Damien Lederer

Histone demethylase KDM6A directly senses oxygen to control chromatin and cell fate

The EGLN-HIF O 2 -Sensing System: Multiple Inputs and Feedbacks

Biomolecular condensates: organizers of cellular biochemistry

The molecular hallmarks of epigenetic control

Histone lysine demethylases as targets for anticancer therapy

Hallmarks of aging: An expanding universe

Phase Transition in Postsynaptic Densities Underlies Formation of Synaptic Complexes and Synaptic Plasticity

Single-cell transcriptomic analysis of Alzheimer’s disease

Modulating the integrated stress response to slow aging and ameliorate age-related pathology

Epigenetics and Human Disease

What is new in CDG?

Glycoproteomics

Loss ofCntnap2Causes Axonal Excitability Deficits, Developmental Delay in Cortical Myelination, and Abnormal Stereotyped Motor Behavior

Betti reaction enables efficient synthesis of 8-hydroxyquinoline inhibitors of 2-oxoglutarate oxygenases

Epigenetic Regulation by Histone Demethylases in Hypoxia

Chromatin and oxygen sensing in the context of JmjC histone demethylases

Congenital Disorders of Glycosylation from a Neurological Perspective

Investigating the functional link between TMEM165 and SPCA1

Liquid phase condensation in cell physiology and disease

Two novel EIF2S3 mutations associated with syndromic intellectual disability with severe microcephaly, growth retardation, and epilepsy

Deletion of KDM6A, a Histone Demethylase Interacting with MLL2, in Three Patients with Kabuki Syndrome

Novel KDM6A (UTX) mutations and a clinical and molecular review of the X‐linked Kabuki syndrome (KS2)

Eight further individuals with intellectual disability and epilepsy carrying bi-allelic CNTNAP2 aberrations allow delineation of the mutational and phenotypic spectrum

RFT1‐congenital disorder of glycosylation (CDG) syndrome: a cause of early‐onset severe epilepsy

Two novel EIF2S3 mutations associated with syndromic intellectual disability with severe microcephaly, growth retardation, and epilepsy

De novo, heterozygous, loss‐of‐function mutations in SYNGAP1 cause a syndromic form of intellectual disability