-
miR149 was able to target Dab2 and promote the cardiac differentiation of mouse MSCs in vitro, which depended upon the Wnt/betacatenin signaling pathway.
-
Dab2 functions as a negative immune regulator of TLR4 endocytosis and signaling; it has a role in the regulatory circuit in controlling the inflammatory response of macrophages to endotoxin
-
The results suggest that Dab2 is required for the excessive calorie-induced differentiation of an adipocyte progenitor cell population that is present in juvenile but depleted in mature animals. The finding provides evidence for a limited pre-adipocyte population in juvenile mammals and the requirement of Dab2 in the regulation of Ras/MAPK signal in the commitment of the precursor cells to adipose tissues.
-
The various novel mechanisms are described by which Dab2 mediates an array of signaling events with vast physiological consequences.
-
The combination of Arh and Dab2 is responsible for the majority of adaptor function in LDLR endocytosis and LDLR-mediated cholesterol homeostasis.
-
cathepsin B (CTSB) inhibition or expression of a CTSB-resistant Dab2 mutant maintains Dab2 expression and shifts long-term TGF-beta-treated cells from autophagy to apoptosis
-
Results identified a novel activation marker, DAB2, which expression is significantly different between microglia activation stages M2a and either M1 or M2b.
-
these findings reveal that DAB2 is critical for controlling inflammatory signaling during phenotypic polarization of macrophages
-
Dab2 expression is induced by hormones
-
Results suggest that endogenous Dab2 exacerbates central nervous system inflammation, potentially acting to up-regulate reactive oxygen species expression in macrophages and microglia, and that it is of potential pathogenic relevance in multiple sclerosis
-
Disabled-2 is required for efficient hemostasis and platelet activation by thrombin in mice.
-
Akt1 and Akt2 are involved in albumin endocytosis, and phosphorylation of Dab2 by Akt induces albumin endocytosis in proximal tubule epithelial cells.
-
Study of dab2 mutant allele in embryos and embryoid bodies confirms a role for Dab2 in extraembryonic endoderm development and epithelial organization. Also, Dab2 has a physiological role in the endocytosis of lipoproteins and cholesterol metabolism.
-
miR-145 regulates the migration and invasion of highly invasive prostate cancer cells through targeting DAB2 gene
-
these results indicate that p96 Dab2 plays a key role in the extra-embryonic endodermal differentiation process.
-
The authors report that Dab2, previously described as an inhibitor of Wnt/beta-catenin signalling, selectively recruits LRP6 to the clathrin-dependent endocytic route, thereby sequestering it from caveolin-mediated endocytosis.
-
Data show that although small RNA-mediated Dab2 knockdown had no affect on the internalization of various clathrin-dependent cargo, TGF-beta receptor recycling was abrogated.
-
TGF-beta modulates the expression of Dab2 and ILEI mRNA required for epithelial-mesenchymal transdifferentiation by inducing phosphorylation of hnRNP E1, resulting in its release from a structural, 33-nucleotide BAT element in the 3'UTR of Dab2 and ILEI.
-
Dab2 is pleiotropic and regulates both visceral endoderm function and lipoprotein receptor trafficking in vivo.
-
Data suggest that Dab2 is a member of a family of cargo-specific adaptor proteins, which regulate clathrin-coat assembly at the plasma membrane.
