Blood flow regulates acvrl1 transcription via ligand-dependent Alk1 activity.

Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant disease characterized by the development of arteriovenous malformations (AVMs) that can result in significant morbidity and mortality. HHT is caused primarily by mutations in bone morphogenetic protein receptors ACVRL1/ALK1, a signaling receptor, or endoglin (ENG), an accessory receptor. Because overexpression of Acvrl1 prevents AVM development in both Acvrl1 and Eng null mice, enhancing ACVRL1 expression may be a promising approach to development of targeted therapies for HHT.

Blood flow regulates transcription via ligand-dependent Alk1 activity.

Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant disease characterized by the development of arteriovenous malformations (AVMs) that can result in significant morbidity and mortality. HHT is caused primarily by mutations in bone morphogenetic protein receptors /ALK1, a signaling receptor, or endoglin (), an accessory receptor. Because overexpression of prevents AVM development in both and null mice, enhancing expression may be a promising approach to development of targeted therapies for HHT.

Transient disruption of mouse home cage activities and assessment of orexin immunoreactivity following concussive- or blast-induced brain injury.

The employment of explosive weaponry in modern warfare exposes populations to shock wave-induced and impact-related brain injuries. Among the most common clinical complaints resulting from traumatic brain injury (TBI) are sleep-wake disturbances. The current study assessed the acute effects of mild concussive brain injury (CBI) and mild blast wave-induced brain injury (BTBI) on mouse behavior and orexin-A expression.