Mairead Kelly
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View article: Beyond Trikafta: new models to assess tissue dependent rescue of N1303K-CFTR
Beyond Trikafta: new models to assess tissue dependent rescue of N1303K-CFTR Open
Rationale Respiratory status of people with Cystic Fibrosis (pwCF) carrying N1303K is improved by Elexacaftor/Tezacaftor/Ivacaftor (ETI) but, contrary to other mutations, the impact on sweat test results is limited. Methods To explore this…
View article: Short-term modification of breathprint by Elexacaftor/Tezacaftor/Ivacaftor in a paediatric cohort
Short-term modification of breathprint by Elexacaftor/Tezacaftor/Ivacaftor in a paediatric cohort Open
View article: Elexacaftor-Tezacaftor-Ivacaftor Reduces Bronchial Dilatations in Adolescents with Cystic Fibrosis
Elexacaftor-Tezacaftor-Ivacaftor Reduces Bronchial Dilatations in Adolescents with Cystic Fibrosis Open
View article: From CFTR to a CF signalling network: a systems biology approach to study Cystic Fibrosis
From CFTR to a CF signalling network: a systems biology approach to study Cystic Fibrosis Open
BACKGROUND: Cystic Fibrosis (CF) is a monogenic disease caused by mutations in the gene coding the Cystic Fibrosis Transmembrane Regulator (CFTR) protein, but its overall physio-pathology cannot be solely explained by the loss of the CFTR …
View article: Beta-adrenergic sweat test in challenging cystic fibrosis diagnosis.
Beta-adrenergic sweat test in challenging cystic fibrosis diagnosis. Open
View article: Prime editing functionally corrects cystic fibrosis-causing CFTR mutations in human organoids and airway epithelial cells
Prime editing functionally corrects cystic fibrosis-causing CFTR mutations in human organoids and airway epithelial cells Open
Prime editing is a recent, CRISPR-derived genome editing technology capable of introducing precise nucleotide substitutions, insertions, and deletions. Here, we present prime editing approaches to correct L227R- and N1303K-CFTR, two mutati…
View article: Beyond Kaftrio : mechanistic insights to maximize N1303K-CFTR rescue
Beyond Kaftrio : mechanistic insights to maximize N1303K-CFTR rescue Open
Introduction N1303K is the fourth most frequent Cystic Fibrosis (CF) causing mutation. People with CF (pwCF) clinical status can be improved by Elexacaftor(ELX)/Tezacaftor(TEZ)/Ivacaftor (ETI) combotherapy. We investigated the mechanism un…
View article: Mitochondrial dynamics and metabolic regulation control T cell fate in the thymus
Mitochondrial dynamics and metabolic regulation control T cell fate in the thymus Open
Several studies demonstrated that mitochondrial dynamics and metabolic pathways control T cell fate in the periphery. However, little is known about their implication in thymocyte development. Our results showed that thymic progenitors (CD…
View article: Putting bicarbonate on the spot: pharmacological insights for CFTR correction in the airway epithelium
Putting bicarbonate on the spot: pharmacological insights for CFTR correction in the airway epithelium Open
Introduction: Cystic fibrosis (CF) is caused by defective Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) proteins. CFTR controls chloride (Cl − ) and bicarbonate (HCO 3 − ) transport into the Airway Surface Liquid (ASL). We inv…
View article: From CFTR to a CF signalling network: a systems biology approach to study Cystic Fibrosis
From CFTR to a CF signalling network: a systems biology approach to study Cystic Fibrosis Open
Background Cystic Fibrosis (CF) is a monogenic disease caused by mutations in the gene coding the Cystic Fibrosis Transmembrane Regulator (CFTR) protein, but its overall physio-pathology cannot be solely explained by the loss of the CFTR c…
View article: mTOR inhibition suppresses salinomycin-induced ferroptosis in breast cancer stem cells by ironing out mitochondrial dysfunctions
mTOR inhibition suppresses salinomycin-induced ferroptosis in breast cancer stem cells by ironing out mitochondrial dysfunctions Open
View article: Putting Bicarbonate on the spot. Implication for theratyping in Cystic Fibrosis
Putting Bicarbonate on the spot. Implication for theratyping in Cystic Fibrosis Open
Cystic fibrosis (CF) is caused by defective Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) protein. CFTR controls chloride (Cl - ) and bicarbonate (HCO 3 - ) transport into the Airway Surface Liquid (ASL).We investigated the im…
View article: WS04.04 CFTR modulator triple combination treatment modifies exhaled breath of children with cystic fibrosis within a week
WS04.04 CFTR modulator triple combination treatment modifies exhaled breath of children with cystic fibrosis within a week Open
View article: mTOR Inhibition Suppresses Salinomycin-Induced Ferroptosis in Breast Cancer Stem Cells by Ironing Out Mitochondrial Dysfunctions
mTOR Inhibition Suppresses Salinomycin-Induced Ferroptosis in Breast Cancer Stem Cells by Ironing Out Mitochondrial Dysfunctions Open
Ferroptosis constitutes a promising therapeutic strategy against cancer by efficiently targeting the highly tumorigenic and treatment-resistant cancer stem cells (CSCs). We previously showed that the lysosomal iron-targeting drug Salinomyc…
View article: Proteomic Profiling of Sweat in Patients with Cystic Fibrosis Provides New Insights into Epidermal Homoeostasis
Proteomic Profiling of Sweat in Patients with Cystic Fibrosis Provides New Insights into Epidermal Homoeostasis Open
Background A high proportion of patients with Cystic Fibrosis (CF) also present the rare skin disease aquagenic palmoplantar keratoderma. A possible link between this condition and absence of a functional CF Transmembrane conductance Regul…
View article: Profiling the response to lumacaftor‐ivacaftor in children with cystic between fibrosis and new insight from a French‐Italian real‐life cohort
Profiling the response to lumacaftor‐ivacaftor in children with cystic between fibrosis and new insight from a French‐Italian real‐life cohort Open
Introduction Clinical trials for CFTR modulators consider mean changes of clinical status at the cohort level, and thus fail to assess the heterogeneity of the response. We aimed to study the different response profiles to lumacaftor‐ivaca…
View article: Melanoma exosomes are taken up by normal melanocytes and conferred invasion ability on normal melanocytes.
Melanoma exosomes are taken up by normal melanocytes and conferred invasion ability on normal melanocytes. Open
(A) HEMa-LP cells and A375 exosomes were labeled using the green fluorescent dye PKH67 and the red fluorescent dye PKH26 respectively. After incubating the labeled A375 exosomes with HEMa-LP cells for 24 h, confocal microscopy image…