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6 hasil untuk "Sara Bitam"

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  1. Artikel Jurnal

    In silico model of the human ClC-Kb chloride channel: pore mapping, biostructural pathology and drug screening

    Maxime Louet; Sara Bitam; Naziha Bakouh dkk.

    Scientific Reports, Vol. 7 No. 1 · 2017 · Inggris · DOAJ Scopus

    Abstract The human ClC-Kb channel plays a key role in exporting chloride ions from the cytosol and is known to be involved in Bartter syndrome type 3 when its permeation capacity is decreased. The ClC-Kb channel has been recently proposed as a potential therapeutic target to treat hypertension. In…

  2. Artikel Jurnal

    An unexpected effect of TNF-α on F508del-CFTR maturation and function [v2; ref status: indexed, http://f1000r.es/5tv]

    Sara Bitam; Iwona Pranke; Monika Hollenhorst dkk.

    F1000Research, Vol. 4 · 2015 · Inggris · DOAJ Scopus

    Cystic fibrosis (CF) is a multifactorial disease caused by mutations in the cystic fibrosis transmembrane conductance regulator gene (CFTR), which encodes a cAMP-dependent Cl- channel. The most frequent mutation, F508del, leads to the synthesis of a prematurely degraded, otherwise partially…

  3. Artikel Jurnal

    An unexpected effect of TNF-α on F508del-CFTR maturation and function [v1; ref status: indexed, http://f1000r.es/5jf]

    Sara Bitam; Iwona Pranke; Monika Hollenhorst dkk.

    F1000Research, Vol. 4 · 2015 · Inggris · DOAJ Scopus

    Cystic fibrosis (CF) is a multifactorial disease caused by mutations in the cystic fibrosis transmembrane conductance regulator gene (CFTR), which encodes a cAMP-dependent Cl- channel. The most frequent mutation, F508del, leads to the synthesis of a prematurely degraded, otherwise partially…

  4. Artikel Jurnal

    New insights into structure and function of bis-phosphinic acid derivatives and implications for CFTR modulation

    Sara Bitam; Ahmad Elbahnsi; Geordie Creste dkk.

    Scientific Reports, Vol. 11 No. 1 · 2021 · Inggris · DOAJ Scopus

    Abstract C407 is a compound that corrects the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) protein carrying the p.Phe508del (F508del) mutation. We investigated the corrector effect of c407 and its derivatives on F508del-CFTR protein. Molecular docking and dynamics simulations combined…

  5. Artikel Jurnal

    Discovery of novel potent ΔF508‐CFTR correctors that target the nucleotide binding domain

    Norbert Odolczyk; Janine Fritsch; Caroline Norez dkk.

    EMBO Molecular Medicine, Vol. 5 No. 10 · 2013 · Inggris · DOAJ Scopus

    Abstract The deletion of Phe508 (ΔF508) in the first nucleotide binding domain (NBD1) of CFTR is the most common mutation associated with cystic fibrosis. The ΔF508‐CFTR mutant is recognized as improperly folded and targeted for proteasomal degradation. Based on molecular dynamics simulation…