Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.26.9 (ribonuclease)
 6,589 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

H(+)-K(+)-ATPase and carbonic anhydrase II (CA II) are two enzymes that are involved in the production and secretion of the hydrogen ion by the gastric parietal cell and maintenance of intracellular pH therein. The present studies were undertaken to examine whether H(+)-K(+)-ATPase and CA II expression change in the rat fundus in association with the development of acid secretory capacity. Changes in enzyme mRNA content in the gastric fundus of developing rat pups 1-6 wk of age were evaluated using dot blots and ribonuclease protection assays. In additional studies the localization of H(+)-K(+)-ATPase and carbonic anhydrase II mRNA was examined by in situ hybridization in Formalin-fixed gastric tissues from rats 1, 3, 6, and 8 wk of age. We observed that H(+)-K(+)-ATPase mRNA content increased with age in the developing rat fundus while CA II mRNA exhibited a reciprocal decrease. These changes in enzyme mRNA were accompanied by concomitant changes in the regional distribution of the cells expressing the genes for the two enzymes. Although the changes in H(+)-K(+)-ATPase mRNA paralleled the development of acid secretory capacity, CA II mRNA levels might be regulated by the requirement for maintenance of intracellular pH during periods of cellular proliferation and by exposure of the gastric surface epithelium to the highly acidic luminal environment of the stomach.
 ...
PMID:H(+)-K(+)-ATPase and carbonic anhydrase II gene expression in the developing rat fundus. 216 89

K+ homeostasis depends on K+ absorption in digestive and renal epithelia. Recently, a cDNA encoding for a putative K(+)-adenosinetriphosphatase (ATPase) alpha-subunit has been characterized. We studied its expression by ribonuclease protection assay and in situ hybridization in the distal colon and the kidney of rats in various physiological states. In the distal colon of control rats, high expression of the colonic putative K(+)-ATPase mRNA was restricted to the surface epithelial cells. A low-K+ diet did not modify this expression, adrenalectomy decreased it, and aldosterone or dexamethasone treatment for 2 days restored normal levels. In the kidney of control rats, levels of K(+)-ATPase mRNA were very low. A low-K+ diet revealed a clear mRNA expression, which is consistent with a recent report [J.A. Kraut, F. Starr, G. Sachs, and M. Reuben. Am. J. Physiol. 268 (Renal Fluid Electrolyte Physiol. 37): F581-F587, 1995]. This expression was restricted to the outer medullary collecting duct, presumably in principal cells. Changes in corticosteroid status did not influence the renal expression. Our results, together with previous studies on K+ absorption and K(+)-ATPase activity, suggest that more than a single molecular form of K(+)-ATPase is likely to be responsible for the regulation of K+ absorption in the colon and distal nephron.
 ...
PMID:Differential regulation of putative K(+)-ATPase by low-K+ diet and corticosteroids in rat distal colon and kidney. 877 35

Channel inducing factor (CHIF) is a novel cDNA recently cloned from a rat distal colon cDNA library of dexamethasone-treated animals. While its expression in Xenopus oocytes evokes a potassium channel activity similar to that induced by Isk (minK), its cellular role is not clear. CHIF exhibits significant homologies with proteins that are putatively regulatory (phospholemman, gamma-subunit of Na(+)-K(+)-ATPase, Mat-8) while it differs from the small-conductance potassium channel Isk. We have studied the tissue specificity of CHIF expression in rat by in situ hybridization. CHIF is selectively present in the distal parts of the nephron (medullary and papillary collecting ducts and end portions of cortical collecting tubule) and in the epithelial cells of the distal colon. No expression of CHIF was found in renal proximal tubule, loop of Henle and distal tubule, proximal colon, small intestine, lung, choroid plexus, salivary glands, or brain. To gain some insight into CHIF function, we have investigated, using in situ hybridization and ribonuclease protection assay, whether CHIF mRNA expression could be altered in some situations. In the distal colon, corticosteroid hormones, sodium restriction, low-potassium diet, and metabolic acidosis significantly increased CHIF mRNA expression. In the kidney, metabolic acidosis was the only condition that showed an increase in CHIF mRNA expression. Some of these treatments also altered the expression of the colonic H(+)-K(+)-ATPase mRNA. In summary, CHIF mRNA is selectively expressed in the medullary collecting duct of the kidney and in the epithelium of the distal colon; its expression varies differently in these two target tissues after alterations in corticosteroid status, potassium depletion, and metabolic acidosis. The precise cell-specific functions of CHIF remain to be established.
 ...
PMID:Cellular localization and regulation of CHIF in kidney and colon. 884 4