Claude Ferec

Professor of Genetic, MD

Université de Bretagne Occidentale

France

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About

Claude Ferec is a Professor of Genetics at Université de Bretagne Occidentale in France. His research primarily focuses on genetic disorders, particularly cystic fibrosis and the regulation of the CFTR gene. Recent studies include the investigation of iron export mechanisms in ferroportin and the implications of gene dosage on pancreatitis risk. He also explores the interplay between the unfolded protein response and inflammation in cystic fibrosis.

Articles (15)

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2025

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2021

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2020

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2020

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2020

Collaborators (4)

cedric le marechal

Professor

Université de Bretagne Occidentale

FRANCE

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David N. Cooper

Professor of Human Molecular Genetics

Cardiff University School of Medicine

UNITED KINGDOM

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Tristan Montier

Université de Bretagne Occidentale

FRANCE

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Isabelle Callebaut

Sorbonne Université

FRANCE

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Claude Ferec

Research Interests

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Articles (15)

Identification of New Key Players for Ferrous Iron Export in the Asymmetric Inner Gate of Human Ferroportin 1

Cis-Regulation of the CFTR Gene in Pancreatic Cells

p.Phe508del-CFTR Trafficking: A Protein Quality Control Perspective Through UPR, UPS, and Autophagy

The Inhibition of the Membrane-Bound Transcription Factor Site-1 Protease (MBTP1) Alleviates the p.Phe508del-Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Defects in Cystic Fibrosis Cells

Cystic Fibrosis: A Journey through Time and Hope

Tissue-Specific Regulation of CFTR Gene Expression

Trypsinogen (PRSS1 and PRSS2) gene dosage correlates with pancreatitis risk across genetic and transgenic studies: a systematic review and re-analysis

The novel c.634+4A>G splicing variant in RHCE results in weak C and e antigen expression in a pregnant woman originated from Japan

The Interplay between the Unfolded Protein Response, Inflammation and Infection in Cystic Fibrosis

Missense RHD single nucleotide variants induce weakened D antigen expression by altering splicing and/or protein expression

Nation‐wide investigation of RHD variants in Thai blood donors: Impact for molecular diagnostics

The corrected breakpoint sequence of the homozygous SPINK1 deletion causing severe infantile isolated exocrine pancreatic insufficiency

Pathogenic and likely pathogenic variants in at least five genes account for approximately 3% of mild isolated nonsyndromic thrombocytopenia

5′ splice site GC>GT and GT>GC variants differ markedly in terms of their functionality and pathogenicity

Variants That Affect Function of Calcium Channel TRPV6 Are Associated With Early-Onset Chronic Pancreatitis

Collaborators (4)

cedric le marechal

David N. Cooper

Tristan Montier

Isabelle Callebaut

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