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In summary, ER retention of pathogenic VLDLR mutants involves binding to calnexin, elevated endoplasmic reticulum stress, and delayed degradation which is dependent on SEL1L.
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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.
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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
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VLDLR expression was negatively regulated by miR-200c Colorectal cancer (CRC) cells and their expression levels were inversely correlated in CRC patients.
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We screened for mutations in RELN 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-mutated patients to be distinguished from VLDLR-mutated patients.
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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/Arg clusters in fibrin make major contributions to this interaction while the contribution of the first cluster is moderate.
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The presence of reelin was elevated in junctional areas as in dysplastic nevi. VLDLR presented positive values in 16 cases (16/ 32) and ApoER2 was weak positive in 7 cases.
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These results for the first time demonstrated that SalA protected against IS/RP-induced endothelial barrier dysfunction through suppression of VLDL receptor expression
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these results suggest that VLDLR functions in vivo as an HCV receptor independent of canonical CD81-mediated HCV entry.
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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
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The results of this study demonstrated the presence of reelin, its receptors VLDLR and ApoER2 as well as Dab1 in the ENS and might indicate a novel role of the reelin system in regulating neuronal plasticity and pre-synaptic functions in the ENS.
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these results suggested that the miR-135a-VLDLR-p38 axis may contribute to gallbladder cancer cell proliferation
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study identified a novel homozygous VLDLR c.2248C>T mutation (p.Q750X) and distinctive MRI findings in 2 siblings with ataxia; also marked vitamin E deficiency was detected in the proband
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these results identify a novel role for the VLDLR as a negative regulator of DC-mediated adaptive immune responses in HDM-induced allergic airway inflammation.
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ectopic expression of HIC1 in U2OS and MDA-MB-231 cell lines decreases expression of the ApoER2 and VLDLR genes, encoding two canonical tyrosine kinase receptors for Reelin.
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an unusual constellation of VLDLR mutations in Cerebellar ataxia, mental retardation and dysequilibrium syndrome 1 is reported
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Results show variation in VLDLR is implicated in disordered gambling
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These results conclude that in the hypoxic hearts of mice and men, the VLDLr gene is regulated by a direct binding of Hif-1alpha to the VLDLr promoter
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Stx5 might play a role in modulating VLDL-R physiology by participating in an abrasively described or completely novel Golgi-bypass pathway.
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In this report, we present 3 patients from 2 different families displaying very low density lipoprotein receptor-associated pontocerebellar hypoplasia, cortical dysplasia, mental retardation, and bipedal gait.
