Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.27.5 (RNase)
17,967 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study evaluated serum ribonuclease activity (SRA) in patients with inflammatory and neoplastic pancreatic diseases. RNase determination was carried out using t-RNA (T) from E. coli MRE 600 at pH 7.4 and polycytidylic acid (poly-C) (P) at pH 6.6 as RNA substrates with RNase A from bovine pancreas as reference enzyme. Healthy volunteers had a SRA of T: 160 +/- 12 and P: 482 +/- 24 ngeq/mL (mean +/- SEM (n]. In patients with acute interstitial pancreatitis (AIP), SRA was similar to healthy controls (T: 166 +/- 14; P: 474 +/- 30 ngeq/mL). Patients with acute necrotizing pancreatitis (ANP) had increased SRA (T: 278 +/- 49; P: 791 +/- 145 ngeq/mL, p less than 0.01, compared to controls). SRA values were also increased in patients with chronic pancreatitis (CP) with T: 224 +/- 15 ngeq/mL (p less than 0.01) and in patients with pancreatic carcinoma (PCA) with T: 331 +/- 35 (p less than 0.001 vs controls, p less than 0.01 vs CP). Increased SRA was detected in patients with renal insufficiency (T: 2576 +/- 195 ngeq/mL, p less than 0.001). Diagnostic discrimination between AIP and ANP was achieved in 69% using T-SRA (sensitivity 31%, specificity 88%), and in 78% using P-SRA (sensitivity 54%, specificity 92%). Discrimination between CP and pancreatic carcinoma was possible in 68% (sensitivity 67%, specificity 71%). The diagnostic value of serum RNase is limited because of its low sensitivity, but increased T-SRA above a cutoff of 250 ngeq/mL and increased P-SRA above a cutoff of 620 ngeq/mL are specific for detecting pancreatic necrosis in the absence of renal impairment. The kidney is a major site for SRA clearance.
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PMID:Serum ribonuclease activity in the diagnosis of pancreatic disease. 203 16

Thrombospondin (TSP) is a trimeric glycoprotein which is synthesized and incorporated into the extracellular matrix by a wide variety of cells. TSP is involved in a number of cellular processes which govern tumor cell behavior including mitogenesis, attachment, migration, and differentiation. To directly assess the role of TSP in tumor cell growth and spread, a human squamous carcinoma cell line, with high TSP production and an invasive phenotype, was transfected with a TSP cDNA antisense expression vector. Five unique transfected clones were obtained with reduced TSP production. Expression of the transfected antisense sequence in these clones was verified by a ribonuclease protection assay. These clones demonstrated reduced growth rates in vitro when compared with a vector transfected control. After subcutaneous inoculation into athymic mice, the antisense clones formed either no tumors or tumors that were slow growing and highly differentiated. This contrasted with the vector-transfected clone which produced poorly differentiated, rapidly growing, invasive tumors. Our results argue in favor of a direct role for TSP in determining the malignant phenotype of certain human tumors.
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PMID:Antisense-mediated reduction in thrombospondin reverses the malignant phenotype of a human squamous carcinoma. 204 Jun 84

The SK-v cells, established from a premalignant vulvar lesion, contain human papillomavirus type 16 (HPV-16) sequences integrated at a single cellular site and derive from a cell clone present in vivo. Transcription of the HPV-16 genome in SK-v cells was analysed by cDNA heteroduplex mapping and sequencing, and by RNase mapping. Viral sequences were shown to be transcribed into virus-cell fusion messengers. The two major transcripts have a coding capacity for a truncated E6 protein, an E7 protein and an E1-E4 fusion protein, but differ in their 3' virus-cell junction. Minor transcripts have a coding capacity for a full-length E6 protein and another truncated version of E6. The transcription pattern in the E6-E7 region was found to be the same both in SK-v cells and in CaSki cells, a line derived from an invasive cervical carcinoma. Immunoprecipitation experiments showed that the E6 protein (18K) and, predominantly, the E7 protein (20K) are expressed in SK-v cells as in CaSki cells. The E7 protein was found in a two- to threefold lower amount in SK-v cells, but showing the same half-life (about 1 h).
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PMID:Expression of the human papillomavirus type 16 genome in SK-v cells, a line derived from a vulvar intraepithelial neoplasia. 215 96

