Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01034 (cystatin C)
 3,397 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the effect of acetone on the viability of CAA, a sample of CAA with a known titer was treated with 90% acetone for 24 hours at room temperature. The remaining viable CAA was quantitated by titrating the treated preparation in MDCC-MSB1 cell culture. Results indicated that CAA is very resistant to inactivation by acetone.
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PMID:The effect of acetone on the viability of chicken anemia agent. 141 9

The TT cell line of human medullary thyroid carcinoma, that retains some of the differentiated functions of thyroid C cells including the synthesis and secretion of calcitonin, was found to contain and release into the culture medium cysteine proteinase inhibitor(s), cystatin(s). The major inhibitor, which is similar to, if not identical with, cystatin C, is constitutively released, or secreted, by TT cells. The rate of secretion of cystatin, quantified by titration of inhibition of papain, was stimulated by dibutyryladenosine 3':5'-cyclic monophosphate, forskolin, the calcium ionophore A 23187, and by the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA). Neither forskolin nor TPA had, however, an effect on the level of the inhibitor in TT cells. Treatment with n-butyrate strongly inhibited the proliferation of TT cells, and led, in 4 to 7 days, to a doubling of the intracellular concentration of cystatins. Northern blot hybridizations to a 32P-labeled riboprobe complementary to human cystatin C cDNA indicated that cAMP, forskolin, and TPA had no effect on the steady-state levels of cystatin C mRNA. These data indicate that release of cystatin(s) from TT cells is regulated by cAMP-calcium-protein kinase C mechanisms that appear to be similar to those that regulate the secretion of calcitonin from these cells. However, in contrast to the calcitonin gene, the expression of the cystatin C gene in these cells is not regulated by cAMP or TPA. By a combination of acetone fractionation, affinity chromatography on Cm-papain-Sepharose, and gel exclusion chromatography a protein of approximately 14 kilodaltons was isolated from TT cells that reacted with antibodies against human cystatin C, and strongly inhibited papain. Cystain secreted by TT cells also had a molecular weight of 14 kilodaltons, and reacted with anti-human cystatin C antibodies. The physiologic and pathologic roles of cystatins in different cell types remain to be established. The TT cells provide a suitable cell type to study the regulation of the expression of the cystatin gene and the mechanism of cystatin release.
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PMID:Cysteine proteinase inhibitor in cultured human medullary thyroid carcinoma cells. 160 39

Racemic anti-benzo[c]phenanthrene-3,4-diol-1,2-epoxide (anti-B[c]PhDE) is a powerful rat mammary carcinogen and is one of the most potent diol-epoxide tumorigens in mouse skin. Activation of ras genes has been proposed to be involved in tumorigenesis by this and related polynuclear aromatic hydrocarbon metabolites. Therefore, we analyzed rat mammary tumors and mouse skin tumors induced by anti-B[c]PhDE for mutations at codons 12, 13 and 61 of the Ki-ras and Ha-ras genes. No Ki-ras mutations were detected in either tumor type. In the rat mammary tumors, no Ha-ras mutations in codons 12 or 13 were observed in 25 tumors analyzed. Only one, a CAA-->CTA mutation, was detected in codon 61, of 42 tumors analyzed. These results indicate that Ki-ras and Ha-ras mutations are not involved in the induction of rat mammary tumors by anti-B[c]PhDE. Mutations in codon 61 of the Ha-ras gene were common, however, in mouse skin tumors induced by this diol-epoxide, being detected in 63% of the tumors analyzed; 90% of these mutations were CAA-->CTA. A dose-dependent difference in the occurrence of the CAA-->CTA mutations was observed; they were present in 75% of the tumors induced by a 100 nmol initiating dose of the diol-epoxide, but in only 34.5% of the tumors induced by a 400 nmol initiating dose. A CAA-->CTA mutation in codon 61 of Ha-ras was also detected in one of four acetone control tumors. In comparison with previous studies of other polynuclear aromatic hydrocarbons and their metabolites, the results suggest that the reactivity with DNA of anti-B[c]PhDE is one factor involved in the induction of A mutations in Ha-ras genes in mouse skin, but further studies are required to evaluate the significance of these mutations in mouse skin tumorigenesis.
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PMID:Contrasting incidence of ras mutations in rat mammary and mouse skin tumors induced by anti-benzo[c]phenanthrene-3,4-diol-1,2-epoxide. 795 41

7H-dibenzo[c,g]carbazole (DBC) is a potent liver and skin carcinogen when topically applied to the back skin of mice. This compound is found in complex mixtures produced during incomplete combustion of fossil fuels as well as in wood and tobacco smoke. The objective of this study was to elucidate the mechanism of action of this compound by assessing the Ha-ras mutational spectra of skin and liver tumors induced in a mouse model system. Low doses (50 nmol) and high doses (100 nmol) of DBC were applied topically to the backs of Hsd:ICR(Br) mice twice weekly. No treatment and solvent application were used as controls. After the mice were killed, the skin and liver tumors were removed, DNA was isolated, and tumor DNA was screened for Ha-ras codon 12, 13, and 61 mutations by using an enriched polymerase chain reaction method. Mutations were confirmed by reverse cyclic dideoxy sequencing. No mutations were found in codons 12 and 13 of DBC-induced tumors, whereas one acetone-control tumor had a codon 13 mutation. Sixty-seven percent of skin tumors and 45% of liver tumors induced by high doses of DBC and 67% of skin tumors induced by low doses of DBC contained codon 61 mutations, whereas liver tumors induced by low doses of DBC did not. The codon 61 mutations were exclusively A:T-->T:A transversions within the second base (CAA-->CTA). These results indicate that DBC is a unique polycyclic aromatic hydrocarbon in that it induces both skin and liver tumors upon topical application and that the mutational spectra are the same in tumors from two target organs, skin and liver, yet different from tumors from a third target organ, lung.
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PMID:Frequent Ha-ras mutations in murine skin and liver tumors induced by 7H-dibenzo[c,g]carbazole. 1036 12

A rapid and sensitive method for quantitative determination of cystatin C (CC) protein in human urine via HPLC was developed and validated. Acetone has been used as a precipitating agent of CC protein from the urine biological matrix. Separation and detection were accomplished by ion pair liquid chromatography and UV detection. Gradient elution mode was utilized to elute CC with a UV detection of 224nm. The analysis time was 14min per sample using Ace C8 (150x4.6mm i.d., 5mum) as a chromatographic column with a flow rate of 1.0mL/min. Calibration curve with good linearity (r(2)=0.99) within the range from 0.390 to 0.001mg/mL was obtained. Limits of detection and quantification were 0.001 and 0.002mg/mL, respectively. Inter-assay and intra-assay variabilities were <15% for all levels and <20% at the limit of quantification level. Major advantages of the method: specific where no false positive results might be obtained and fast where sample pretreatment needs only 1h.
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PMID:Novel liquid chromatographic determination of cystatin C in human urine. 1923 47