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Our findings described an atherogenic phenotype characterized by low VLDL-C but high VLDLR mRNA expression in peripheral WBCs, which suggested that VLDLR in all types of peripheral WBCs may be involved in lipid deposition, and VLDL-C and VLDLR may co-determine the development of atherosclerosis.
In the second family, we identified a previously unreported homozygous missense change, c.154T > C (p.Cys52Arg) in the VLDLR gene
VLDLR expression was negatively regulated by miR (zeige MLXIP Proteine)-200c Colorectal cancer (CRC (zeige CALR Proteine)) cells and their expression levels were inversely correlated in CRC (zeige CALR Proteine) patients.
We screened for mutations in RELN (zeige RELN Proteine) or VLDLR and compared the phenotype of these patients with that of previously reported patients. differences in clinical severity, involvement of the cerebellar hemispheres, together with the severity of the neocortical defect, enables RELN (zeige RELN Proteine)-mutated patients to be distinguished from VLDLR-mutated patients.
Data suggest that, in the binding of fibrin beta N-domains and the (1-8) peptide fragment of VLDLR (very low density lipoprotein receptor), the second and third Lys (zeige LYZ Proteine)/Arg clusters in fibrin make major contributions to this interaction while the contribution of the first cluster is moderate.
The presence of reelin (zeige RELN Proteine) was elevated in junctional areas as in dysplastic nevi. VLDLR presented positive values in 16 cases (16/ 32) and ApoER2 (zeige LRP8 Proteine) was weak positive in 7 cases.
These results for the first time demonstrated that SalA protected against IS/RP-induced endothelial barrier dysfunction through suppression of VLDL receptor expression
these results suggest that VLDLR functions in vivo as an HCV receptor independent of canonical CD81 (zeige CD81 Proteine)-mediated HCV entry.
the results obtained indicate that minimal fibrin-binding structures are located within the second and third CR domains of the VLDL receptor and the presence of the fourth CR domain is required for high-affinity binding
The results of this study demonstrated the presence of reelin (zeige RELN Proteine), its receptors VLDLR and ApoER2 (zeige LRP8 Proteine) as well as Dab1 (zeige DAB1 Proteine) in the ENS and might indicate a novel role of the reelin (zeige RELN Proteine) system in regulating neuronal plasticity and pre-synaptic functions in the ENS.
Mice lacking Vldlr expression also had altered call repertoires, and this effect was exacerbated by deficiency in Apoer2 (zeige LRP8 Proteine).
studies uncover functions of VLDLR and mTORC1 in lactation and osteoclastogenesis, illuminating key mechanisms and therapeutic insights for bone and metabolic diseases.
Further, luciferase assay confirmed VLDLR as a direct target of miR-17-5p in vascular smooth muscle cells (VSMCs).
fenofibrate upregulated VLDLR transcriptional activity through PPAR (zeige PPARA Proteine) response element binding to the VLDLR promoter.
C-terminal truncation of the reelin (zeige RELN Proteine) protein disrupts the interaction of reelin (zeige RELN Proteine) with VLDLR, resulting in abnormal development of the cerebral cortex and hippocampus.
Study showed that the two major VLDLR splice variants have differential activities in regulating Wnt (zeige WNT2 Proteine) signaling due to their different ectodomain shedding rates, which identified the functional difference of these splice variants.
The absence of PCSK9 (zeige PCSK9 Proteine) results in a sex- and tissue-specific subcellular distribution of the LDLR (zeige LDLR Proteine) and VLDLR, which is determined by estradiol levels.
In the retinas of Vldlr(-/-) mice with low fatty acid uptake but high circulating lipid levels, we found that Ffar1 (zeige FFAR1 Proteine) suppresses expression of the glucose transporter Glut1 (zeige SLC2A1 Proteine)
neuronal stress differentially regulates lipoprotein receptor expression in neurons, with VLDLR upregulation as a common element as a modulator of neuronal Wnt (zeige WNT2 Proteine) signaling
Subretinal vascularization (SRV) in the Vldlr-/- model is associated with mistargeted neurites and that SRV is preceded by altered retinal vascular development.
The low density lipoprotein receptor (LDLR) gene family consists of cell surface proteins involved in receptor-mediated endocytosis of specific ligands. This gene encodes a lipoprotein receptor that is a member of the LDLR family and plays important roles in VLDL-triglyceride metabolism and the reelin signaling pathway. Mutations in this gene cause VLDLR-associated cerebellar hypoplasia. Alternative splicing generates multiple transcript variants encoding distinct isoforms for this gene.
, very low-density lipoprotein receptor
, VTG receptor
, very low density lipoprotein (VLDL)/vitellogenin receptor
, vitellogenin receptor