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VLDLRVery Low Density Lipoprotein Receptor
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By studying frog oocytes in the laboratory we were able to discover that the VLDLR protein acts as a 'delivery truck' or chaperone that helps deliver mPR to the plasma membrane and hence mediates its action after progesterone treatment."
Binding of reelin to its receptors VLDLR and/or ApoER2 induces the phosphorylation of adaptor protein Dab1by the Src family kinases Src and Fyn [20,21].
TTest analysis for these genes between the vehicle-exposed and the G-treated cells--at a significance level of 0.05--indicated that ACSL1, ABCA1, DHCR24, ACAT2, ACACA, ABCG1, ACAD9, ACACB, IDI1, PPARG, SCD, SCARB1, HMGCS1, EBP, DHCR7, FASN, HMGCR, and GPAM were down-regulated upon G treatment; whereas NR1H2, PPARA, INSIG2, CPTP1, APOE, VLDLR, ABCC2, and SREBF2 were activated after exposure to G (Fig.
Shimokata, "Association of polymorphisms in CYP17A1, MTP, and VLDLR with bone mineral density in community-dwelling Japanese women and men," Genomics, vol.
Awan et al., "Circulating proprotein convertase subtilisin/kexin 9 (PCSK9) regulates VLDLR protein and triglyceride accumulation in visceral adipose tissue," Arteriosclerosis, Thrombosis, and Vascular Biology, vol.
Circulating proprotein convertase subtilisin/kexin 9 (PCSK9) regulates VLDLR protein and triglycer ide accumulation in visceral adipose tissue.
Apo E receptors and its functions in the CNS: Of the two major apolipoproteins found in the cerebro spinal fluid (CSF), apo E can associate with a number of extracellular molecules and bind to four major CNS apo E receptors, VLDLR, Apo ER2, LDLR and LRP.
Interestingly, VLDLR expression is a determinant factor in inflammation and in M1-like activation of macrophages in AT [66].
To date, few lncRNAs (i.e., VLDLR, ROR, and TUC339) have been reported in circulating HCC EVs: (i) exposure of HCC cells to diverse anticancer agents such as sorafenib, camptothecin, and doxorubicin increased the expression of lnc-VLDLR in transformed hepatocytes as well as its recruitment inside EVs released from these cells.
Placenta transports cholesterol from maternal circulation to the fetus by cholesterol transporters that include low-density lipoprotein receptor (LDLR), the very low-density lipoprotein receptor (VLDLR), and the SRBI receptor [15].
Several cell receptors were identified as being potential HCV cell entry to the cell, mainly transmembrane lectins as dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) and its liver and lymphatic endothelium homologue (L-SIGN), scavenger member 1 receptor-class B (SR-BI), tight junction proteins such as claudin-1 (CLDN-1) and occludin (OCLN), cluster of differentiation 81 (CD81) protein, and, recently, the very-low-density lipoprotein receptor (VLDLR) [5,6].
To obtain the VLDLR fraction from the serum of a patient with type III hyperlipoproteinemia, we conducted ultracentrifugation and gel filtration.