monensin and 3-3--dioctadecylindocarbocyanine

monensin has been researched along with 3-3--dioctadecylindocarbocyanine* in 1 studies

Other Studies

1 other study(ies) available for monensin and 3-3--dioctadecylindocarbocyanine

Article	Year
Lovastatin increases surface low density lipoprotein receptor expression by retarding the receptor internalization rate in proliferating lymphocytes. Biochemical and biophysical research communications, 1997, Jun-09, Volume: 235, Issue:1 We examined the effects of Lovastatin on LDL receptor (LDL-R) expression and rate of internalization in interleukin-2 (IL-2) expanded phytohemagglutinin-stimulated lymphocytes. Lovastatin increased the surface LDL-R expression, but not DiI-LDL uptake, by up to 30% regardless of whether cell proliferation was affected. It caused a dose-dependent reduction in the LDL-R internalization rate as determined with monensin. Lovastatin had no effect on IL-2 receptor internalization. Inhibition of DNA synthesis by hydroxyurea or protein tyrosine kinase activity by genistein failed to affect the LDL-R internalization rate. Co-incubation of cells with Lovastatin and mevalonate or LDL completely restored the rate of LDL-R internalization. We conclude that Lovastatin increases the apparent surface LDL-R expression by retarding the rate of LDL-R internalization. The effect is mediated through the mevalonate pathway but not the anti-mitogenic property of Lovastatin. Topics: Carbocyanines; Cell Division; Endocytosis; Flow Cytometry; Fluorescent Dyes; Genistein; Hydroxyurea; Interleukin-2; Isoflavones; Lipoproteins, LDL; Lovastatin; Lymphocyte Activation; Lymphocytes; Mevalonic Acid; Monensin; Phytohemagglutinins; Receptors, Interleukin-2; Receptors, LDL	1997

Article

Year

Lovastatin increases surface low density lipoprotein receptor expression by retarding the receptor internalization rate in proliferating lymphocytes.

Biochemical and biophysical research communications, 1997, Jun-09, Volume: 235, Issue:1

We examined the effects of Lovastatin on LDL receptor (LDL-R) expression and rate of internalization in interleukin-2 (IL-2) expanded phytohemagglutinin-stimulated lymphocytes. Lovastatin increased the surface LDL-R expression, but not DiI-LDL uptake, by up to 30% regardless of whether cell proliferation was affected. It caused a dose-dependent reduction in the LDL-R internalization rate as determined with monensin. Lovastatin had no effect on IL-2 receptor internalization. Inhibition of DNA synthesis by hydroxyurea or protein tyrosine kinase activity by genistein failed to affect the LDL-R internalization rate. Co-incubation of cells with Lovastatin and mevalonate or LDL completely restored the rate of LDL-R internalization. We conclude that Lovastatin increases the apparent surface LDL-R expression by retarding the rate of LDL-R internalization. The effect is mediated through the mevalonate pathway but not the anti-mitogenic property of Lovastatin.

Topics: Carbocyanines; Cell Division; Endocytosis; Flow Cytometry; Fluorescent Dyes; Genistein; Hydroxyurea; Interleukin-2; Isoflavones; Lipoproteins, LDL; Lovastatin; Lymphocyte Activation; Lymphocytes; Mevalonic Acid; Monensin; Phytohemagglutinins; Receptors, Interleukin-2; Receptors, LDL

1997