Annette Schenck

Restoring polyamines protects from age-induced memory impairment in an autophagy-dependent manner.

Novel features of dFMR1, the Drosophila orthologue of the fragile X mental retardation protein.

Transcriptional regulation of glial cell specification.

CYFIP/Sra-1 controls neuronal connectivity in Drosophila and links the Rac1 GTPase pathway to the fragile X protein.

82-FIP, a novel FMRP (fragile X mental retardation protein) interacting protein, shows a cell cycle-dependent intracellular localization.

NUFIP1 (nuclear FMRP interacting protein 1) is a nucleocytoplasmic shuttling protein associated with active synaptoneurosomes.

CYFIP2 is highly abundant in CD4+ cells from multiple sclerosis patients and is involved in T cell adhesion.

WAVE/SCAR, a multifunctional complex coordinating different aspects of neuronal connectivity.

FMRP interferes with the Rac1 pathway and controls actin cytoskeleton dynamics in murine fibroblasts.

Phosphorylation of WAVE1 regulates actin polymerization and dendritic spine morphology.

HSPC300 and its role in neuronal connectivity.

The endosomal protein Appl1 mediates Akt substrate specificity and cell survival in vertebrate development.

SLC29A3 gene is mutated in pigmented hypertrichosis with insulin-dependent diabetes mellitus syndrome and interacts with the insulin signaling pathway.

CNTNAP2 and NRXN1 are mutated in autosomal-recessive Pitt-Hopkins-like mental retardation and determine the level of a common synaptic protein in Drosophila.

Protein complexes containing CYFIP/Sra/PIR121 coordinate Arf1 and Rac1 signalling during clathrin-AP-1-coated carrier biogenesis at the TGN.

CDK19 is disrupted in a female patient with bilateral congenital retinal folds, microcephaly and mild mental retardation.

Epigenetic regulation of learning and memory by Drosophila EHMT/G9a.

CYFIP dependent actin remodeling controls specific aspects of Drosophila eye morphogenesis.

Mutations in the chromatin modifier gene KANSL1 cause the 17q21.31 microdeletion syndrome.

Analysis of adhesion molecules and basement membrane contributions to synaptic adhesion at the Drosophila embryonic NMJ.

Disruption of an EHMT1-associated chromatin-modification module causes intellectual disability.

Range of genetic mutations associated with severe non-syndromic sporadic intellectual disability: an exome sequencing study.

Mutations in DDHD2, encoding an intracellular phospholipase A(1), cause a recessive form of complex hereditary spastic paraplegia.

Homozygous and heterozygous disruptions of ANK3: at the crossroads of neurodevelopmental and psychiatric disorders.

CEP89 is required for mitochondrial metabolism and neuronal function in man and fly.

GATAD2B loss-of-function mutations cause a recognisable syndrome with intellectual disability and are associated with learning deficits and synaptic undergrowth in Drosophila.

Human intellectual disability genes form conserved functional modules in Drosophila.

Ubiquitin ligase HUWE1 regulates axon branching through the Wnt/β-catenin pathway in a Drosophila model for intellectual disability.

The genetics of cognitive epigenetics.

Drosophila models of early onset cognitive disorders and their clinical applications.

Genome sequencing identifies major causes of severe intellectual disability.

Altered GPM6A/M6 dosage impairs cognition and causes phenotypes responsive to cholesterol in human and Drosophila.

Mitochondrial diseases: Drosophila melanogaster as a model to evaluate potential therapeutics.

The epigenetic regulator G9a mediates tolerance to RNA virus infection in Drosophila.

Converging evidence does not support GIT1 as an ADHD risk gene.

Conditional depletion of intellectual disability and Parkinsonism candidate gene ATP6AP2 in fly and mouse induces cognitive impairment and neurodegeneration.

Systematic Phenomics Analysis Deconvolutes Genes Mutated in Intellectual Disability into Biologically Coherent Modules.

De novo loss-of-function mutations in WAC cause a recognizable intellectual disability syndrome and learning deficits in Drosophila.

Disruption of POGZ Is Associated with Intellectual Disability and Autism Spectrum Disorders.

A New Fiji-Based Algorithm That Systematically Quantifies Nine Synaptic Parameters Provides Insights into Drosophila NMJ Morphometry.

BOD1 Is Required for Cognitive Function in Humans and Drosophila.

A homozygous FITM2 mutation causes a deafness-dystonia syndrome with motor regression and signs of ichthyosis and sensory neuropathy.

Targeted sequencing identifies 91 neurodevelopmental-disorder risk genes with autism and developmental-disability biases.