Recent Citations
Vector Biolabs’ adenovirus/AAV products & services have been cited in over 1,000 peer-reviewed papers. You’ll find the most recent and notable of these publications here.
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Control of Feeding Behavior by Cerebral Ventricular Volume Transmission of Melanin-Concentrating Hormone
/in PUB-7150 Featured /by Haig DidizianClassical mechanisms through which brain-derived molecules influence behavior include neuronal synaptic communication and neuroendocrine signaling. Here we provide evidence for an alternative neural communication mechanism that is relevant for food intake control involving cerebroventricular volume transmission of the neuropeptide melanin-concentrating hormone (MCH). Results reveal that the cerebral ventricles receive input from approximately one-third of MCH-producing […]
Macrophage cells secrete factors including LRP1 that orchestrate the rejuvenation of bone repair in mice
/in PUB-7684 Featured /by Haig DidizianThe pace of repair declines with age and, while exposure to a young circulation can rejuvenate fracture repair, the cell types and factors responsible for rejuvenation are unknown. Here we report that young macrophage cells produce factors that promote osteoblast differentiation of old bone marrow stromal cells. Heterochronic parabiosis exploiting young mice in which macrophages […]
Amino Acid Restriction Triggers Angiogenesis via GCN2/ATF4 Regulation of VEGF and H2S Production
/in PUB-6922 Featured /by Haig DidizianAngiogenesis, the formation of new blood vessels by endothelial cells (ECs), is an adaptive response to oxygen/nutrient deprivation orchestrated by vascular endothelial growth factor (VEGF) upon ischemia or exercise. Hypoxia is the best-understood trigger of VEGF expression via the transcription factor HIF1a. Nutrient deprivation is inseparable from hypoxia during ischemia, yet its role in angiogenesis […]
Kir2 inward rectification–controlled precise and dynamic balances between Kir2 and HCN currents initiate pacemaking activity
/in PUB-6797 Featured /by Haig DidizianSpontaneous rhythmic action potential or pacemaking activity of pacemaker cells controls rhythmic signaling such as heartbeat. The mechanism underlying the origin of pacemaking activity is not well understood. In this study, we created human embryonic kidney (HEK) 293 cells that show pacemaking activity through heterologous expression of strong inward rectifier K+ channels (Kir2.1), hyperpolarization-activated cyclic […]
Autophagy maintains tumour growth through circulating arginine
/in PUB-7685 Featured /by Haig DidizianAutophagy captures intracellular components and delivers them to lysosomes, where they are degraded and recycled to sustain metabolism and to enable survival during starvation1,2,3,4,5. Acute, whole-body deletion of the essential autophagy gene Atg7 in adult mice causes a systemic metabolic defect that manifests as starvation intolerance and gradual loss of white adipose tissue, liver glycogen […]
PDGFRa+ pericryptal stromal cells are the critical source of Wnts and RSPO3 for murine intestinal stem cells in vivo
/in PUB-6923 Featured /by Haig DidizianWnts and R-spondins (RSPOs) support intestinal homeostasis by regulating crypt cell proliferation and differentiation. Ex vivo, Wnts secreted by Paneth cells in organoids can regulate the proliferation and differentiation of Lgr5-expressing intestinal stem cells. However, in vivo, Paneth cell and indeed all epithelial Wnt production is completely dispensable, and the cellular source of Wnts and […]
Bile diversion, a bariatric surgery, and bile acid signaling reduce central cocaine reward
/in PUB-7382 Featured /by Haig DidizianThe gut-to-brain axis exhibits significant control over motivated behavior. However, mechanisms supporting this communication are poorly understood. We reveal that a gut-based bariatric surgery chronically elevates systemic bile acids and attenuates cocaine-induced elevations in accumbal dopamine. Notably, this surgery reduces reward-related behavior and psychomotor sensitization to cocaine. Utilizing a knockout mouse model, we have determined […]
The protein kinase PERK/EIF2AK3 regulates proinsulin processing not via protein synthesis but by controlling endoplasmic reticulum chaperones
/in PUB-6862 Featured /by Haig DidizianLoss-of-function mutations of the protein kinase PERK (EIF2AK3) in humans and mice cause permanent neonatal diabetes and severe proinsulin aggregation in the endoplasmic reticulum (ER), highlighting the essential role of PERK in insulin production in pancreatic ß cells. As PERK is generally known as a translational regulator of the Unfolded Protein Response (UPR), the underlying […]