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anti-Human VLDLR Anticorps:
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Cow (Bovine) Monoclonal VLDLR Primary Antibody pour ICC, IF - ABIN4365609
Roberts, Barnard, Liang, Vaziri: Effect of diet on adipose tissue and skeletal muscle VLDL receptor and LPL: implications for obesity and hyperlipidemia. dans Atherosclerosis 2002
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Human Polyclonal VLDLR Primary Antibody pour FACS, IF (p) - ABIN705555
Fredriksson, Mishra, Lam, Mushaben, Cuento, Meyer, Yao, Keeran, Nugent, Qu, Yu, Yang, Raghavachari, Dagur, McCoy, Levine: The very low density lipoprotein receptor attenuates house dust mite-induced airway inflammation by suppressing dendritic cell-mediated adaptive immune responses. dans Journal of immunology (Baltimore, Md. : 1950) 2014
Human Polyclonal VLDLR Primary Antibody pour FACS, IHC (p) - ABIN651940
Sakai, Tiebel, Ljungberg, Sullivan, Lee, Terashima, Li, Kobayashi, Lu, Chan, Oka: A neuronal VLDLR variant lacking the third complement-type repeat exhibits high capacity binding of apoE containing lipoproteins. dans Brain research 2009
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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 (Montrer MLXIP Anticorps)-200c Colorectal cancer (CRC (Montrer CALR Anticorps)) cells and their expression levels were inversely correlated in CRC (Montrer CALR Anticorps) patients.
We screened for mutations in RELN (Montrer RELN Anticorps) 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 (Montrer RELN Anticorps)-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 (Montrer LYZ Anticorps)/Arg clusters in fibrin make major contributions to this interaction while the contribution of the first cluster is moderate.
The presence of reelin (Montrer RELN Anticorps) was elevated in junctional areas as in dysplastic nevi. VLDLR presented positive values in 16 cases (16/ 32) and ApoER2 (Montrer LRP8 Anticorps) 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 (Montrer CD81 Anticorps)-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 (Montrer RELN Anticorps), its receptors VLDLR and ApoER2 (Montrer LRP8 Anticorps) as well as Dab1 (Montrer DAB1 Anticorps) in the ENS and might indicate a novel role of the reelin (Montrer RELN Anticorps) 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 (Montrer LRP8 Anticorps).
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 (Montrer PPARA Anticorps) response element binding to the VLDLR promoter.
C-terminal truncation of the reelin (Montrer RELN Anticorps) protein disrupts the interaction of reelin (Montrer RELN Anticorps) 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 (Montrer WNT2 Anticorps) signaling due to their different ectodomain shedding rates, which identified the functional difference of these splice variants.
The absence of PCSK9 (Montrer PCSK9 Anticorps) results in a sex- and tissue-specific subcellular distribution of the LDLR (Montrer LDLR Anticorps) 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 (Montrer FFAR1 Anticorps) suppresses expression of the glucose transporter Glut1 (Montrer SLC2A1 Anticorps)
neuronal stress differentially regulates lipoprotein receptor expression in neurons, with VLDLR upregulation as a common element as a modulator of neuronal Wnt (Montrer WNT2 Anticorps) 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