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pseudohypoaldosteronism/protease
Saite tiek saglabāta starpliktuvē
10 rezultātiem
Pseudohypoaldosteronism type 1 and the genes encoding prostasin, alpha-spectrin, and Nedd4.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Pseudohypoaldosteronism type 1 (PHA1), a rare disorder of infancy, presents with potential life-threatening salt wasting and failure to thrive. Thus far, PHA1 has been attributed to mutations affecting the mineralocorticoid receptor or any of the three subunits assembling the amiloride-sensitive
The epithelial sodium channel: activation by membrane-bound serine proteases.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
The epithelial sodium channel (ENaC) was cloned just 10 years ago. Since that time, the study of human monogenic diseases (pseudohypoaldosteronism type 1 [PHA-1] and Liddle syndrome), as well as mouse models mimicking salt-losing syndromes (PHA-1) or salt-sensitive hypertension (Liddle syndrome),
No evidence of hearing loss in pseudohypoaldosteronism type 1 patients.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
CONCLUSIONS
The fact that pseudohypoaldosteronism type 1 (PHA-1) patients with a defect in the alpha subunit of epithelial sodium channels (ENaC) in the cochlea have normal hearing suggests compensation by alternative sodium transport mechanisms. Consequently, hearing loss due to defective cochlear
Activation of the epithelial sodium channel (ENaC) by serine proteases.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
The study of human monogenic diseases [pseudohypoaldosteronism type 1 (PHA-1) and Liddle's syndrome] as well as mouse models mimicking the salt-losing syndrome (PHA-1) or salt-sensitive hypertension (Liddle's syndrome) have established the epithelial sodium channel ENaC as a limiting factor in vivo
Paracellular transport in the collecting duct.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
The paracellular pathway through the tight junction provides an important route for chloride reabsorption in the collecting duct of the kidney. This review describes recent findings of how defects in paracellular chloride permeation pathway may cause kidney diseases and how such a pathway may be
Cell surface expression and biosynthesis of epithelial Na+ channels.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
The epithelial Na+ channel (ENaC) complex is composed of three homologous subunits: alpha, beta and gamma. Mutations in ENaC subunits can increase the number of channels on the cell surface, causing a hereditary form of hypertension called Liddle's syndrome, or can decrease channel activity, causing
Small molecule activator of the human epithelial sodium channel.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
The epithelial sodium channel (ENaC), a heterotrimeric complex composed of alpha, beta, and gamma subunits, belongs to the ENaC/degenerin family of ion channels and forms the principal route for apical Na(+) entry in many reabsorbing epithelia. Although high affinity ENaC blockers, including
Regulation of the epithelial sodium channel by accessory proteins.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
The epithelial sodium channel (ENaC) is of fundamental importance in the control of sodium fluxes in epithelial cells. Modulation of sodium reabsorption through the distal nephron ENaC is an important component in the overall control of sodium balance, blood volume and thereby of blood pressure.
Urinary extracellular vesicles as markers to assess kidney sodium transport.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
OBJECTIVE
This article summarizes studies that have analyzed sodium transporters in urinary extracellular vesicles (uEVs) in relation to hypertension.
RESULTS
The majority of kidney sodium transporters are detectable in uEVs. Patients with loss or gain of function mutations in sodium transporter
Colon-specific deletion of epithelial sodium channel causes sodium loss and aldosterone resistance.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Aldosterone promotes electrogenic sodium reabsorption through the amiloride-sensitive epithelial sodium channel (ENaC). Here, we investigated the importance of ENaC and its positive regulator channel-activating protease 1 (CAP1/Prss8) in colon. Mice lacking the αENaC subunit in colonic superficial
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