Mice lacking the metalloprotease-disintegrin MDC9 (ADAM9) have no evident major abnormalities during development or adult life.
about
TACE cleavage of proamphiregulin regulates GPCR-induced proliferation and motility of cancer cellsEvidence for regulation of the tumor necrosis factor alpha-convertase (TACE) by protein-tyrosine phosphatase PTPH1Role of ADAM-9 disintegrin-cysteine-rich domains in human keratinocyte migrationA Disintegrin and Metalloprotease (ADAM): Historical Overview of Their FunctionsCatalytic properties of ADAM19Proteolytic processing of Alzheimer's β-amyloid precursor proteinTrafficking and proteolytic processing of APPDeficits in spatial learning and motor coordination in ADAM11-deficient miceADAM9 is involved in pathological retinal neovascularizationEssential role for ADAM19 in cardiovascular morphogenesisDistinct roles for ADAM10 and ADAM17 in ectodomain shedding of six EGFR ligandsCalsyntenin-1 shelters APP from proteolytic processing during anterograde axonal transport.Selective roles for tumor necrosis factor alpha-converting enzyme/ADAM17 in the shedding of the epidermal growth factor receptor ligand family: the juxtamembrane stalk determines cleavage efficiency.The waved with open eyelids (woe) locus is a hypomorphic mouse mutation in Adam17.The secretases: enzymes with therapeutic potential in Alzheimer disease.A disintegrin and metalloproteinase 9 is involved in ectodomain shedding of receptor-binding cancer antigen expressed on SiSo cells.L1 is sequentially processed by two differently activated metalloproteases and presenilin/gamma-secretase and regulates neural cell adhesion, cell migration, and neurite outgrowthProteases and proteolysis in Alzheimer disease: a multifactorial view on the disease process.Secreted and membrane-bound isoforms of protease ADAM9 have opposing effects on breast cancer cell migration.ADAM10 mediates ectodomain shedding of the betacellulin precursor activated by p-aminophenylmercuric acetate and extracellular calcium influx.Characterization of oxygen-induced retinopathy in mice carrying an inactivating point mutation in the catalytic site of ADAM15.The purinergic receptor P2X7 triggers alpha-secretase-dependent processing of the amyloid precursor proteinMembrane-anchored growth factors, the epidermal growth factor family: beyond receptor ligands.TACE is required for the activation of the EGFR by TGF-alpha in tumorsEpidermal growth factor (EGF) ligand release by substrate-specific a disintegrin and metalloproteases (ADAMs) involves different protein kinase C (PKC) isoenzymes depending on the stimulusMice carrying a hypomorphic Evi1 allele are embryonic viable but exhibit severe congenital heart defectsPotential role for ADAM15 in pathological neovascularization in mice.ADAM9 inhibition increases membrane activity of ADAM10 and controls α-secretase processing of amyloid precursor proteinmiR-126-3p Inhibits Thyroid Cancer Cell Growth and Metastasis, and Is Associated with Aggressive Thyroid Cancer.Preconditioning-mimetics bradykinin and DADLE activate PI3-kinase through divergent pathways.Behavioral phenotypes of amyloid-based genetically modified mouse models of Alzheimer's disease.ADAM proteases, ErbB pathways and cancer.Endothelial deletion of ADAM17 in mice results in defective remodeling of the semilunar valves and cardiac dysfunction in adults.Alzheimer's disease: the lipid connection.Loss of the metalloprotease ADAM9 leads to cone-rod dystrophy in humans and retinal degeneration in mice.Implication of ADAM-8, -9, -10, -12, -15, -17, and ADAMTS-1 in implantational remodeling of a mouse uterus.ADAM function in embryogenesisPotential late-onset Alzheimer's disease-associated mutations in the ADAM10 gene attenuate {alpha}-secretase activity.Shedding of collagen XVII/BP180 in skin depends on both ADAM10 and ADAM9.Increased abundance of ADAM9 transcripts in the blood is associated with tissue damage.
P2860
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P2860
Mice lacking the metalloprotease-disintegrin MDC9 (ADAM9) have no evident major abnormalities during development or adult life.
description
2002 nî lūn-bûn
@nan
2002 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
2002 թվականի մարտին հրատարակված գիտական հոդված
@hy
2002年の論文
@ja
2002年論文
@yue
2002年論文
@zh-hant
2002年論文
@zh-hk
2002年論文
@zh-mo
2002年論文
@zh-tw
2002年论文
@wuu
name
Mice lacking the metalloprotea ...... ing development or adult life.
@ast
Mice lacking the metalloprotea ...... ing development or adult life.
@en
Mice lacking the metalloprotease-disintegrin MDC9
@nl
type
label
Mice lacking the metalloprotea ...... ing development or adult life.
@ast
Mice lacking the metalloprotea ...... ing development or adult life.
@en
Mice lacking the metalloprotease-disintegrin MDC9
@nl
prefLabel
Mice lacking the metalloprotea ...... ing development or adult life.
@ast
Mice lacking the metalloprotea ...... ing development or adult life.
@en
Mice lacking the metalloprotease-disintegrin MDC9
@nl
P2093
P2860
P1476
Mice lacking the metalloprotea ...... ing development or adult life.
@en
P2093
Carl P Blobel
Gisela Weskamp
Katia Manova
Shigeki Higashyama
Thomas A Brodie
Thomas Ludwig
P2860
P304
P356
10.1128/MCB.22.5.1537-1544.2002
P407
P577
2002-03-01T00:00:00Z