G. Mollet

发表

Computational identification of promoters and first exons in the human genome

Michael Q. Zhang, I. Grosse, R. Davuluri, 2001, Nature Genetics.

The gene mutated in juvenile nephronophthisis type 4 encodes a novel protein that interacts with nephrocystin

A. Nayır, G. Mollet, R. Salomon, 2002, Nature Genetics.

Determination of the genomic structure of the COL4A4 gene and of novel mutations causing autosomal recessive Alport syndrome.

G. Mollet, C. Antignac, C. Antignac, 1998, American journal of human genetics.

Structure of the human type IV collagen gene COL4A3 and mutations in autosomal Alport syndrome.

G. Mollet, C. Antignac, C. Antignac, 2001, Journal of the American Society of Nephrology : JASN.

Endoplasmic reticulum–retained podocin mutants are massively degraded by the proteasome

K. Tory, G. Mollet, C. Antignac, 2018, The Journal of Biological Chemistry.

Mutation-dependent recessive inheritance of NPHS2-associated steroid-resistant nephrotic syndrome

K. Tory, G. Mollet, O. Gribouval, 2014, Nature Genetics.

An inducible mouse model of podocin-mutation-related nephrotic syndrome

Michael J. Randles, G. Mollet, C. Antignac, 2017, PloS one.

Podocin inactivation in mature kidneys causes focal segmental glomerulosclerosis and nephrotic syndrome.

M. Dallman, G. Mollet, C. Antignac, 2009, Journal of the American Society of Nephrology : JASN.

Endoplasmic reticulum stress drives proteinuria-induced kidney lesions via Lipocalin 2

G. Mollet, C. Antignac, B. Knebelmann, 2016, Nature Communications.

Characterization of the nephrocystin/nephrocystin-4 complex and subcellular localization of nephrocystin-4 to primary cilia and centrosomes.

G. Mollet, R. Salomon, F. Silbermann, 2005, Human molecular genetics.

Increased lysosomal proteolysis counteracts protein accumulation in the proximal tubule during focal segmental glomerulosclerosis.

G. Mollet, C. Antignac, E. Christensen, 2013, Kidney international.

TBC1D8B Loss-of-Function Mutations Lead to X-Linked Nephrotic Syndrome via Defective Trafficking Pathways.

G. Mollet, O. Gribouval, C. Antignac, 2019, American journal of human genetics.

Loss-of-Function Mutations Lead to X-Linked Nephrotic Syndrome

Agnieszka, G. Mollet, O. Gribouval, 2018 .

Mutations in the evolutionarily highly conserved KEOPS complex genes cause nephrotic syndrome with microcephaly

Annapurna, Wierenga, E. Roeder, 2018 .

Abolishment of proximal tubule albumin endocytosis does not affect plasma albumin during nephrotic syndrome in mice.

G. Mollet, C. Antignac, E. Christensen, 2017, Kidney international.

A slit-diaphragm-associated protein network for dynamic control of renal filtration

A. Köttgen, B. Fakler, O. Kretz, 2022, Nature Communications.

C-terminal oligomerization of podocin mediates interallelic interactions

K. Tory, G. Mollet, Eszter Balogh, 2019 .

C-terminal oligomerization of podocin mediates interallelic interactions.

K. Tory, G. Mollet, C. Antignac, 2018, Biochimica et biophysica acta. Molecular basis of disease.

NPHS2 Mutations in Steroid‐Resistant Nephrotic Syndrome: A Mutation Update and the Associated Phenotypic Spectrum

A. Mégarbané, K. Dahan, G. Mollet, 2014, Human mutation.

Podocyte Purinergic P2X4 Channels Are Mechanotransducers That Mediate Cytoskeletal Disorganization.

