Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Query: EC:3.1.26.9 (
ribonuclease
)
6,589
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The tight junction forms the intercellular barrier separating tissue compartments. The characteristics of this barrier are remarkably diverse among different epithelia and endothelia and are not explained by our limited knowledge of its molecular composition. Two isoforms of the 220-kDa tight junction protein ZO-1 result from alternative RNA splicing and differ by an internal 80-amino acid domain, termed alpha (E. Willott, M. S. Balda, M. Heintzman, B. Jameson, and J. M. Anderson. Am. J. Physiol. 262 (Cell Physiol. 31): C1119-C1124, 1992). Using antibodies specific for each isoform and double-labeled immunofluorescence microscopy, we observed that the
ZO-1
alpha- isoform is restricted to junctions of endothelial cells and highly specialized epithelial cells of both seminiferous tubules (Sertoli cells) and renal glomeruli (podocytes); in contrast, the
ZO-1
alpha+ isoform is expressed in cells of all other epithelia examined. Both immunoblotting and
ribonuclease
protection analysis confirmed this pattern of expression. This distribution does not correlate with differences in junctional resistance or ultrastructural complexity. Instead, we observe a correlation with junctional plasticity;
ZO-1
alpha- is expressed in structurally dynamic junctions, whereas
ZO-1
alpha+ is expressed in those which are less dynamic. This is the first molecular distinction among tight junctions and reveals a fundamental dichotomy with implications for how the paracellular barriers of endothelia and epithelia are regulated.
...
PMID:Two classes of tight junctions are revealed by ZO-1 isoforms. 768 77
Hepatocyte tight junctions form the intercellular barrier between bile and blood. Cholestasis due to common bile duct ligation (CBDL) results in structural changes in the tight junction (TJ) and an overt paracellular leak, although the molecular basis for these alterations is undefined. Using the epithelial isoform of the TJ protein
ZO-1
(
ZO-1
alpha +) as a marker for molecular changes in hepatocyte TJs, we investigated the effects of CBDL on
ZO-1
alpha + immunofluorescence (IF) localization and on
ZO-1
alpha + mRNA and protein expression over 2 wk of CBDL.
ZO-1
alpha + IF staining was altered after 2 days of CBDL and appeared to accumulate in pericanalicular regions after 7 and 9 days. Quantitative immunoblotting and
ribonuclease
protection revealed a marked increase in hepatic
ZO-1
alpha + protein expression and
ZO-1
alpha + mRNA levels, respectively. In contrast to changes in
ZO-1
alpha + IF, which occurred throughout the lobule, and changes in mRNA and protein expression, which were maximal after 9 days of ligation, the maximal hepatocyte proliferation occurred within 2 days after CBDL and was confined to periportal regions. CBDL results in altered hepatic localization and increased expression of the TJ protein
ZO-1
alpha + and appears to represent a specific response by hepatocytes to pathological junction injury independent of cell proliferation.
...
PMID:Altered expression and localization of the tight junction protein ZO-1 after common bile duct ligation. 833 99