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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 (显示 MLXIP ELISA试剂盒)-200c Colorectal cancer (CRC (显示 CALR ELISA试剂盒)) cells and their expression levels were inversely correlated in CRC (显示 CALR ELISA试剂盒) patients.
We screened for mutations in RELN (显示 RELN ELISA试剂盒) 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 (显示 RELN ELISA试剂盒)-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 (显示 LYZ ELISA试剂盒)/Arg clusters in fibrin make major contributions to this interaction while the contribution of the first cluster is moderate.
The presence of reelin (显示 RELN ELISA试剂盒) was elevated in junctional areas as in dysplastic nevi. VLDLR presented positive values in 16 cases (16/ 32) and ApoER2 (显示 LRP8 ELISA试剂盒) 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 (显示 CD81 ELISA试剂盒)-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 (显示 RELN ELISA试剂盒), its receptors VLDLR and ApoER2 (显示 LRP8 ELISA试剂盒) as well as Dab1 (显示 DAB1 ELISA试剂盒) in the ENS and might indicate a novel role of the reelin (显示 RELN ELISA试剂盒) system in regulating neuronal plasticity and pre-synaptic functions in the ENS.
these results suggested that the miR (显示 MLXIP ELISA试剂盒)-135a-VLDLR-p38 (显示 CRK ELISA试剂盒) axis may contribute to gallbladder cancer cell proliferation
C-terminal truncation of the reelin (显示 RELN ELISA试剂盒) protein disrupts the interaction of reelin (显示 RELN ELISA试剂盒) 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 (显示 WNT2 ELISA试剂盒) signaling due to their different ectodomain shedding rates, which identified the functional difference of these splice variants.
The absence of PCSK9 (显示 PCSK9 ELISA试剂盒) results in a sex- and tissue-specific subcellular distribution of the LDLR (显示 LDLR ELISA试剂盒) 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 (显示 FFAR1 ELISA试剂盒) suppresses expression of the glucose transporter Glut1 (显示 SLC2A1 ELISA试剂盒)
neuronal stress differentially regulates lipoprotein receptor expression in neurons, with VLDLR upregulation as a common element as a modulator of neuronal Wnt (显示 WNT2 ELISA试剂盒) signaling
Subretinal vascularization (SRV) in the Vldlr-/- model is associated with mistargeted neurites and that SRV is preceded by altered retinal vascular development.
VLDLR requires RasGRF1 (显示 RASGRF1 ELISA试剂盒)/CaMKII (显示 CAMK2G ELISA试剂盒) to alter dendritic spine formation.
This study demonstrated that VLDLR is expressed in distinct spatiotemporal patterns in developing mouse cerebral cortex.
LRP5 (显示 LRP5 ELISA试剂盒) signaling is a prerequisite for neovascularization in VLDLR knockout mice. LRP5 (显示 LRP5 ELISA试剂盒) may be an effective target for inhibiting intraretinal neovascularization.
these results identify a novel role for the VLDLR as a negative regulator of DC-mediated adaptive immune responses in HDM (显示 HDAC3 ELISA试剂盒)-induced allergic airway inflammation.
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