
IndraLab
Statements
sparser
"This process involves: (1) the binding of a Wnt ligand to the extracellular cysteine rich domain on the transmembrane Frizzled receptor, (2) phosphorylation/activation of the protein disheveled by low-density lipoprotein receptor-related protein (LDLR-LRP) -5 or -6 co-receptors, (3) blocking of glycogen synthase kinase-3β activity (GSK-3β) by sequestering GSK-3β via the inhibitory protein frequently rearranged in advanced T cell lymphomas (Frat), and (4) inactivation of the “destruction complex” resulting in decreased phosphorylation and down-regulating proteasomal degradation of β-catenin [ xref , xref , xref , xref ]."
sparser
"For example, interactions with the LDL receptor and Lrp1 support the M6PR-independent delivery of cathepsin D to lysosomes ( xref ), whereas glucocerebrosidase, whose loss causes a lysosome storage disorder known as Gaucher’s disease, is routed through a LIMP-2–dependent mechanism ( xref )."
sparser
"The different rates of uptake of CRLPs oxCRLPs and pCRLPs by macrophages demonstrated here, therefore, could be explained by effects on interaction with the LDLr and the LRP caused by differences both in the conformation of apoE and in the number of apoE molecules able to bind to the receptors, even though the total amount of apoE associated with the particles is not changed."
sparser
"However, ligand binding to LRP1, a member of LDLR family, transactivates the Trk receptors through an SFK-dependent pathway in PC12 cells and neurons [ xref ], demonstrating that apolipoprotein E-receptors have neurotrophic activity that is dependent on Trk receptor transactivation."
sparser
"The use of mice deficient in SMC LRP (LRP smc−∕− ) associated with LDLR knockout (LDLR −∕− ) resulted in a severe vSMC proliferation within the aorta, disruption of elastic laminae, and enhancement of atherosclerosis, suggesting that vSMC LRP plays an important atheroprotective role via clearance capacities not limited to LDL endocytosis alone (Boucher et al., xref )."
sparser
"None of the LDLa repeats of LRAD3 contains all of the necessary acidic amino acids that are required for generating an acidic pocket capable of docking lysine side chains that protrude from certain LDL receptor family member ligands, such as the receptor associated protein (RAP) ( xref ) ( xref ), suggesting that potential ligands are likely to be distinct from those that interact with the LDL receptor or LRP1."
sparser
"Another effect of reduced recycling of apoE4 is due to the tight binding of apoE4 to LDLR and LRP1 in the endosomal compartment [ xref ], which in turn affects the interaction of the amyloid precursor protein (APP) and LRP1 that is crucial for the generation of Aβ [ xref , xref ]."
sparser
"Finally, siRNA-CaP-rHDL was prepared by
incubating siRNA-CaP-LNC with apolipoprotein E3 (ApoE3), which was previously
confirmed to be responsible for binding to low-density lipoprotein receptor
(LDLR) and low-density lipoprotein receptor-related protein 1 (LRP1) that are
expressed in the BBB, blood–brain tumour barrier (BBTB) and glioblastoma
cells xref xref xref xref xref ."
sparser
"ApoCI is an inhibitor of LPL activity, and inhibits the binding of VLDL to LDL-receptor related protein (LRP), xref , xref as well as the apoE-mediated binding of VLDL to the LDLR and the LRP. xref , xref ApoCI is a potent activator of lecithin:cholesterol acyltransferase (LCAT), xref , xref leading to elevated HDL-cholesterol ester concentrations. xref xref – xref In apoCI-deficient mice, the primary metabolic defect is an impaired VLDL uptake by the liver in vivo. xref Interestingly, whereas overexpression of human APOC1 in transgenic mice predominantly inhibits the uptake of VLDL by the liver, the absence of endogenous apoCI in mice appears to have the same effect, although to a lesser extent."
sparser
"The fact that both Dab2 and ARH increased the size of CCPs relative to CCPs in which AP2 is the predominant adaptor (i.e., under conditions of TfnR overexpression) might reflect the need to accommodate the very large ligands bound by LDLR and LRP ( xref ) (i.e., LDL particles, d∼22 nm and α2-macroglobulin, d∼18.5 nm; xref ), respectively."
sparser
"It is unclear whether the apoC-III 0a and apoC-III 0b glycoforms affect the affinity of TRLs for SDC1, but in previous studies the absence or presence of murine apoC-III 0a on TRLs did not seem to affect the capacity of SDC1 to mediate TRL clearance. xref This thus suggests no preferential binding of apoC-III 0a to HSPGs. xref Combined, these observations support the idea that the apoC-III 0a glycoform (or murine apoC-III) is a very potent inhibitor of TRL binding to LDLR and LRP1 and shifts clearance of apoC-III 0a bearing TRLs to SDC1 by default (and not by greater affinity)."