CD320 Molecule (CD320) Kits ELISA

Human CD320 Molecule (CD320) interaction partners

1. It has been proposed that the transcobalamin 2 receptor (TCN2R) is associated with idiopathic recurrent spontaneous abortion (RSA). The findings showed no significant association between TCN2R rs2336573 polymorphisms and the risk/protection of recurrent spontaneous abortion.

2. the crystal structure of human holo-transcobalamin (TC) in complex with the extracellular domain of CD320, visualizing the structural basis of the TC-CD320 interaction, is reported.

3. There was no significant difference in the expression of soluble csf CD320 between patients and controls.

4. Although not significant when corrected for multiple testing, eight single nucleotide polymorphisms (SNPs) in two genes, transcobalamin II (TCN2) and the transcobalamin II-receptor (TCblR), were found to influence several clinical traits of cobalamin deficiency.

5. The soluble transcobalamin receptor is present in cerebrospinal fluid and correlates to dementia-related biomarkers tau proteins and amyloid-beta.

6. Transcobalamin II (TCN2 67A>G and TCN2 776C>G) and transcobalamin II receptor (TCblR 1104C>T) polymorphisms in Korean patients with idiopathic recurrent spontaneous abortion

7. The high urinary concentration and the strong correlation between urinary and serum sCD320 suggests that sCD320 is filtered in the kidney.

8. Data indicate that only the extracellular region (aa 32-229) of TCblR/CD320 is needed for transcobalamin-cobalamin (TC-Cbl) binding.

9. Proliferating cancer cells express measurable levels of TCII and TCII-R.

10. TCblr SNP were associated with omphalocele suggests that disruption of methylation reactions, in which folate, vitamin B12, and homocysteine play critical parts, may be a risk factor for omphalocele.

11. Our data suggest that variation in TCblR plays a role in neural tube defect risk and that these variants may modulate cobalamin metabolism.

12. the cell cycle associated expression of TCblR appears to be tightly regulated in synchrony with the proliferative phase of the cell cycle.

13. Analysis of TCblR/CD320, the gene for the receptor for cellular uptake of transcobalamin-bound cobalamin, identified a homozygous single codon deletion, c.262_264GAG (p.E88del), resulting in the loss of a glutamic acid residue.

14. Confocal microscopy of tonsil sections revealed co-localization of CD320 with CD19 and CD38 but not with CD3 indicating that germinal center B cells expressed CD320 in addition to follicular dendritic cells.

15. This gene encodes a receptor for cellular uptake of transcobalamin-bound vitamin B12.

Mouse (Murine) CD320 Molecule (CD320) interaction partners

1. This study evaluated the role of transcobalamin (TC), the transcobalamin receptor (CD320) , and megalin in various tissues during pregnancy.

2. CD320 role in the hippocampal long-term potentiation and the hippocampal pyramidal neurons.

3. Severe cobalamin depletion in the central nervous system (CNS) after birth in TCblR knockouts indicates that TCblR is the only receptor responsible for cobalamin uptake in the CNS

4. In vivo, endogenous PCSK9 regulates VLDLR protein levels and triglyceride accumulation in adipose tissue.

5. Diabetic rats showed severe hyperlipidemia on d 21 and 28, with a dramatic decline in VLDL-R protein in skeletal muscle (>90%), heart (approximately 50%) and a loss of adipose tissues itself.

6. Reelin binds several receptors, including the VLDL receptor in cultured hippocampus neurons.

7. VLDL and LDL lowering by gene transfer of the VLDL receptor combined with a low-fat diet regimen induces regression and reduces macrophage content in advanced atherosclerotic lesions in LDL receptor-deficient mice

8. These data demonstrate a cell-autonomous function of ApoER2, and most likely VLDLR and Dab1, in postnatal migration of neuroblasts in the forebrain, which is suggested to depend on ligands other than Reelin.

9. The high affinity of apoE4 to the LDLR enhances VLDL sequestration on the hepatocyte surface but delays their internalization.

10. Data show that thrombospondin-1 (THBS-1) is a novel physiological ligand for ApoER2 and VLDLR, and that lack of THBS-1 results in anatomical abnormalities of the RMS and leads to a reduction of postnatal neuronal precursors entering the OB.