Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P14784 (IL-2 receptor)
 3,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The levels of soluble form of E-Selectin (sEs), or endothelial-leukocyte adhesion molecule-1, were measured in 96 sera derived from 72 HIV-infected patients at different stages of the disease, 60 healthy blood donors, and 50 HIV-negative patients with infections, using a quantitative ELISA. Levels of sEs in HIV-infected individuals without AIDS, according to the 1993 classification system of the Centers for Disease Control, were higher than normal (mean +/- SEM 48 +/- 4 versus 35 +/- 3 ng/ml, p = 0.003). Patients with established AIDS, who were afebrile and had no evidence of acute concurrent infection, had even higher sEs serum levels (70 +/- 9 ng/ml, p = 0.009, compared to those without AIDS). A significant increase in clinical category disease progression was present. Individual concentrations of sEs correlated directly with levels of soluble intercellular adhesion molecule-1 (p < 0.00001) and IL-2 receptor (p = 0.001), but not with CD4+ T-cell counts. Zidovudine treatment was not associated with changes in sEs serum levels. Elevated sEs levels were also found in HIV-seronegative patients with other bacterial and protozoal infections. Since sEs is a biologically active molecule, further studies should investigate the pathogenetic significance of circulating sEs in HIV-related disease progression, and assess the prognostic value of sEs determination for these patients.
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PMID:Levels of the circulating cell adhesion molecule E-selectin and disease progression in HIV infection. 852 77

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.
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PMID:Lovastatin increases surface low density lipoprotein receptor expression by retarding the receptor internalization rate in proliferating lymphocytes. 919 47