Dab2 deficiency in myeloid cells promotes inflammation in livers and atherosclerotic plaques in an Ldl receptor knockout mouse model of atherosclerosis.
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.
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.
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