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Loss of T cell control during persistent polyomavirus infection, in the setting of a limited antiviral antibody response, facilitates emergence of antibody-escape viruses carrying the potential for neurovirulence.

Genetics and genomics approaches reveal a conserved post-transcriptional regulatory mechanism that promotes adult axon regeneration from worm to mammals.

During mouse preimplantation development, the complete loss of actomyosin contractility abolishes cytokinesis but not apico-basal polarisation, lineage specification, or fluid accumulation, which are the critical steps to the formation of the blastocyst.

Impairing TDP-43 RNA-binding capacity through a single acetylation-mimic mutation alters TDP-43 function and recapitulates biochemical, molecular, and behavioral features of sporadic TDP-43 proteinopathies, thus providing opportunities for new research into pathogenic mechanisms and therapeutic interventions.

Spontaneous growth arrest of transformed melanocytes (resulting in benign “moles”) does not result from cell-autonomous oncogene-induced senescence, but can be explained by collective mechanisms used in normal tissue size control.

Proof of concept that viral vector-mediated gene transfer improves bladder function in a preclinical model of an inherited early-onset lower urinary tract disease.

In the SOD1^G93A mouse model of amyotrophic lateral sclerosis (ALS), expression of transmembrane signaling molecule ephrinB2 in spinal cord astrocytes contributes to motor neuron damage and loss of diaphragm function.

The first born excitatory cerebellar nuclei neurons influence the survival of their Purkinje cell partners which stimulate the expansion of granule cells and interneurons to produce functional local circuits.

A genetic screen in combination with biochemical approaches reveal hijacking of the host β-catenin destruction complex by the parasite T. gondii to reprogram immune gene expression.