Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

C-erbB-2 is a human proto-oncogene which has homologies with the well known proto-oncogene c-erbB. The c-erbB-2 gene is amplified and overexpressed in some human adenocarcinomas. Its expression, in terms of RNA levels in normal human fetal kidney, lung and liver, has also been reported. In the present study, various fetal tissues from three human abortuses obtained at 9, 14 and 24 weeks of gestation, were studied immunohistologically by the ABC method and immunochemically by Western blot analysis for the distribution of c-erbB-2 gene product at the protein level. A polyclonal antibody raised in rabbit by immunization with a synthetic polypeptide corresponding to part of the predicted intracytoplasmic domain was used. Strong immunoreactivity was observed on the membrane of most of the epithelial cells examined, including transitional cells of the renal pelvis and ureter, glandular cells of the gastrointestinal tract, renal tubuli, bronchi and pancreas, and stratified epithelium of the oral cavity, trachea and esophagus in this gestational period. A much more intense reaction was observed on the basolateral sides than on the apical side of these cells. No immunoreactivity was found in the liver, adrenal gland, striated and smooth muscles, brain, endothelium or fibroblasts. Western blot analysis confirmed increased expression of the c-erbB-2 gene product in fetal kidney and intestine but not in the brain. As the protein seems to be poorly expressed in normal adult epithelial cells except for renal tubuli, the present results suggest that the protein is a membrane-associated receptor protein which controls some specific reaction of fetal epithelium.
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PMID:C-erbB-2 gene product, a membrane protein commonly expressed on human fetal epithelial cells. 247 78

1. The varying profile of cell types along the muscle wall of the guinea-pig upper urinary tract was examined electrophysiologically, using intracellular microelectrodes, and morphologically, using both electron and confocal microscopy. 2. Simple 'pacemaker' oscillations (frequency of 8 min-1) of the membrane potential were recorded in both the pelvi-calyceal junction (83 % of cells) and the proximal renal pelvis (15 % of cells), but never in the distal renal pelvis or ureter. When filled with the cell marker, neurobiotin, 'pacemaker' cells were spindle shaped and approximately 160 microm in length. 3. In most cells of the ureter (100 %) and in both the proximal (75 %) and distal (89 %) renal pelvis, spontaneous action potentials (frequency of 3-5 min-1) consisted of an initial spike, followed by a number of potential oscillations superimposed on a plateau phase. When filled with neurobiotin, cells firing these 'driven' action potentials, were spindle shaped and > 250 microm in length. 4. Greater than 80 % of smooth muscle cells in the pelvi-calyceal junction were 'atypical', having < 40 % of their sectional areas occupied by loosely packed contractile filaments. Most of the smooth muscle cells in the ureter (99.7 %) and both the proximal (83 %) and distal (97.5 %) renal pelvis were of 'typical' appearance in that they contained cytoskeletal and contractile elements occupying > 60 % of cross-sectional area. 5. A third type of spontaneously discharging cell fired 'intermediate' action potentials (3-4 min-1), consisting of a single spike followed by a quiescent plateau and an abrupt repolarization. These cells were morphologically similar to interstitial cells of Cajal (ICC). However, these 'ICC-like' cells were not immuno-reactive for c-Kit, the proto-oncogene for tyrosine kinase. 6. In summary, 'atypical' smooth muscle cells were predominant in the pelvi-calyceal junction and fired 'pacemaker' potentials at a frequency significantly higher than 'driven' action potentials recorded in 'typical' smooth muscle cells throughout the renal pelvis and ureter. 'Intermediate' action potentials were recorded in 'ICC-like' cells in both the pelvi-calyceal junction and renal pelvis. We suggest that these 'ICC-like' cells act as a preferential pathway, conducting and amplifying pacemaker signals to initiate action potential discharge in the driven areas of the upper urinary tract.
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PMID:Identification of the cells underlying pacemaker activity in the guinea-pig upper urinary tract. 1045 97

Almost 1% of human infants are born with urogenital abnormalities, many of which are linked to irregular connections between the distal ureters and the bladder. During development, ureters migrate by an unknown mechanism from their initial integration site in the Wolffian ducts up to the base of the bladder in a process that we call ureter maturation. Rara(-/-) Rarb2(-/-) mice display impaired vitamin A signaling and develop syndromic urogenital malformations similar to those that occur in humans, including renal hypoplasia, hydronephrosis and mega-ureter, abnormalities also seen in mice with mutations in the proto-oncogene Ret. Here we show that ureter maturation depends on formation of the 'trigonal wedge', a newly identified epithelial outgrowth from the base of the Wolffian ducts, and that the distal ureter abnormalities seen in Rara(-/-) Rarb2(-/-) and Ret(-/-) mutant mice are probably caused by a failure of this process. Our studies indicate that formation of the trigonal wedge may be essential for correct insertion of the distal ureters into the bladder, and that these events are mediated by the vitamin A and Ret signaling pathways.
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PMID:Distal ureter morphogenesis depends on epithelial cell remodeling mediated by vitamin A and Ret. 1219 22