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Myelin-associated inhibitors and chondroitin sulfate proteoglycans are not the primary mechanism stopping sensory axons regenerating into the spinal cord, although their removal can markedly enhance regeneration when combined with an intervention that elevates axon growth capacity sufficiently robustly.

A panel of seven new mouse strains with chromosomal duplications is used to identify a minimal genetic region required in three copies to cause congenital heart defects typical of human Down syndrome.

SLC7A8 a neutral amino acid transporter has a key role in the maintenance of hearing during aging and its absence causes early onset of hearing loss.

Combined evidence of human genetics, in vitro cardiomyocyte differentiation, and mouse model indicates that SORBS2 is a regulator of second heart field development and its deficiency causes seemingly opposite atrial septal defects.

A novel DUB-regulated mechanism controls polarized axon growth and guidance.

Mouse in vivo and in vitro analysis and human genetic screening highlight the role of anti-Müllerian hormone (AMH) signaling in GnRH neuronal development and function, and identify mutations in AMH and AMHR2 in CHH patients.

Identified as a binding factor of transcription factor MYRF, the LRR-TM protein PAN-1 promotes the cell-membrane localization and nuclear translocation of MYRF, which drives synaptic rewiring in Caenorhabditis elegans.

Zebrafish knockouts can be generated in a few hours directly from wild-type eggs and are suitable for studying continuous traits, including behaviour.

Within populations, there is standing variation in paralog expression levels, paralog expression levels are heritable, and variation in paralog expression can modify the phenotypes associated with mutation of one of the paralogs.

Quantification of fluorescently labeled mRNAs reveals that Fgf4 regulates Notch oscillations in the segmentation clock that controls somitogenesis.