Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long-Evans (Eker) rats carry a mutation that predisposes them to develop spontaneous renal cell tumors of two morphologic patterns: solid chromophilic masses or cystic lesions lined by eosinophilic cells. Previous studies have suggested that these tumors arise from the proximal tubules. In the present study, lectin-binding characteristics and cytokeratin expression of various stages of hereditary rat renal epithelial neoplasia were examined to localize the portion of the nephron from which tumors arise. Lectin-binding histochemistry has been used as a marker of cell surface glycoprotein expression, thought to be important in the differentiation of benign from malignant epithelial lesions and in the determination of their cell of origin. The presence or absence of keratin intermediate filaments in the rat nephron has been used to identify nephron segments. The polyclonal antibody to high- and low-molecular-weight cytokeratin stained the cells of the collecting ducts but not the proximal or distal tubules. Binding to the proximal tubules by the lectins Conavalia ensiformis (Con A), Dolichas biflorus, Ricinus communis (RCA-1), and Triticum vulgare and to the distal tubules by Con A, RCA-1, Arachis hypogaea (PNA) with and without neuraminidase, and the antibody for cytokeratins was demonstrated. The lectin binding and cytokeratin staining patterns of rat hereditary renal cell carcinoma, adenoma and the preneoplastic lesions of atypical tubules and hyperplasias suggest that cystic adenomas arise from the distal nephron, principally the collecting duct, whereas the solid atypical tubules, hyperplasias, and adenomas arise from the proximal nephron, principally the proximal tubule.
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PMID:Preneoplastic and neoplastic lesions of rat hereditary renal cell tumors express markers of proximal and distal nephron. 748 12

To distinguish biological molecular processes of osmotic stress occurring in inner medulla, we utilized microarrays to monitor expression profiles. RNAs from three segments (cortex, outer medulla, and inner medulla) of mouse kidney were isolated and applied to microarrays. We found 35 genes expressed highly in inner medulla. Next, microarrays for the RNAs from mouse medullary collecting duct cell line (mIMCD) cells and osmotically adapted mIMCD cells (HT cells) were performed (designed as resistant to 1270mOsm/H(2)O). Of 35 genes highly expressed in inner medulla, 6 genes such as; B-cell translocation gene protein (BTG), myc-basic motif homologue, gelsolin, cell surface glycoprotein, laminin beta2, and tubulo-interstitial nephritis antigen, were also expressed highly in HT cells. Using real-time PCR, we confirmed the expression of six genes. Additionally acute osmotic stress induced the BTG. By comparing the inner medulla to a mIMCD3, we identified genes which respond to acute and chronic hyperosmotic stress.
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PMID:Osmoadaptation-related genes in inner medulla of mouse kidney using microarray. 1531 98