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)

The expression and distribution of deoxyribonuclease I (DNase I) in rat parotid gland, kidney, small intestine and keratinized epithelium was further analysed at the level of its mRNA by in situ hybridization and correlated to immunohistochemical results using polyclonal anti-DNase I antibodies. High amounts of DNase I-specific mRNA and immunoreactivity were detected in the parotid gland, kidney and small intestine in agreement with previous immunohistochemical results. In the parotid gland, both the DNase I-specific mRNA and antigenicity were detected within the secretory cells. In the kidney, DNase I gene transcripts were localized in distal tubules and the collecting duct system. In this organ an identical localization of DNase I antigenicity was obtained. In the small intestine only the enterocytes covering the villi were shown to express DNase I-specific mRNA; the highest level being detected within the enterocytes along the lower third of the villi. In contrast, the highest level of immunoreactivity was found in enterocytes covering the middle and upper thirds of the villi. Within the stratified epithelium of the tongue, DNase I gene transcription and protein expression started in lower parts of the stratum spinosum and reached into the stratum granulosum. However, the gradient of DNase I gene transcript expression appeared to be shifted to lower layers of the stratum spinosum when compared to DNase I immunoreactivity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Localization of deoxyribonuclease I gene transcripts and protein in rat tissues and its correlation with apoptotic cell elimination. 764 Oct 69

Despite its key role in potassium homeostasis, transcriptional control of the H(+)-K(+)-ATPase alpha(2)-subunit (HKalpha(2)) gene in the collecting duct remains poorly characterized. cAMP increases H(+)-K(+)-ATPase activity in the collecting duct, but its role in activating HKalpha(2) transcription has not been explored. Previously, we demonstrated that the proximal 177 bp of the HKalpha(2) promoter confers basal collecting duct-selective expression. This region contains several potential cAMP/Ca(2+)-responsive elements (CRE). Accordingly, we examined the participation of CRE-binding protein (CREB) in HKalpha(2) transcriptional control in murine inner medullary collecting duct (mIMCD)-3 cells. Forskolin and vasopressin induced HKalpha(2) mRNA levels, and CREB overexpression stimulated the activity of HKalpha(2) promoter-luciferase constructs. Serial deletion analysis revealed that CREB inducibility was retained in a construct containing the proximal 100 bp of the HKalpha(2) promoter. In contrast, expression of a dominant negative inhibitor (A-CREB) resulted in 60% lower HKalpha(2) promoter-luciferase activity, suggesting that constitutive CREB participates in basal HKalpha(2) transcriptional activity. A constitutively active CREB mutant (CREB-VP16) strongly induced HKalpha(2) promoter-luciferase activity, whereas overexpression of CREBdLZ-VP16, which lacks the CREB DNA-binding domain, abolished this activation. In vitro DNase I footprinting and gel shift/supershift analysis of the proximal promoter with recombinant glutathione S-transferase (GST)-CREB-1 and mIMCD-3 cell nuclear extracts revealed sequence-specific DNA-CREB-1 complexes at -86/-60. Mutation at three CRE-like sequences within this region abolished CREB-1 DNA-binding activity and abrogated CREB-VP16 trans-activation of the HKalpha(2) promoter. In contrast, mutation of the neighboring -104/-94 kappabeta element did not alter CREB-VP16 trans-activation of the HKalpha(2) promoter. Thus CREB-1, binding to one or more CRE-like elements in the -86/-60 region, trans-activates the HKalpha(2) gene and may represent an important link between rapid and delayed effects of cAMP on HKalpha(2) activity.
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PMID:CREB trans-activates the murine H(+)-K(+)-ATPase alpha(2)-subunit gene. 1516 20