Lista de obras - Silke Haerteis - Dominio Público Uruguay

A mutation in the β-subunit of ENaC identified in a patient with cystic fibrosis-like symptoms has a gain-of-function effect

artículo científico publicado en 2012

Activation of the Human Epithelial Sodium Channel (ENaC) by Bile Acids Involves the Degenerin Site

artículo científico publicado en 2016

An inhibitory peptide derived from the α-subunit of the epithelial sodium channel (ENaC) shows a helical conformation

artículo científico publicado en 2012

Atomic force microscopy imaging reveals the formation of ASIC/ENaC cross-clade ion channels.

artículo científico publicado en 2015

Atomic force microscopy reveals the architecture of the epithelial sodium channel (ENaC)

scientific journal article

Bile acids inhibit human purinergic receptor P2X4 in a heterologous expression system

scientific article published on 15 April 2019

Cathepsin S causes inflammatory pain via biased agonism of PAR2 and TRPV4.

artículo científico publicado en 2014

Cathepsin S causes inflammatory pain via biased agonism of PAR2 and TRPV4.

artículo científico publicado en 2014

Cholesterol depletion of the plasma membrane prevents activation of the epithelial sodium channel (ENaC) by SGK1.

artículo científico publicado en 2009

Demonstration of proteolytic activation of the epithelial sodium channel (ENaC) by combining current measurements with detection of cleavage fragments

artículo científico publicado en 2014

Four subunits (αβγδ) of the epithelial sodium channel (ENaC) are expressed in the human eye in various locations.

artículo científico publicado en 2012

Functional characterization of a partial loss-of-function mutation of the epithelial sodium channel (ENaC) associated with atypical cystic fibrosis

artículo científico publicado en 2009

Ion channels in sarcoma: pathophysiology and treatment options

scientific article published on 03 August 2019

Neutrophil Elastase Activates Protease-activated Receptor-2 (PAR2) and Transient Receptor Potential Vanilloid 4 (TRPV4) to Cause Inflammation and Pain.

artículo científico publicado en 2015

Pharmacological and electrophysiological characterization of the human bile acid-sensitive ion channel (hBASIC).

artículo científico publicado en 2013

Plasmin and chymotrypsin have distinct preferences for channel activating cleavage sites in the γ subunit of the human epithelial sodium channel.

artículo científico publicado en 2012

Plasmin in nephrotic urine activates the epithelial sodium channel

artículo científico publicado en 2008

Proteolytic activation of the human epithelial sodium channel by trypsin IV and trypsin I involves distinct cleavage sites.

artículo científico publicado en 2014

Sensitisation of TRPV4 by PAR2 is independent of intracellular calcium signalling and can be mediated by the biased agonist neutrophil elastase

artículo científico publicado en 2014

The Chorioallantoic Membrane Model: A 3D in vivo Testbed for Design and Analysis of MC Systems

scientific article published on 20 October 2024

The bile acid receptor TGR5 activates the TRPA1 channel to induce itch in mice.

artículo científico publicado en 2014

The degenerin region of the human bile acid-sensitive ion channel (BASIC) is involved in channel inhibition by calcium and activation by bile acids.

artículo científico publicado en 2018

Lista de obras de Silke Haerteis

A mutation in the β-subunit of ENaC identified in a patient with cystic fibrosis-like symptoms has a gain-of-function effect

Activation of the Human Epithelial Sodium Channel (ENaC) by Bile Acids Involves the Degenerin Site

An inhibitory peptide derived from the α-subunit of the epithelial sodium channel (ENaC) shows a helical conformation

Atomic force microscopy imaging reveals the formation of ASIC/ENaC cross-clade ion channels.

Atomic force microscopy reveals the architecture of the epithelial sodium channel (ENaC)

Bile acids inhibit human purinergic receptor P2X4 in a heterologous expression system

Cathepsin S causes inflammatory pain via biased agonism of PAR2 and TRPV4.

Cathepsin S causes inflammatory pain via biased agonism of PAR2 and TRPV4.

Cholesterol depletion of the plasma membrane prevents activation of the epithelial sodium channel (ENaC) by SGK1.

Demonstration of proteolytic activation of the epithelial sodium channel (ENaC) by combining current measurements with detection of cleavage fragments

Four subunits (αβγδ) of the epithelial sodium channel (ENaC) are expressed in the human eye in various locations.

Functional characterization of a partial loss-of-function mutation of the epithelial sodium channel (ENaC) associated with atypical cystic fibrosis

Ion channels in sarcoma: pathophysiology and treatment options

Neutrophil Elastase Activates Protease-activated Receptor-2 (PAR2) and Transient Receptor Potential Vanilloid 4 (TRPV4) to Cause Inflammation and Pain.

Pharmacological and electrophysiological characterization of the human bile acid-sensitive ion channel (hBASIC).

Plasmin and chymotrypsin have distinct preferences for channel activating cleavage sites in the γ subunit of the human epithelial sodium channel.

Plasmin in nephrotic urine activates the epithelial sodium channel

Proteolytic activation of the human epithelial sodium channel by trypsin IV and trypsin I involves distinct cleavage sites.

Sensitisation of TRPV4 by PAR2 is independent of intracellular calcium signalling and can be mediated by the biased agonist neutrophil elastase

The Chorioallantoic Membrane Model: A 3D in vivo Testbed for Design and Analysis of MC Systems

The bile acid receptor TGR5 activates the TRPA1 channel to induce itch in mice.

The degenerin region of the human bile acid-sensitive ion channel (BASIC) is involved in channel inhibition by calcium and activation by bile acids.