The human MDR1 gene encoding P-glycoprotein, an energy-dependent drug-efflux pump, was initially isolated from a multidrug-resistant KB carcinoma cell. When a 3 kb genomic sequence isolated from normal human tissue including the major downstream promoter and the first and second exons of the MDR1 gene was compared to the equivalent fragment from KB cells, the MDR1 gene from KB carcinoma cells was found to have a point mutation in the first exon. Although this mutation does not affect the downstream promoter sequence or the coding sequence of the MDR1 gene, it creates a single base mismatch between the 5' KB genomic fragment previously used for RNase protection analysis of MDR1 RNA expression in normal tissues and thereby reduces the sensitivity of this assay. Using the DNA fragment from normal tissues rather than KB cells, we have reanalyzed MDR1 mRNA levels in 12 renal carcinomas and 4 colon adenocarcinomas. By this RNase protection assay, MDR1 RNA levels are as high in these tumors as in the multidrug-resistant cell line, KB-8-5. The ribonuclease protection assay indicated that the major downstream promoter was mainly used in these clinical samples including two samples of RNA from metastatic renal cancer. This assay appears to be a very sensitive and specific assay for detecting MDR1 mRNA levels and mRNA initiation sites in clinical samples.
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PMID:Detection of multidrug resistance (MDR1) gene RNA expression in human tumors by a sensitive ribonuclease protection assay. 248 65

The human papillomavirus type 11 enhancer, when linked to the minimal simian virus 40 early promoter, has been dissected into two domains in monkey kidney CV-1 cells, one being constitutive (designated CEI) and the other inducible by trans-acting E2 proteins encoded by homologous and heterologous papillomaviruses (H. Hirochika, T.R. Broker, and L.T. Chow, J. Virol. 61:2599-2606, 1987; H. Hirochika, R. Hirochika, T.R. Broker, and L.T. Chow, Genes Dev. 2:54-67, 1988). We have demonstrated that the natural promoter regulated by this enhancer is located immediately upstream of the E6 open reading frame (the E6 promoter). We have mapped the cap site to nucleotide 99 by RNase protection. We further demonstrate a second constitutive enhancer element, CEII, which is required for transcription from the E6 promoter in the human cervical carcinoma cell lines C-33A and HeLa but not in CV-1 cells. By deletion mapping, we have localized this cell type-specific domain to 71 base pairs by using chloramphenicol acetyltransferase assays. Deletion of either CEI or CEII dramatically decreased the constitutive activity of the enhancer and the E6 promoter, whereas multimerization of either domain in the absence of the other could independently restore expression. Furthermore, when either of these elements was deleted, the full-length E2 protein of human papillomavirus type 11 abolished the remaining basal E6 promoter activity, demonstrating for the first time that the enhancer-activating E2 protein of human papillomaviruses can also function as a transcriptional repressor for the homologous E6 viral promoter. The presence of multiple copies of each element in tandem overcomes the repression by the E2 protein. The effects of CEII are at the level of transcription, without changing the cap site. By gel shift assay, we have shown that a protein present in nuclear extracts of C-33A and HeLa cervical carcinoma cells binds to the newly identified constitutive element II. This protein did not bind the simian virus 40 enhancer, nor did it bind to the enhancer region of many other papillomaviruses tested. UV cross-linking experiments revealed major 44-kilodalton and minor 34-kilodalton proteins that bound specifically to CEII. These two proteins are either related or bind to CEII with high cooperativity. We conclude that transcriptional activities directed by the enhancer and E6 promoter reflect an intricate balance among viral and cellular factors. We present a model on the regulation of the E6 promoter by host and viral transcription factors.
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PMID:Identification of a novel constitutive enhancer element and an associated binding protein: implications for human papillomavirus type 11 enhancer regulation. 254 7

