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)

Mice deficient for B cell leukemia/lymphoma gene 2 [bcl-2(-/-) mice] manifest congenital renal hypoplasia and develop multicystic kidney disease and renal failure postnatally. To characterize postpartum renal development, to identify the cellular origin of the cysts, and to provide insight into the role that bcl-2 deficiency plays in the cystogenic process, we examined the morphology of kidneys from bcl-2 (-/-) mice and wild-type littermates [bcl-2 (+/+)] from birth (P0) to postpartum day 28 (P28), determined whether abnormalities of cellular proliferation and apoptosis accompany cyst development, and characterized expression of the bcl-2-related protein, bax. Between P0 and P7, kidneys from bcl-2 (-/-) and bcl-2 (+/+) mice undergo a comparable increase in weight and have similar histological appearances. However, during the next 2 wk of life, weight gain in kidneys from bcl-2 (-/-) mice is reduced compared with that in kidneys from bcl-2 (+/+) animals, and cysts develop in tubules with staining characteristics of proximal tubule, distal tubule/medullary thick ascending limb of Henle's loop, and collecting duct. Unaffected glomeruli and proximal tubules in kidneys of bcl-2 (-/-) mice undergo compensatory growth. Cystogenesis is accompanied by enhanced incorporation of 5-bromo-2'-deoxyuridine in cells within cortex and medulla and apoptosis of cells within cysts and in the renal interstitium. Bax protein is expressed in the distal tubule in kidneys of bcl-2 (+/+) and bcl-2 (-/-) mice and in some, but not all cysts. We conclude that abnormal regulation of DNA synthesis and apoptosis accompany cystogenesis in bcl-2 (-/-) mice during postpartum kidney development. Continued expression of bax could enhance apoptotic cell death.
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PMID:Abnormal postpartum renal development and cystogenesis in the bcl-2 (-/-) mouse. 876 Feb 59

One of the most remarkable transformations of cells during organogenesis is the epithelial transformation of nephrogenic mesenchyme to secretory nephrons. During recent years, gene targeting and organ culture approaches have been used efficiently to resolve key molecules involved in this multistage process. Nephrons are induced by the tips of the branching ureteric bud that later forms the collecting duct network. The first signal in nephron induction is obviously maintaining the mesenchyme; the second enhances cell proliferation and brings together the set of cells that contribute to one single nephron. This stage is characterized by two types of condensations (first the cap stage and then pre-tubular condensation). The final step, epithelial transformation, is a cell-autonomous process. Although the molecular cascade in nephron induction is being resolved in the rat, the same signals seem to work less efficiently in the mouse. In the rat, fibroblast growth factor-2 maintains the nephrogenic mesenchyme; leukaemia inhibitory factor together with transforming growth factor beta-2 induce its condensation; and autocrine secretion of Wnt-4 converts it to epithelium.
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PMID:Nephron induction. 1238 1