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Literature summary for 3.4.24.81 extracted from

  • Jorissen, E.; Prox, J.; Bernreuther, C.; Weber, S.; Schwanbeck, R.; Serneels, L.; Snellinx, A.; Craessaerts, K.; Thathiah, A.; Tesseur, I.; Bartsch, U.; Weskamp, G.; Blobel, C.P.; Glatzel, M.; De Strooper, B.; Saftig, P.
    The disintegrin/metalloproteinase ADAM10 is essential for the establishment of the brain cortex (2010), J. Neurosci., 30, 4833-4844.
    View publication on PubMedView publication on EuropePMC

Inhibitors

Inhibitors Comment Organism Structure
GI254023X
-
Mus musculus

Natural Substrates/ Products (Substrates)

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

Organism UniProt Comment Textmining
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
brain
-
Mus musculus
-

Substrates and Products (Substrate)

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

Synonyms Comment Organism
ADAM10
-
Mus musculus
ADAM10 alpha-secretase Mus musculus

General Information

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