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:3.1.27.1 (RNase)
16,360 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum Ribonuclease (RNase, EC. 3. 1. 4. 22) of normal persons and of patients with chronic pancreatitis, or pancreatic cancer was determined with poly (C) as substrate. Strikingly abnormal elevations occured in the serum RNase of patients with pancreatic cancer (p less than 0.001). Average serum RNase values of 18 normal persons, 10 patients with chronic pancreatitis and 26 patients with pancreatic cancer were 92, 118, and 249 units, respectively. In patients with pancreatic cancer, we compared the RNase level with four histologic types (ductar cell adenocarcinoma, anaplastic cell carcinoma, acinar cell carcinoma, and islet cell carcinoma). Adenocarcinoma showed higher activity than the other histologic types (p less than 0.005). When we compared the serum of pancreatic cancer and pancreatic cancer tumor extract with normal serum and normal pancreas extract, strikingly different phosphocellulose chromatographic pattern were evident. The correlation of increased serum RNase levels with tumor histology and different chromatographic pattern may explain the new enzyme production in cancer patients, and have biological significance in the development of pancreatic cancer.
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PMID:Serum ribonucleases in pancreatic cancer: relation to tumor histology. 21 87

Northern blot and ribonuclease protection assay were used to identify alpha 2-adrenoceptor subtypes in human colonic adenocarcinoma (HT29), neuroblastoma x glioma rat-mouse hybrid NG108-15 (NG108) and opossum kidney (OK) cell lines. Radioligand binding studies showed that the alpha 2-adrenoceptor expressed in HT29, NG108 and OK cells represent the pharmacological alpha 2A, alpha 2B and alpha 2C subtypes respectively. In our Northern blot analysis, hybridization of poly(A)+ RNA from HT29, NG108 and OK cells with human kidney alpha 2-adrenoceptor cDNA probe (alpha 2-C4) identified a single band of 4.4, 4.2 and 4.4 kb respectively in each cell line. Hybridization with a human platelet alpha 2-adrenoceptor genomic probe (alpha 2-C10) resulted in two bands for HT29 cells with the size of 4.4 kb and 3.9 kb. No bands were seen for HT29, NG108 and OK cells when hybridized with a third alpha 2-adrenoceptor human genomic DNA probe which is localized in chromosome 2 (alpha 2-C2). For the HT29 cells, the 3.9 kb band was seen only when using the alpha 2-C10 probe. Thus, this band probably represents alpha 2-C10 mRNA. To further characterize the alpha 2-adrenoceptor mRNA expressed in HT29, NG108 and OK cells, the sensitive ribonuclease protection assay was performed. A single band about 900 bp was protected when the poly(A)+ RNA from NG108 and OK cells was hybridized with an alpha 2-C4 RNA probe and digested with RNAases. Hybridization of mRNA from HT29 cells with alpha 2-C10 RNA probe and digestion with RNAases protected a 500 bp fragment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Northern blot and ribonuclease protection study of alpha 2-adrenoceptor subtypes in cultured cell lines. 132 48

In order to locate the promoter region of the human alpha 2A adrenergic receptor gene we used RNase protection analysis and antisense RNA probes to map the cap site of the alpha 2 transcripts. Prior sequence analysis has shown two potential TATA box motifs in the human alpha 2A adrenergic receptor gene, TATATAT and TATAAAA, located 427 and 1037 base pairs (bp), respectively, upstream of the protein coding region. RNase protection experiments and primer extension show that transcription starts downstream of the distal TATAAAA, indicating that the 5'-untranslated region is approximately 1 kilobase in length. We have used the chloramphenicol acetyltransferase reporter gene and transient transfection into HT29, a human adenocarcinoma cell line that expresses the alpha 2A receptor, to show that as little as 150 bp upstream of the cap site can direct transcription. Sequence analysis shows that although this region contains the TATA box motif it lacks a CCAAT box motif. DNase I footprint analysis of a fragment from -17 to -193 (where +1 is the transcription initiation site), using nuclear extracts from HT29, showed hypersensitive sites (-68/-69) and two protected regions: -70 to -87, which includes a 10-bp palindrome, and -92 to -105, which includes a GC box, a common motif for Sp1 nuclear factor binding. Gel mobility shift assays indicate that Sp1 or a related factor may bind to this GC box. Deletion of the GC box and the palindrome from chloramphenicol acetyltransferase constructs abolishes transcription. We propose that these cis sequences may function in lieu of a CCAAT box to regulate transcription of the human alpha 2A adrenergic receptor gene.
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PMID:Promoter region of the human alpha 2A adrenergic receptor gene. 138 31

