Matrix metalloproteinase 7 controls pancreatic acinar cell transdifferentiation by activating the Notch signaling pathway. - sprookjes - yvandenbroek - TriplyDB

Matrix metalloproteinase 7 controls pancreatic acinar cell transdifferentiation by activating the Notch signaling pathway.

Matrix metalloproteinase 7 controls pancreatic acinar cell transdifferentiation by activating the Notch signaling pathway.

http://www.wikidata.org/entity/Q36288566

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Reserve stem cells: Differentiated cells reprogram to fuel repair, metaplasia, and neoplasia in the adult gastrointestinal tract Matrix metalloproteinases in stem cell regulation and cancer Therapeutic potential of targeting acinar cell reprogramming in pancreatic cancer Identification of amino acid residues of matrix metalloproteinase-7 essential for binding to cholesterol sulfate Protein kinase C iota regulates pancreatic acinar-to-ductal metaplasia Charge-Triggered Membrane Insertion of Matrix Metalloproteinase-7, Supporter of Innate Immunity and Tumors Increasing Notch signaling antagonizes PRC2-mediated silencing to promote reprograming of germ cells into neurons Acinar cell carcinoma: a report of 19 cases with a brief review of the literature Beta-catenin blocks Kras-dependent reprogramming of acini into pancreatic cancer precursor lesions in mice.microRNA-139-5p exerts tumor suppressor function by targeting NOTCH1 in colorectal cancer KRAS, Hedgehog, Wnt and the twisted developmental biology of pancreatic ductal adenocarcinoma.EZH2 couples pancreatic regeneration to neoplastic progression.Matrix metalloproteinase-10 promotes Kras-mediated bronchio-alveolar stem cell expansion and lung cancer formation Cholesterol sulfate alters substrate preference of matrix metalloproteinase-7 and promotes degradations of pericellular laminin-332 and fibronectin Organoid models of human and mouse ductal pancreatic cancer Neurogenin 3 Expressing Cells in the Human Exocrine Pancreas Have the Capacity for Endocrine Cell Fate.Notch1 is not required for acinar-to-ductal metaplasia in a model of Kras-induced pancreatic ductal adenocarcinoma Stat3 and MMP7 contribute to pancreatic ductal adenocarcinoma initiation and progression.Notch signaling proteins: legitimate targets for cancer therapy.The unholy trinity: inflammation, cytokines, and STAT3 shape the cancer microenvironment.Protein kinase D1 drives pancreatic acinar cell reprogramming and progression to intraepithelial neoplasia Expression of matrix metalloproteinase-7 is an unfavorable prognostic factor in intrahepatic cholangiocarcinoma Defensins Potentiate a Neutralizing Antibody Response to Enteric Viral Infection.Matrilysin (MMP-7) inhibition of BMP-7 induced renal tubular branching morphogenesis suggests a role in the pathogenesis of human renal dysplasia.Transdifferentiation of tadpole pancreatic acinar cells to duct cells mediated by Notch and stromelysin-3.Basal autophagy maintains pancreatic acinar cell homeostasis and protein synthesis and prevents ER stress.Matrix metalloproteinase 9 (MMP-9)-dependent processing of βig-h3 protein regulates cell migration, invasion, and adhesion Remodeling the exocrine pancreas at metamorphosis in Xenopus laevis.Macrophage-secreted cytokines drive pancreatic acinar-to-ductal metaplasia through NF-κB and MMPs.ADAM proteases: ligand processing and modulation of the Notch pathway Matrilysin-1 mediates bronchiolization of alveoli, a potential premalignant change in lung cancer.Osteoclast-derived matrix metalloproteinase-7, but not matrix metalloproteinase-9, contributes to tumor-induced osteolysis.Mitogen-activated Protein Kinase Kinase Activity Maintains Acinar-to-Ductal Metaplasia and Is Required for Organ Regeneration in Pancreatitis.Senescence-associated SIN3B promotes inflammation and pancreatic cancer progression.Proteolytic cleavage of Notch: "HIT and RUN".The role of Adams in Notch signaling.Notch signaling in pancreatic cancer: oncogene or tumor suppressor?MiR-139-5p: promising biomarker for cancer.KLF4 Is Essential for Induction of Cellular Identity Change and Acinar-to-Ductal Reprogramming during Early Pancreatic Carcinogenesis.Acinar cell plasticity and development of pancreatic ductal adenocarcinoma.

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P2860

Matrix metalloproteinase 7 controls pancreatic acinar cell transdifferentiation by activating the Notch signaling pathway.

http://www.wikidata.org/entity/Q36288566

description

2007 nî lūn-bûn

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2007年の論文

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年学术文章

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2007年學術文章

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2007年學術文章

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name

Matrix metalloproteinase 7 con ...... g the Notch signaling pathway.

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Matrix metalloproteinase 7 con ...... g the Notch signaling pathway.

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Matrix metalloproteinase 7 con ...... g the Notch signaling pathway.

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Howard C Crawford

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Johnny A Johnson

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P2860

The disintegrin/metalloprotease ADAM 10 is essential for Notch signalling but not for alpha-secretase activity in fibroblasts

PTF1 is an organ-specific and Notch-independent basic helix-loop-helix complex containing the mammalian Suppressor of Hairless (RBP-J) or its paralogue, RBP-L.

Notch signaling controls multiple steps of pancreatic differentiation

A novel proteolytic cleavage involved in Notch signaling: the role of the disintegrin-metalloprotease TACE

Intestinal tumorigenesis is suppressed in mice lacking the metalloproteinase matrilysin

Calcium depletion dissociates and activates heterodimeric notch receptors

Kuzbanian controls proteolytic processing of Notch and mediates lateral inhibition during Drosophila and vertebrate neurogenesis

Notch/gamma-secretase inhibition turns proliferative cells in intestinal crypts and adenomas into goblet cells

Matrix metalloproteinase-7 is expressed by pancreatic cancer precursors and regulates acinar-to-ductal metaplasia in exocrine pancreas.

The Nestin progenitor lineage is the compartment of origin for pancreatic intraepithelial neoplasia

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