Low density lipoprotein-receptor plays a major role in the binding of very low density lipoproteins and their remnants on HepG2 cells.

摘要: Abstract The binding to HepG2 cells of very low density lipoproteins (VLDL) and their remnants (IDL) was alternatively, in the past, attributed lipoprotein receptor (LDLr) or an apoE-specific receptor. In order resolve this issue, we have compared those labelled with iodine-125 normal LDLr deficient cells. Those were obtained by a constitutive antisense strategy level is 14% By saturation curve analysis, show that VLDL IDL bind high affinity sites on eliminated conducting assay presence 200-fold excess HDL3 respective concentrations 125 I -labelled IDL. For -VLDL cells, found dissociation constant (Kd) 21.2±3.7 μg prot./ml (S.E., N=5) maximal capacity (Bmax) 0.0312±0.0063 prot./mg cell prot, while measured Kd 5.3±0.8 Bmax 0.0081±0.0014 This indicates responsible for 74% non-LDLr has higher than LDLr. A 53% loss -IDL (Bmax:0.028±0.005 versus 0.059±0.006), no significant statistical difference between affinities. study shows almost only contributor binding, it shares another physiological importance confirmed equivalent degradation