Calcyclin is a member of the S-100 family of calcium-binding proteins, whose expression is enhanced when quiescent cells are exposed to mitogenic signals. The function of calcyclin is unknown, but it is thought to be involved in modulating the intracellular calcium concentration following mitogenic stimuli. Since activation of protein kinase C (PKC) also occurs following stimulation of quiescent cells by a variety of mitogens, we have investigated the relationship between calcyclin expression and PKC activation in three human endometrial adenocarcinoma cell lines. The addition of 10(-7) M 4 beta-phorbol 12-myristate 13-acetate (PMA) to HEC-50 and HEC-1B cell cultures resulted in a change in cell morphology, an inhibition of proliferation, an increase in calcyclin transcription rate, and an increase in calcyclin mRNA and calcyclin protein levels. In contrast, PMA had no effect on cell morphology or cell proliferation in the Ishikawa adenocarcinoma cell line but enhanced calcyclin expression. Another bioactive phorbol ester had the same effect, whereas the calcium ionophore A23187 and the non-phorbol-ester-type tumor promoter thapsigargin had no effect on calcyclin expression. The effect of PMA on calcyclin expression was blocked by the simultaneous addition of the PKC inhibitor staurosporine and by protein synthesis inhibition with cycloheximide. RNase protection assays and primer extension analysis demonstrated that PMA enhanced transcription from all three of the previously identified transcription start sites in the calcyclin gene. These data clearly demonstrate a dissociation between calcyclin expression and cellular proliferation and suggest that the enhanced calcyclin expression which is seen in quiescent cells following mitogenic stimuli may result from activation of the PKC system.
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PMID:Differential effects of phorbol esters on proliferation and calcyclin expression in human endometrial carcinoma cells. 146 12

The molecular mechanisms that regulate intestine-specific gene expression and the transition from proliferating, undifferentiated crypt cells to nonproliferating, differentiated villus cells are unknown. Sucrase-isomaltase is an apical membrane disaccharidase that is found exclusively in enterocytes of adult intestine and is expressed in a complex pattern along the intestinal crypt-villus axis. To investigate the regulation of sucrase-isomaltase, we have cloned and sequenced 3.6 kilobases of the 5'-flanking region of the human sucrase-isomaltase gene. The transcriptional start site was mapped in human small intestine and in a colonic adenocarcinoma cell line (Caco-2) using an anchored polymerase chain reaction, primer extension, and RNase protection assays. The 5'-flanking DNA of the gene was linked to either chloramphenicol acetyltransferase or luciferase reporter genes and used for transfection into Caco-2, HeLa, and HepG2 cells. This analysis demonstrated that intestine-specific transcription of the sucrase-isomaltase gene involves both proximal and distal regulatory elements. Use of sucrase-isomaltase as a model gene will allow investigation of the mechanisms that regulate transcription of enterocyte-specific genes, developmental gene expression in the small intestine and colon, and the process of differentiation as epithelial cells migrate from intestinal crypts onto the villus in adult intestine.
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PMID:Isolation and characterization of the human sucrase-isomaltase gene and demonstration of intestine-specific transcriptional elements. 156 17

The mRNA expression of protooncogenes c-Ki-ras, c-myc, and c-fos was studied in five pancreatic carcinomas and five normal pancreatic tissues using RNase protection assay and Northern blot analysis. The expression of those protooncogenes was detected in total mRNA from all specimens. However, the amounts in carcinomas and in normal tissues differed. C-Ki-ras mRNA in all the tumors was expressed up to sixfold more than in normal tissues. C-fos mRNA was also overexpressed up to tenfold in four of five tumors. In contrast, c-myc mRNA levels were varied and did not differ significantly between tumors and normal tissues. The results suggest that the overexpression of c-Ki-ras and c-fos mRNA are implicated in the development of pancreatic adenocarcinoma.
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PMID:Overexpression of c-Ki-ras and c-fos in human pancreatic carcinomas. 158 54

