Linked Life Data

10935448

Source:http://linkedlifedata.com/resource/pubmed/id/10935448

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-8-17
pubmed:abstractText
Beta-catenin acts as a key mediator of the Wnt/Wingless signaling pathway involved in cell proliferation, differentiation and survival. Recent studies have shown that an unstable interaction between beta-catenin and the mutant presenilin-1 induces neuronal apoptosis, and that beta-catenin levels are decreased in the brains of patients with Alzheimer's disease (AD). Since activated microglia and astrocytes play a role in the process of neuronal degeneration in AD, the cytokine/growth factor-regulated expression of beta-catenin in human neural cell lines, including NTera2 teratocarcinoma-derived differentiated neurons (NTera2-N), IMR-32 neuroblastoma, SKN-SH neuroblastoma and U-373MG astrocytoma, was studied quantitatively following exposure to epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), brain-derived neurotrophic factor (BDNF), tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, IL-6, interferon (IFN)-gamma, transforming growth factor (TGF)-beta1, dibutyryl cyclic adenosine 3',5'-cyclic monophosphate (cAMP) (dbcAMP) or phorbol 12-myristate 13-acetate (PMA). Beta-catenin mRNA expressed constitutively in all of these cell lines was unaffected by treatment with any factors examined. In contrast, beta-catenin protein levels were reduced markedly in NTera2-N cells by exposure to dbcAMP, EGF or bFGF, and in U-373MG cells by treatment with dbcAMP or PMA, but were unaffected in any cell lines by BDNF, TNF-alpha, IL-1beta, IL-6, IFN-gamma or TGF-beta1. These results indicate that beta-catenin is expressed constitutively in human neural cells and downregulated at a protein level by a set of growth factors in a cell type-specific manner.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0919-6544
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
113-23
pubmed:dateRevised
2008-3-10
pubmed:meshHeading
pubmed-meshheading:10935448-Astrocytoma, pubmed-meshheading:10935448-Brain Neoplasms, pubmed-meshheading:10935448-Bucladesine, pubmed-meshheading:10935448-Cadherins, pubmed-meshheading:10935448-Cell Differentiation, pubmed-meshheading:10935448-Cytokines, pubmed-meshheading:10935448-Cytoskeletal Proteins, pubmed-meshheading:10935448-Gene Expression Regulation, Neoplastic, pubmed-meshheading:10935448-Glioma, pubmed-meshheading:10935448-Growth Substances, pubmed-meshheading:10935448-HL-60 Cells, pubmed-meshheading:10935448-HeLa Cells, pubmed-meshheading:10935448-Humans, pubmed-meshheading:10935448-Neuroblastoma, pubmed-meshheading:10935448-Neurons, pubmed-meshheading:10935448-Retinal Neoplasms, pubmed-meshheading:10935448-Retinoblastoma, pubmed-meshheading:10935448-Tetradecanoylphorbol Acetate, pubmed-meshheading:10935448-Trans-Activators, pubmed-meshheading:10935448-Transcription, Genetic, pubmed-meshheading:10935448-Tumor Cells, Cultured, pubmed-meshheading:10935448-beta Catenin
pubmed:year
2000
pubmed:articleTitle
Beta-catenin expression in human neural cell lines following exposure to cytokines and growth factors.
pubmed:affiliation
Department of Internal Medicine, Saga Medical School, Japan. satoj1@post.saga-med.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't