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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.
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-200c Colorectal cancer (CRC) cells and their expression levels were inversely correlated in CRC patients.
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.
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.
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.
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-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, 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.
these results suggested that the miR-135a-VLDLR-p38 axis may contribute to gallbladder cancer cell proliferation
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
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.
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.
an unusual constellation of VLDLR mutations in Cerebellar ataxia, mental retardation and dysequilibrium syndrome 1 is reported
Results show variation in VLDLR is implicated in disordered gambling
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
Stx5 might play a role in modulating VLDL-R physiology by participating in an abrasively described or completely novel Golgi-bypass pathway.
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.
Mice lacking Vldlr expression also had altered call repertoires, and this effect was exacerbated by deficiency in Apoer2.
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 response element binding to the VLDLR promoter.
C-terminal truncation of the reelin protein disrupts the interaction of reelin 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 signaling due to their different ectodomain shedding rates, which identified the functional difference of these splice variants.
The absence of PCSK9 results in a sex- and tissue-specific subcellular distribution of the LDLR 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 suppresses expression of the glucose transporter Glut1
neuronal stress differentially regulates lipoprotein receptor expression in neurons, with VLDLR upregulation as a common element as a modulator of neuronal Wnt 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/CaMKII to alter dendritic spine formation.
This study demonstrated that VLDLR is expressed in distinct spatiotemporal patterns in developing mouse cerebral cortex.
LRP5 signaling is a prerequisite for neovascularization in VLDLR knockout mice. LRP5 may be an effective target for inhibiting intraretinal neovascularization.
Nuclear factor (erythroid-derived 2)-like 2 activation-induced hepatic very-low-density lipoprotein receptor overexpression in response to oxidative stress contributes to alcoholic liver disease in mice.
Clusterin is a ligand for apolipoprotein E receptor 2 (ApoER2) and very low density lipoprotein receptor (VLDLR) and signals via the Reelin-signaling pathway.
The Reelin receptors ApoER2 and VLDLr play essential roles in Reelin-mediated migration and positioning of mesencephalic dopaminergic neurons.
VLDLR contributes to adipose tissue inflammation and mediates VLDL-induced lipid accumulation and induction of inflammation and ER stress in adipocytes and macrophages.
Dab1 mediated the association of CIN85 with ApoER2 or VLDLR in neurons.
there are reelin-independent functions of very-low-density lipoprotein receptor (VLDLR) and low-density lipoprotein receptor-related protein 8 in geniculate nucleus 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