A PTH-related peptide (PTHRP) has been identified and its cDNA cloned from human tumors associated with the syndrome of humoral hypercalcemia of malignancy. The human PTHRP gene has been recently isolated and found to be a complex transcriptional unit using multiple promoters and containing alternatively spliced 3' exons which result in three mRNA classes, each class encoding a PTHRP with a unique carboxy-terminus. The PTHRP gene appears to be expressed in a number of normal tissues, and PTHRP transcripts have been previously reported to be overexpressed in a small sample of human parathyroid adenomas. In the present study we surveyed RNA prepared from a total of 60 abnormal human parathyroid glands for PTHRP gene expression using a combination of Northern blotting and RNase protection techniques. Apparent overexpression of PTHRP mRNA was observed in two thirds of parathyroid adenomas, whereas no overexpression was found in 7 examples of sporadic primary hyperplasia, 5 examples of secondary hyperplasia, and 3 examples of parathyroid carcinoma. Apparent overexpression was also observed in 1 of 4 cases of multiple endocrine neoplasia type 1, 1 of 2 examples of multiple endocrine neoplasia type 2, and 1 gland considered to represent tertiary hyperparathyroidism. Northern analysis of poly(A)+ RNA prepared from three representative adenomas using region-specific probes indicated that two putative promoters are used and revealed a pattern of preferential splicing of transcripts to include the most distal 3' exon. These findings suggest that the PTHRP gene is commonly overexpressed in adenomatous parathyroid glands, but not in sporadic primary hyperplasia, that this overexpression does not seem to be dependent on the use of a single specific promoter, and that adenomatous parathyroid cells appear to preferentially use one of several alternative splicing pathways. It is presently not known whether PTHRP is secreted by abnormal parathyroid tissues and, if so, in what form.
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PMID:Expression of transcripts encoding a parathyroid hormone-related peptide in abnormal human parathyroid tissues. 257 15

Magnetic resonance spectroscopy (MRS) can identify abnormal lipoproteins in the plasma of patients with premalignant and malignant tumours. Proteolipid complexes, 8-11 nm and 25-28 nm in size, were isolated from the plasma of a patient with a borderline ovarian tumour. These complexes, which generated a characteristically long MRS T2 relaxation value (greater than 400 ms), were disrupted by ribonuclease. None of the conventional lipoproteins had a T2 value above 160 ms. Chemical analysis of the proteolipid complexes showed a 20% glycolipid component, and MRS identified a fucosylated molecule as the origin of the long T2 value. 9 months after resection of all tumour, a visible lipoprotein band, possibly lipoprotein (a), persisted in the plasma but neither the long T2 relaxation value nor the 8-11 nm or 25-28 nm particles were present. The long T2 relaxation value in the MRS profile, found in isolated proteolipid and unfractionated plasma and serum of other patients with carcinoma of the ovary and colon, provides a non-invasive method of assaying for cancer.
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PMID:Proteolipid identified by magnetic resonance spectroscopy in plasma of a patient with borderline ovarian tumour. 288 35

Acid tumor-derived suppressor factors (TDSFs, isoelectric pH less than 3.0) in extracts of murine fibrosarcomas and human colorectal adenocarcinoma cell lines induce normal murine spleen cells to inhibit delayed-type hypersensitivity (DTH) to the sensitizer dinitrochlorobenzene (DNCB). We sought to determine if TDSF from normal and neoplastic human colon and rectum also inhibited normal human peripheral blood mononuclear cells (PBMC) responses to mitogen and to alloantigens. Collagenase-DNase digests of five freshly isolated carcinomas and paired autologous normal tissues were subjected to preparative isoelectric focusing (pIEF) over a pH range of 2.5 to 9.5. Fractions with isoelectric pH less than 3.0 from three of the five tumors induced normal C3H/HeN spleen cells to inhibit DTH to DNCB. Acid fractions from three tumors and four normal tissues also significantly inhibited the PBMC proliferative response to mitogen and alloantigens. However, the ability of acid fractions to suppress lymphocyte proliferation did not correlate with the induction of suppression of DTH to DNCB. Incubation of human PBMC with acid proliferation inhibitors did not induce suppressor cells that would inhibit the subsequent proliferative response of fresh, autologous PBMC. The acid suppressant from colorectal carcinoma was sensitive to treatment with trypsin but not RNase or DNase, whereas murine TDSF is sensitive to RNase and resistant to treatment with trypsin. The suppressive moiety from one tumor had an apparent mass of 45 kDa by gel filtration chromatography, in contrast to murine TDSF that has a mass of more than 300 kDa. Thus, the acid inhibitor in digests of human colorectal carcinoma is distinct from the TDSF that induces suppressor cells for DTH to DNCB.
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PMID:Tumor-derived suppressor factors (TDSFs) in normal and neoplastic colon and rectum. 294 30

