Inhibitors | Comment | Organism | Structure |
---|---|---|---|
GI254023X | - |
Mus musculus |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
amyloid precursor protein + H2O | Mus musculus | ADAM10 plays a central role in the developing brain by controlling mainly Notch-dependent pathways but likely also by reducing surface shedding of other neuronal membrane proteins including amyloid precursor protein | ? | - |
? | |
beta-amyloid precursor protein + H2O | Mus musculus | - |
? | - |
? | |
Notch1 + H2O | Mus musculus | ADAM10 plays a central role in the developing brain by controlling mainly Notch-dependent pathways but likely also by reducing surface shedding of other neuronal membrane proteins including amyloid precursor protein | ? | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
brain | - |
Mus musculus | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
amyloid precursor protein + H2O | - |
Mus musculus | ? | - |
? | |
amyloid precursor protein + H2O | ADAM10 plays a central role in the developing brain by controlling mainly Notch-dependent pathways but likely also by reducing surface shedding of other neuronal membrane proteins including amyloid precursor protein | Mus musculus | ? | - |
? | |
beta-amyloid precursor protein + H2O | - |
Mus musculus | ? | - |
? | |
Notch1 + H2O | - |
Mus musculus | ? | - |
? | |
Notch1 + H2O | ADAM10 plays a central role in the developing brain by controlling mainly Notch-dependent pathways but likely also by reducing surface shedding of other neuronal membrane proteins including amyloid precursor protein | Mus musculus | ? | - |
? |
Synonyms | Comment | Organism |
---|---|---|
ADAM10 | - |
Mus musculus |
ADAM10 | alpha-secretase | Mus musculus |
General Information | Comment | Organism |
---|---|---|
malfunction | Adam10-/- mice die at embryonic day 9.5, due to major defects in development of somites and vasculogenesis. Generation of Adam10 conditional knock-out (cKO) mice using a Nestin-Cre promotor, limiting ADAM10 inactivation to neural progenitor cells (NPCs) and NPC-derived neurons and glial cells. The cKO mice die perinatally with a disrupted neocortex and a severely reduced ganglionic eminence, due to precocious neuronal differentiation resulting in an early depletion of progenitor cells. Premature neuronal differentiation is associated with aberrant neuronal migration and a disorganized laminar architecture in the neocortex. Neurospheres derived from Adam10 cKO mice have a disrupted sphere organization and segregated more neurons at the expense of astrocytes. Notch-1 processing is affected, leading to downregulation of several Notch-regulated genes in Adam10 | Mus musculus |
malfunction | ADAM10 deletion causes reduced Notch signaling in vivo. Adam10-deficient mice die at embryonic day 9.5, due to major defects in development of somites and vasculogenesis. Adam10 conditional knock-out mice die perinatally with a disrupted neocortex and a severely reduced ganglionic eminence, due to precocious neuronal differentiation resulting in an early depletion of progenitor cells | Mus musculus |
physiological function | ADAM10 plays a central role in the developing brain by controlling mainly Notch-dependent pathways but likely also by reducing surface shedding of other neuronal membrane proteins including amyloid precursor protein | Mus musculus |
physiological function | ADAM10 represents the most important amyloid precursor protein alpha-secretase in brain. ADAM10 plays a central role in the developing brain by controlling mainly Notch-dependent pathways but likely also by reducing surface shedding of other neuronal membrane proteins including amyloid precursor protein | Mus musculus |