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)

ADP ribosylation in the presence of cholera or pertussis toxin indicated the presence of G-proteins in Nb2 cell membranes. Two protein bands, with mol wt of 43.5K and 46.5K, were radiolabeled by cholera toxin, while a single protein (41.5K mol wt) was ADP ribosylated by pertussis toxin. Northern hybridization of total RNA from Nb2 cells with specific cDNA probes indicated the presence of mRNA transcripts encoding Gs, Gi2, Go, and, to a lesser extent, Gi3. A characteristic of receptors coupled to G-proteins is that their binding properties are regulated by guanine nucleotides. The binding of [125I]human GH to the lactogen receptor as well as the binding of [125I]IL-2 to the IL-2 receptor were decreased in a dose-dependent manner by GTP, GDP, and the analog guanosine 5'-O-(3-thiotriphosphate). GMP, however, had no effect. The addition of pyruvate kinase and phosphoenolpyruvate to regenerate GTP from GDP greatly increased the apparent potency of GTP. Cholera toxin inhibited PRL- and interleukin-2-stimulated DNA synthesis and cell proliferation in the Nb2 cells. In contrast, pertussis toxin had a differential effect on PRL- and IL-2-stimulated cells. Pertussis toxin, at an optimal concentration of 0.01 ng/ml, significantly enhanced the stimulatory effects of PRL on DNA synthesis (P less than or equal to 0.01; n = 9) and cell proliferation (P less than or equal to 0.05; n = 9) compared with the effect of PRL alone. However, at higher concentrations the toxin inhibited PRL-stimulated DNA synthesis and cell proliferation. Complete inhibition was achieved with 1000 ng/ml toxin. In contrast to the biphasic effect on PRL-stimulated cells, pertussis toxin was only weakly inhibitory to cells treated with IL-2. At the highest concentration tested, pertussis toxin (1000 ng/ml) inhibited IL-2-stimulated DNA synthesis and cell growth by only 30-35%. (Bu)2cAMP (IC50 = 0.019 mM) or methylxanthine (MIX; IC50 = 0.25 mM) also inhibited PRL-stimulated DNA synthesis. In the absence of mitogen, neither agent, from 0.0001-1 mM, had any effect on DNA synthesis. Similarly, IL-2-stimulated DNA synthesis in Nb2 cells was inhibited by (Bu)2cAMP (IC50 = 0.019 mM) or MIX (IC50 = 0.072 mM). However, MIX was approximately 3 times as potent in inhibiting the cell response to IL-2 as that to PRL. The susceptibility of Nb2 cells to both bacterial toxins suggests a role for G-proteins in regulating PRL- or IL-2-stimulated mitogenesis in these cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:G-proteins modulate prolactin- and interleukin-2-stimulated mitogenesis in rat Nb2 lymphoma cells. 246 72

The onset and persistence of psoriatic lesions are linked to the presence of an inflammatory infiltrate of CD3+ lymphocytes that includes CD4+ and CD8+ subsets. Since a primary susceptibility factor for psoriasis is the Class I HLA-Cw6 molecule, we set out to learn more about the features of the epidermal CD8+ lymphocytes. The markers tested were GMP-17, a cytotoxic granule protein found in activated cytotoxic lymphocytes (CTLs), and the alpha chain of the IL-2 receptor (CD25), a plasma membrane molecule found on activated T cells. Lymphocytes in lesional skin expressed the GMP-17 protein, whereas lymphocytes in non-lesional skin, resolving lesional skin and normal skin had little or no GMP-17. By flow cytometry analysis, lesional epidermal GMP-17+ cells were CD8+CD3+, with a subpopulation expressing the activation marker CD25+. Due to the abundance of activated GMP-17+CD8+CD3+ lymphocytes (the phenotype of activated cytotoxic cells) in psoriatic lesions compared to non-lesional and normal skin, we hypothesize that they are contributing directly to the psoriatic phenotype.
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PMID:Intraepidermal lymphocytes in psoriatic lesions are activated GMP-17(TIA-1)+CD8+CD3+ CTLs as determined by phenotypic analysis. 952 96

Objective: A systematic review and meta-analysis of diagnostic biomarkers for noninvasive diagnosis of acute allograft rejection following liver transplantation. Background: Noninvasive blood and urine markers have been widely explored in recent decades for diagnosing acute rejection after liver transplantation. However, none have been translated into routine clinical use so far due to uncertain diagnostic accuracy, and liver biopsy remains the gold standard. Methods: Systematic literature searches of Medline, Cochrane and Embase were conducted up to February 2019 to identify studies evaluating the use of noninvasive markers in diagnosing allograft rejection following liver transplantation. Meta-analysis was performed using a random effects model with DerSimonian-Laird weighting and the hierarchical summary receiver operating curve. Results: Of 560 identified studies, 15 studies (1,445 patients) met the inclusion criteria. The following markers were tested: acid labile nitroso-compounds (NOx), serum amyloid A protein, procalcitonin, peripheral blood eosinophil count, peripheral blood T-cell activation and interleukin 2 (IL-2) receptor, guanylate-binding protein-2 mRNA, graft-derived cell-free DNA, pi-glutathione S-transferase, alpha-glutathione S-transferase and serum HLA class I soluble antigens. Only eosinophil count was tested in multiple studies, and they demonstrated high heterogeneity (I 2 = 72% [95% CI: 0.5-0.99]). IL-2 receptor demonstrated the highest sensitivity (89% [95% CI: 0.78-0.96]) and specificity (81% [95% CI: 0.69-0.89]). Conclusion: IL-2 receptor expression demonstrated the highest diagnostic accuracy, while the peripheral eosinophil count was the only marker tested in more than one study. Presently, liver biopsy remains superior to noninvasive diagnostic biomarkers as most studies exhibited inferior designs, hindering possible translation into clinical application.
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PMID:Diagnostic Biomarkers to Diagnose Acute Allograft Rejection After Liver Transplantation: Systematic Review and Meta-Analysis of Diagnostic Accuracy Studies. 3103 58