-term daily usage of rofecoxib in patients with rheumatoid arthritis. The Adenomatous Poly Prevention on Vioxx (APPROVe) trial further evaluated cardiovascular effects of rofecoxib and recently led to removal of this drug from the marketplace. Coxibs affect renal function via blockade of normal COX-2 functions. COX-2 expression increases in high renin states and in response to a high-sodium diet or water deprivation. PGI2 and PGE2 are the most important renal prostanoids. PGI2 inhibition results in hyperkalemia. PGE2 inhibition results in sodium retention, which leads to hypertension, peripheral edema and potentially exacerbation of heart failure. This review article discusses beneficial and deleterious effects associated with prostanoids produced by COX-1 and COX-2 in various organs and how blockade of these products translates into clinical medicine.
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PMID:Cyclooxygenase-2 inhibitors: a painful lesson. 1678 94