Disabled-2 inactivation is an early step in ovarian tumorigenicity.
about
The adaptor molecule Disabled-2 links the transforming growth factor beta receptors to the Smad pathway.The mechanism of growth-inhibitory effect of DOC-2/DAB2 in prostate cancer. Characterization of a novel GTPase-activating protein associated with N-terminal domain of DOC-2/DAB2Disabled-2 (Dab2) is required for transforming growth factor beta-induced epithelial to mesenchymal transition (EMT)Dab2 links CIN85 with clathrin-mediated receptor internalizationDual roles for the Dab2 adaptor protein in embryonic development and kidney transportEarly events in ovarian oncogenesisDAB2IP in cancerEndocytosis and Physiology: Insights from Disabled-2 Deficient MiceCell cycle-dependent phosphorylation of Disabled-2 by cdc2Disabled-2 is transcriptionally regulated by ICSBP and augments macrophage spreading and adhesion.Homozygous loss of BHD causes early embryonic lethality and kidney tumor development with activation of mTORC1 and mTORC2Disabled-2 colocalizes with the LDLR in clathrin-coated pits and interacts with AP-2The inhibitory role of DOC-2/DAB2 in growth factor receptor-mediated signal cascade. DOC-2/DAB2-mediated inhibition of ERK phosphorylation via binding to Grb2Characterization of a novel negative regulator (DOC-2/DAB2) of c-Src in normal prostatic epithelium and cancerType II transforming growth factor-beta receptor recycling is dependent upon the clathrin adaptor protein Dab2p67 isoform of mouse disabled 2 protein acts as a transcriptional activator during the differentiation of F9 cellsGenome-wide association study identifies five loci associated with susceptibility to pancreatic cancer in Chinese populationsA single common portal for clathrin-mediated endocytosis of distinct cargo governed by cargo-selective adaptors.Sulfatides partition disabled-2 in response to platelet activation.Transcription profiles of non-immortalized breast cancer cell lines.Xenopus Dab2 is required for embryonic angiogenesisDynamic expression of Dab2 in the mouse embryonic central nervous system.Loss of GATA4 and GATA6 expression specifies ovarian cancer histological subtypes and precedes neoplastic transformation of ovarian surface epitheliaPutative tumour-suppressor gene DAB2 is frequently down regulated by promoter hypermethylation in nasopharyngeal carcinoma.Ovarian cancer: pathology, biology, and disease modelsRestoration of positioning control following Disabled-2 expression in ovarian and breast tumor cells.Loss of disabled-2 expression is an early event in esophageal squamous tumorigenesis.Epigenetic downregulation of human disabled homolog 2 switches TGF-beta from a tumor suppressor to a tumor promoter.Epigenetic regulation of a novel tumor suppressor gene (hDAB2IP) in prostate cancer cell lines.Regulation of ovarian cancer progression by microRNA-187 through targeting Disabled homolog-2.Lessons from border cell migration in the Drosophila ovary: A role for myosin VI in dissemination of human ovarian cancer.Hormonal induction and roles of Disabled-2 in lactation and involution.Vitamin D transport proteins megalin and disabled-2 are expressed in prostate and colon epithelial cells and are induced and activated by all-trans-retinoic acidmiR-93-directed downregulation of DAB2 defines a novel oncogenic pathway in lung cancer.Differential requirement for Dab2 in the development of embryonic and extra-embryonic tissues.Loss of Dab2 expression in breast cancer cells impairs their ability to deplete TGF-β and induce Tregs development via TGF-β.Identification of genes differentially expressed in myogenin knock-down bovine muscle satellite cells during differentiation through RNA sequencing analysis.Dab2, a negative regulator of DC immunogenicity, is an attractive molecular target for DC-based immunotherapy.Disabled-2 heterozygous mice are predisposed to endometrial and ovarian tumorigenesis and exhibit sex-biased embryonic lethality in a p53-null backgroundInvasion of normal human fibroblasts induced by v-Fos is independent of proliferation, immortalization, and the tumor suppressors p16INK4a and p53.
P2860
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P2860
Disabled-2 inactivation is an early step in ovarian tumorigenicity.
description
1999 nî lūn-bûn
@nan
1999 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի մայիսին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
Disabled-2 inactivation is an early step in ovarian tumorigenicity.
@ast
Disabled-2 inactivation is an early step in ovarian tumorigenicity.
@en
type
label
Disabled-2 inactivation is an early step in ovarian tumorigenicity.
@ast
Disabled-2 inactivation is an early step in ovarian tumorigenicity.
@en
prefLabel
Disabled-2 inactivation is an early step in ovarian tumorigenicity.
@ast
Disabled-2 inactivation is an early step in ovarian tumorigenicity.
@en
P2093
P2860
P356
P1433
P1476
Disabled-2 inactivation is an early step in ovarian tumorigenicity.
@en
P2093
P2860
P2888
P304
P356
10.1038/SJ.ONC.1202649
P407
P577
1999-05-01T00:00:00Z
P5875
P6179
1050723976