Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P41181 (
collecting duct
)
5,183
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Development-dependent mRNA expression of the chloride channels ClC-2 and
ICln
was studied by quantitative reverse transcriptase-polymerase chain reaction in rat ureteric bud and cortical
collecting duct
primary monolayer cultures. Abundance of ClC-2 mRNA increased in ureteric bud cells between embryonic day 15 (E15) and E17, peaked at postnatal day 3 (P3), and was down-regulated at P7 when morphogenesis is complete, suggesting a specific embryonic function. Expression of
ICln
mRNA, in contrast, up-regulated continuously with development.
...
PMID:Chloride channels ClC-2 and ICln mRNA expression differs in renal epithelial ontogeny. 973 73
Kidney collecting-duct cells swell in response to changes in medulla osmolality caused by the transition from antidiuresis to diuresis. Regulatory volume decrease (RVD) mechanisms must be activated to face this hypotonic stress. In
Aquaporin-2
(
AQP2
)-expressing renal CD8 cells, hypotonicity decreased cell surface expression of
AQP2
and increased the amount of
AQP2
localized intracellularly, whereas the total amount of
AQP2
phosphorylated at ser-256 decreased. Analysis of cAMP dynamics using fluorescence resonance energy transfer (FRET) showed that hypotonicity causes a reduction of cAMP, consistent with a decrease in phospho-
AQP2
. Moreover, hypotonicity caused a profound actin reorganization, associated with the loss of stress fibers and formation of F-actin patches (microspikes) at the cell border. Those changes were regulated by the monomeric GTPase Cdc42. Interestingly, expression of the dominant-negative Cdc42 (N17-Cdc42) prevented the hypotonicity-induced microspike formation and the generation of Cl(-) currents. Hypotonicity also caused the relocation from the cytosol to the plasma membrane and increase in interaction with actin of
ICln
(nucleotide-sensitive chloride current protein), which is essential for the generation of ion currents activated during RVD. Together, the profound actin remodeling, internalization of
AQP2
and translocation of
ICln
to the plasma membrane during hypotonicity may contribute to RVD after cell swelling in renal medulla.
...
PMID:Hypotonicity induces aquaporin-2 internalization and cytosol-to-membrane translocation of ICln in renal cells. 1713 47