The density of the alpha 2A-adrenergic receptor in the HT29 cell line, a human colonic adenocarcinoma, increases when the cells are placed in fetal calf serum (FCS)-free culture medium and decreases again, in a concentration-dependent manner, when they are re-exposed to FCS. In an attempt to identify the FCS components responsible for this phenomenon, we examined the effect of insulin and of various growth factors on receptor expression. Incubation of HT29 cells with insulin resulted in a time- and dose-dependent lowering of the alpha 2-adrenergic receptor number. The decrease of [3H] RX821002 binding sites after a 48-h period of treatment reached 70-75% with 170 nM insulin, and a half-maximal effect was observed at 2.6 nM. This value is in agreement with the EC50 of the hormone for stimulating the glycolytic activity of HT29 cells (8 nM) and is sufficiently low to indicate that the decrease of alpha 2-adrenergic receptor number is mediated through stimulation of insulin receptors. Direct quantification of [3H] UK14304 binding sites and the study of the inhibition of [3H]RX821002 binding by (-)-epinephrine indicated that the degree of receptor coupling to Gi protein was not affected when the receptor number was decreased by insulin treatment. The reduction in receptor number did result in an attenuation of the inhibitory effect of UK14304 on forskolin-induced cAMP accumulation in a manner which was consistent with the existence of a large population of spare receptors in untreated cells. The action of insulin is not due to an accelerated rate of receptor degradation and can be mimicked by other growth factors (epidermal growth factor and insulin-like growth factors I and II) acting through stimulation of tyrosine kinase receptors. RNase mapping experiments with a 0.35-kilobase riboprobe prepared from the human alpha 2 C10-adrenergic receptor gene demonstrated that the decrease of receptor number induced by the different treatments is a reflection of changes occurring at the level of its mRNA. The use of cycloheximide indicated that the effect of insulin on alpha 2-adrenergic receptor mRNA does not require protein synthesis. The half-life of the alpha 2-adrenergic receptor mRNA measured after the addition of actinomycin D was unchanged by insulin which suggests that a decrease in the transcription rate is the predominant factor responsible for the observed regulation of receptor expression.
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PMID:Regulation of the alpha 2A-adrenergic receptor in the HT29 cell line. Effects of insulin and growth factors. 167 44

We have characterized the expression of MYCL2, an intronless X-linked gene related to MYCL1. RNase protection analysis of a panel of human normal and tumor tissues has revealed that MYCL2 is expressed almost exclusively in human adult normal testis; much lower levels of transcript were detected in one human lung adenocarcinoma. No MYCL2 transcript was found in human testis RNA obtained from second trimester fetuses. This observation suggests a germ cell rather than somatic cell origin of the transcript and possible developmental regulation of MYCL2. Northern blot analysis of poly(A)+ RNA from adult human normal testis with an antisense riboprobe revealed a transcript of approximately 4.8-kb, which is in agreement with the size predicted from the MYCL2 nucleotide sequence. Antisense transcripts were found spanning regions of MYCL2 corresponding to all three exons of MYCL1. No sizable open reading frame was seen for the MYCL2 antisense transcripts suggesting that they may represent either regulatory sequences or an intron of a gene encoded by the complementary strand. RNase protection assays and the 5' RACE protocol (Rapid Amplification of cDNA Ends) were used to address the localization of the transcription start site of the MYCL2 sense transcript and different putative promoters and transcription regulatory elements have been identified.
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PMID:Testis-specific expression of the human MYCL2 gene. 171 81

The amino acid sequence and disulfide bond pairing of human tumor derived angiogenin, the first tumor angiogenesis factor to be isolated in pure form from human sources, have been determined by conventional sequencing techniques adapted and applied to nanomole and subnanomole levels of material. Angiogenin, obtained from conditioned media of a human colonic adenocarcinoma cell line, is a single-chain protein consisting of 123 amino acids with the following sequences: less than Glu1-Asp-Asn-Ser-Arg-Tyr-Thr-His- Phe-Leu-Thr-Gln-His-Tyr-Asp15-Ala-Lys-Pro-Gln-Gly-Arg-Asp-Asp- Arg-Tyr-Cys-Glu-Ser-Ile-Met30- Arg-Arg-Arg-Gly-Leu-Thr-Ser-Pro-Cys-Lys-Asp-Ile-Asn-Thr- Phe45-Ile-His-Gly-Asn-Lys-Arg-Ser -Ile-Lys-Ala-Ile-Cys-Glu-Asn-Lys60-Asn-Gly-Asn-Pro-His-Arg-Glu-Asn -Leu-Arg-Ile -Ser-Lys-Ser-Ser75 -Phe-Gln-Val-Thr-Thr-Cys-Lys-Leu-His-Gly-Gly-Ser-Pro-Trp-Pro90-Pro -Cys-Gln-Tyr -Arg-Ala-Thr-Ala -Gly-Phe-Arg-Asn-Val-Val-Val105-Ala-Cys-Glu-Asn-Gly-Leu-Pro-Val- His-Leu-Asp-Gln-Ser-Ile-Phe120-Arg-Arg-Pro123-OH. Three disulfide bonds link the half-cystinyl residues 26-81, 39-92, and 57-107. The sequence is homologous to that of the pancreatic ribonucleases with 35% identity and many of the remaining residues conservatively replaced. Similarities are especially apparent around the major active-site residues His-12, Lys-41, and His-119 of ribonuclease which are conserved as are three of the four disulfide bonds.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amino acid sequence of human tumor derived angiogenin. 286 94

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


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