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Results 1 - 10 of 57 > >>
EC Number General Information Commentary Reference
Display the word mapDisplay the reaction diagram Show all sequences 3.4.24.81malfunction 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 709644
Display the word mapDisplay the reaction diagram Show all sequences 3.4.24.81malfunction 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 709644
Display the word mapDisplay the reaction diagram Show all sequences 3.4.24.81malfunction B-cell specific ADAM10 deficient mice have severely diminished primary and secondary responses after T-dependent immunization, display impaired germinal center formation, have fewer follicular T helper cells, decreased follicular dendritic cell networks, and altered chemokine expression in draining lymph nodes 720159
Display the word mapDisplay the reaction diagram Show all sequences 3.4.24.81malfunction deletion of ADAM10 prevents development of the entire marginal zone B cell lineage 720143
Display the word mapDisplay the reaction diagram Show all sequences 3.4.24.81malfunction enzyme depletion in forebrain neurons leads to posttranslational increase of cellular prion protein levels 753409
Display the word mapDisplay the reaction diagram Show all sequences 3.4.24.81malfunction enzyme inhibition selectively increases glioma sphere-forming cell, but not neural stem cell, migration out of tumourspheres towards fibronectin 754777
Display the word mapDisplay the reaction diagram Show all sequences 3.4.24.81malfunction enzyme knockdown inhibits the CNE-2 nasopharyngeal carcinoma cell proliferation and migration 753146
Display the word mapDisplay the reaction diagram Show all sequences 3.4.24.81malfunction enzyme knockout in cranial neural crest cells leads to embryonic death, craniofacial dysmorphia and bone defects 752662
Display the word mapDisplay the reaction diagram Show all sequences 3.4.24.81malfunction enzyme-deficient embryos die at E 9.5 due to developmental defects in somitogenesis, neurogenesis and vasculogenesis 752839
Display the word mapDisplay the reaction diagram Show all sequences 3.4.24.81malfunction inhibition of ADAM10 activity in the intestine of mice results in a lack of compartmentalization of Paneth cells within the crypt stem cell niche 720511
Results 1 - 10 of 57 > >>