P Tate

The methyl-CpG binding protein MeCP2 is essential for embryonic development in the mouse

The major form of MeCP2 has a novel N-terminus generated by alternative splicing

Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl-CpG-binding protein 2

Genomic structure and chromosomal mapping of the murine and human Mbd1, Mbd2, Mbd3, and Mbd4 genes

The Story of Rett Syndrome: From Clinic to Neurobiology

Widespread Translational Remodeling during Human Neuronal Differentiation

DNA Methylation and Its Basic Function

Rett Syndrome and MeCP2: Linking Epigenetics and Neuronal Function

Complexities of Rett Syndrome and MeCP2: Figure 1.

Transcriptional repression by the methyl-CpG-binding protein MeCP2 involves a histone deacetylase complex

Epigenetic modifications and human disease

Mecp2-Null Mice Provide New Neuronal Targets for Rett Syndrome

Model of autism: increased ratio of excitation/inhibition in key neural systems

Alterations in DNA Methylation: A Fundamental Aspect of Neoplasia

Isolation, physical mapping, and Northern analysis of the X-linked human gene encoding methyl CpG-binding protein, MECP2

PARASITE-INDUCED CHANGES IN BEHAVIOR AND COLOR MAKEGAMMARUS PULEXMORE PRONE TO FISH PREDATION

Parasites: Small Players with Crucial Roles in the Ecological Theater

Mouse neurexin-1α deletion causes correlated electrophysiological and behavioral changes consistent with cognitive impairments

David Keilin, 1887-1963

The X-linked methylated DNA binding protein, Mecp2, is subject to X inactivation in the mouse

Genetic and Physical Mapping of a Gene Encoding a Methyl CpG Binding Protein, Mecp2, to the Mouse X Chromosome