Sera from 230 hepatocellular carcinoma patients were tested for antinuclear antibodies by anticomplement immunofluorescence in 16 types of transformed, diploid or primary cells of human, monkey, chimpanzee or rat origin. As controls, we tested 85 sera from patients with chronic liver diseases, 48 sera from patients with nonhepatic cancers and 164 sera of normal controls. Exactly 11.2% of all cancer patients but only 3.6% of noncancer patients had complement-fixing antinuclear antibody that reacted with all substrates. Only sera from hepatocellular carcinoma reacted with subsets of the tumor cell substrates. These sera reacted with hepatocellular carcinoma cells and nonhepatic cancer cells (antitumor) or only with one or more of the human hepatocellular carcinoma cell lines, PLC/PRF/5, Hep3B and Mahlavu, that were derived from HBsAg-positive patients (antihepatocellular carcinoma). Three of these reacted only with hepatitis B virus DNA-positive cells (PLC/PRF/5 and Hep3B) that contained "hepatitis B-associated nuclear antigen," 1 reacted only with hepatitis B virus DNA-negative Mahlavu cells, 1 reacted with PLC/PRF/5 and Mahlavu and 3 reacted with all 3 cells. The nuclear antigen in Mahlavu was expressed as a homogeneous fluorescence that spared the nucleoli, was present in a lower percentage of cells than hepatitis B-associated nuclear antigen and was more thermostable than hepatitis B-associated nuclear antigen. However, it resembled hepatitis B-associated nuclear antigen in kinetics of expression and susceptibility to digestion with DNase, RNase and proteinase K. The nature of the nuclear antigens in the hepatocellular carcinoma cells is poorly understood but one possibility is that they may represent the expression of viral or tumor-related genes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The spectrum of complement-fixing antinuclear antibodies in patients with hepatocellular carcinoma. 299 Nov 5

Until now the fluorescence assay with ethidium bromide has only been used on pure DNA. This assay depends on the difference in fluorescence between single- and double-stranded DNA (dsDNA). Cross-links in DNA are measured by the return of fluorescence of dsDNA after heat denaturation at pH 12. Under these conditions denatured DNA gives very low fluorescence. In the present study this assay was applied to tumor cells. The mouse Ehrlich ascites tumor cell line (EAT) and a human small-cell carcinoma line (GLC4) were incubated for 4 hr at 37 degrees C, with the cross-linking agent cis-diamino-dichloro platinum (cDDP). The samples of whole cells were thereafter resuspended in potassium phosphate buffer with 10 mM EDTA, 4M NaCl, 0.1% Sarkosyl pH 7.2, for 16 hr at 37 degrees C. Measurements were performed with a spectrofluorometer with excitation wavelength 525 nm, emission wavelength 580 nm. There was a linear relationship for cDDP concentrations of 0-150 microM and the extent of DNA cross-links in EAT (r = 0.958). In GLC4 there was a linear relationship at low cDDP concentrations of 0-50 microM (r = 0.968) while between 50 and 150 microM a plateau was reached. RNase added to the lysate of whole cells had no influence on the extent of cross-links. This assay was compared with the alkaline elution assay, and results were identical.
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PMID:Detection of DNA cross-links in tumor cells with the ethidium bromide fluorescence assay. 300 75


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