T. Gudermann, G. Mollet, F. Schaefer, 2016, Journal of the American Society of Nephrology : JASN.

Urokinase‐type plasminogen activator contributes to amiloride‐sensitive sodium retention in nephrotic range glomerular proteinuria in mice

G. Mollet, C. Antignac, H. Birn, 2019, Acta physiologica.

A homozygous KAT2B variant modulates the clinical phenotype of ADD3 deficiency in humans and flies

R. Bodmer, A. Afenjar, G. Mollet, 2018, PLoS genetics.

A homozygous missense mutation in the ciliary gene TTC21B causes familial FSGS.

G. Mollet, O. Gribouval, F. Silbermann, 2014, Journal of the American Society of Nephrology : JASN.

Pseudouridylation defect due to DKC1 and NOP10 mutations causes nephrotic syndrome with cataracts, hearing impairment, and enterocolitis

H. Williams, D. Curtis, K. Tory, 2020, Proceedings of the National Academy of Sciences.

Loss-of-function mutations in WDR73 are responsible for microcephaly and steroid-resistant nephrotic syndrome: Galloway-Mowat syndrome.

N. Boddaert, G. Mollet, O. Gribouval, 2014, American Journal of Human Genetics.

Disruption of pathways regulated by Integrator complex in Galloway–Mowat syndrome due to WDR73 mutations

G. Mollet, C. Antignac, C. Bole-Feysot, 2021, Scientific Reports.

Sodium retention by uPA‐plasmin‐ENaC in nephrotic syndrome—Authors reply

G. Mollet, C. Antignac, H. Birn, 2019, Acta Physiologica.

Cathepsin B increases ENaC activity leading to hypertension early in nephrotic syndrome

G. Mollet, O. Schilling, A. Alli, 2019, Journal of cellular and molecular medicine.

Mutations in INF2 are a major cause of autosomal dominant focal segmental glomerulosclerosis.

G. Mollet, O. Gribouval, C. Antignac, 2011, Journal of the American Society of Nephrology : JASN.

Maternal environment interacts with modifier genes to influence progression of nephrotic syndrome.

M. Kretzler, G. Mollet, C. Antignac, 2008, Journal of the American Society of Nephrology : JASN.

Neurological involvement in monogenic podocytopathies

G. Mollet, O. Boyer, G. Dorval, 2021, Pediatric Nephrology.

Defects in t6A tRNA modification due to GON7 and YRDC mutations lead to Galloway-Mowat syndrome

N. Boddaert, D. Magen, P. Revy, 2019, Nature Communications.

Mutations in KEOPS-complex genes cause nephrotic syndrome with primary microcephaly

Jeremy F. P. Ullmann, Sebastian A. Leidel, E. Roeder, 2017, Nature Genetics.

INF2 mutations in Charcot-Marie-Tooth disease with glomerulopathy.

G. Mollet, O. Gribouval, C. Antignac, 2011, The New England journal of medicine.

Generation of an induced pluripotent stem cell (iPSC) line (IMAGINi007) from a patient with steroid-resistant nephrotic syndrome carrying the homozygous p.R138Q mutation in the podocin-encoding NPHS2 gene.

G. Mollet, C. Antignac, N. Lefort, 2020, Stem cell research.

The gene mutated in juvenile nephronophthisis type 4 encodes a novel protein that interacts with nephrocystin

A. Nayır, G. Mollet, R. Salomon, 2002, Nature Genetics.

Literature Abstracts

G. Mollet, M. Gubler, L. Forestier, 2001, Pediatric Nephrology.

Podocyte Purinergic P2X4 Channels Are Mechanotransducers That Mediate Cytoskeletal Disorganization.

T. Gudermann, G. Mollet, F. Schaefer, 2016, Journal of the American Society of Nephrology : JASN.

Podocin inactivation in mature kidneys causes focal segmental glomerulosclerosis and nephrotic syndrome.

M. Dallman, G. Mollet, C. Antignac, 2009, Journal of the American Society of Nephrology : JASN.

Adeno-associated virus gene therapy prevents progression of kidney disease in genetic models of nephrotic syndrome

Colin J. Chu, G. Mollet, C. Antignac, 2023, Science Translational Medicine.

Literature Abstracts

G. Mollet, L. Heidet, C. Arrondel, 2001, Pediatric Nephrology.