3D bioprinted neural scaffolds: a transformative avenue for GM2 gangliosidosis therapy.
Confidence:
0.21
· 7 полей извлечено
Идентификация (6 полей)
Механизм действия (21 полей)
Mechanism
—
0.00
Mutations (obesity/lean)
MC4R mutation with defective Gq/11α signaling; FGFR1 deletion in AgRP neurons; mutations disrupting hunger, energy balance, fat storage; MC4R and ADCY3 subcellular localization at neuronal primary cilia
0.90
Activity (obesity)
—
0.00
Activity temporal
—
0.00
Energy balance
FGFR1 in AgRP neurons impairs energy homeostasis; MC4R mutation leads to hyperphagia; obesity-related genetic disorders disrupt energy balance
0.90
Appetite
MC4R mutation leads to hyperphagia; obesity-related genetic disorders disrupt hunger regulation
0.90
Fat metabolism
obesity-related genetic disorders disrupt fat storage
0.70
Lipolysis
—
0.00
Thermogenesis
—
0.00
Muscle metabolism
—
0.00
Inflammation
—
0.00
Glucose metabolism
—
0.00
AA metabolism
—
0.00
Hormonal pathways
MC4R mutation with defective Gq/11α signaling
0.80
Cell death
—
0.00
Adipocyte fibrosis
—
0.00
Upstream (biochem)
—
0.00
Upstream (physiol)
—
0.00
Downstream (biochem)
—
0.00
Downstream (physiol)
—
0.00
PTMs
—
0.00
Экспрессия (8 полей)
Tissue expression
—
0.00
In vitro
neuron-laden agarose-laminin hydrogel; 3D bioprinted retinal Müller cells
0.90
In vivo
—
0.00
In silico
—
0.00
Genetic association
—
0.00
Ex vivo
—
0.00
Animal model
mouse model of juvenile neuronal ceroid lipofuscinosis
0.90
Diet/model
—
0.00