Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three distinct genes encode an identical calmodulin protein in mammalian cells. In addition, multiple mRNA transcripts, with approximate sizes of 1.6 kb and 4.4 kb, are visualized on Northern blots hybridized to calmodulin-I cDNA probes. To elucidate the mechanism generating multiple calmodulin mRNAs, the complete sequence of the 4194 base human calmodulin-I mRNA was determined from cDNA clones and 3' rapid amplification of complementary ends (3' RACE). The 5' untranslated region of calmodulin-I mRNA contains a GC-rich domain containing multiple repeats of GGC interrupted by a GCA sequence, as well as a tandem repeat sequence of eight GCA triplets. The 3' untranslated region of calmodulin-I mRNA contains two canonical and one aberrant (ATTAAA) polyadenylation signal, consistent with the sizes of 1.6 kb and 4.4 kb mRNAs visualized on Northern blots, and a potential minor 4.2 kb mRNA detected by 3' RACE. Hybridization experiments using specific probes upstream and downstream of the polyadenylation signals demonstrated that alternate use of polyadenylation signals is the molecular mechanism for multiple calmodulin-I mRNA transcripts in human cells. Thirteen adenine rich elements with the motif AUUUA were detected in the 3' untranslated region. Three such motifs are embedded in regions that are conserved with the rat 3' untranslated region of calmodulin-I mRNA. One of these is surrounded by an adenine-uridine rich region that can form an 11-base pair stem structure. We propose that sequences in the 3' untranslated region of calmodulin-I mRNA may play a role in the regulation of calmodulin expression.
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PMID:Multiple mRNA species are generated by alternate polyadenylation from the human calmodulin-I gene. 759 66

The immunohistochemical study was performed on temporal artery biopsies from eight patients with giant cell (temporal) arteritis: three before treatment, four after a short period of corticosteroid therapy (from 1 day to 7 days) and one during relapse occurring after a treatment of 9 years; from four subjects with clinical symptoms but without histological features of giant cell arteritis and from five negative controls. Before treatment, biopsies of patients with temporal arteritis showed an inflammatory infiltrate with macrophages and T cells, essentially CD4+ and memory T cells (CD45 RO+), expressing the markers of activation IL2 receptor and HLA DR. Few B and NK cells were also detected. Adhesion molecules, LFA1 and I-CAM1, were strongly expressed by T cells and macrophages. In contrast, the ligand to the CD2, the CD58 marker, was rarely detected. These immunohistochemical features were also observed after a short corticosteroid treatment (by intravenous methylprednisolone or oral prednisone), with presence of activated T cells, memory T cells, macrophages and I-CAM1 and LFA1 expressing cells in the infiltrate. A temporal biopsy, performed after a long time of corticosteroid therapy, showed activated T cells, macrophages and memory cells in o,ne arteriole. In controls, this study showed some mononuclear cells dispersed in intima and adventia, but without activated or memory T cells. Our results support the presence of immune local response in temporal arteritis, incompletely improved by a short corticosteroid treatment.
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PMID:[Immunohistochemical study of lesions in Horton's temporal arteritis before and during corticotherapy]. 897 74