Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.10.1 (ERK)
 95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma met-enkephalin (MET-ENK) levels are increased in type 1 diabetic women and in pregnant diabetic women in comparison with normal women. Plasma MET-ENK levels further increase in the peripartum period both in diabetic and non-diabetic females, probably due to the analgesic and behavioural properties of the opioid system.
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PMID:High levels of circulating met-enkephalin in pregnant and menstruating type 1 diabetic women. 218 95

This study analyses distribution patterns of the delta F508 mutation of the cystic fibrosis transmembrane conductance regulator gene (CFTR) gene and the cystic fibrosis (CF)-linked marker loci MET, D7S23, D7S399, and D7S8 in a sample of 167 (116 complete) CF families from Bohemia and Moravia (Czechoslovakia). DNA typing was performed by polymerase chain reaction amplification, restriction analysis, and agarose or polyacrylamide gel electrophoresis. The frequency of the delta F508 mutation in this sample is 67% and the frequency of the B haplotype is 77.6% on CF chromosomes. Linkage disequilibrium was found between delta F508 and all markers tested.
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PMID:Frequency of the delta F508 mutation and flanking marker haplotypes at the CF locus from 167 Czech families. 221 Jul 55

Differential polypeptide expression in gene transfer cell lines of limited genetic complexity was analyzed as a gene mapping strategy. Subcellular fractionation preceding two-dimensional gel electrophoretic analysis simplified protein patterns and revealed subcellular location of differentially expressed polypeptides. As a model system, human MET oncogene polypeptide was identified in gene transfer lines by this approach. Genes encoding five putative human proteins were identified and provisionally assigned to chromosomal region 7q21-31 or to chromosome 1.
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PMID:Polyacrylamide gel analysis of polypeptides in gene transfer cell lines. 221 22

We have previously shown that two alleles of the MET locus are independently rearranged in the chemically-treated human cell line MNNG-HOS. One allele is the TPR-MET oncogene which was activated by fusion of the MET locus on chromosome 7 with the TPR locus on chromosome 1. The second allele is found on a der(7)t(1;7)(q23;q32) chromosome and is characterized by a deletion of the amino-terminus of the MET extracellular ligand binding domain. Here we present a pulsed field gel electrophoresis analysis which reveals that the two MET allele rearrangements in MNNG-HOS cells are more complex than originally thought. The breakpoint in MET on der(7) has been molecularly cloned and, unexpectedly, we found that rearrangement in this allele involves sequences derived from chromosome 2. Moreover, the rearrangement producing der(7) involves an inversion of the MET locus or a more complex alteration. Analysis of hybrid cells containing TPR-MET demonstrated that both the upstream and downstream portions of MET are conserved in this rearrangement and that oncogene activation occurred by an insertion of TPR sequences into the MET locus. These findings illustrate that when examined at the molecular level some chromosome abnormalities can be extremely complex and, thus, are of limited value in gene mapping studies.
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PMID:Analysis by pulsed field gel electrophoresis reveals complex rearrangements in two MET alleles in a chemically-treated human cell line, MNNG-HOS. 225 Sep 12

To predict the nature of non-calcifying lung tumors, we performed a prospective study of 46 cases with L-[methyl 11C]methionine (MET, 24 cases) and 18F-fluorodeoxyglucose (FDG, 22 cases) using positron emission tomography (PET). Mean tumor/muscle radioactivity ratios are 5.3 +/- 2.0 (n = 14) for malignant and 1.9 +/- 0.9 (n = 10) for benign with MET (p less than 0.001), and 4.4 +/- 2.2 (n = 12) and 1.5 +/- 0.3 (n = 10), respectively, with FDG (p less than 0.001). The ratios indicate that malignant tumors have higher metabolic demand than benign lesions. Tumors less than 1 cm in diameter were difficult to accurately evaluate due to PET resolution. Compared to the diagnosis at pathology, the MET study showed a sensitivity of 93% (13/14), a specificity of 60% (6/10), and an accuracy of 79% (19/24). The FDG study showed 83% (10/12), 90% (9/10), 86% (19/22), respectively. No significant differences were observed between the two tracers. This study suggests that PET studies using either MET or FDG may be very useful for the differential diagnosis of lung tumors.
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PMID:Differential diagnosis of lung tumor with positron emission tomography: a prospective study. 226 88

Activation of the MET protooncogene by a rearrangement involving the fusion of TPR and MET specific gene sequences has been observed in a human osteosarcoma cell line (HOS) treated in vitro with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). No information has been available about the possible occurrence of this rearrangement in human tumors. To facilitate rapid screening of human cell lines and tumor samples for this specific gene rearrangement, we developed a sensitive detection method based on polymerase chain reaction (PCR) amplification of TPR-MET mRNA. cDNA was generated from cellular transcripts by using one of the PCR primers, which was then used as a template for PCR amplification of a 205-base-pair region carrying the breakpoint. An end-labeled internal probe was hybridized in solution to an aliquot of the PCR product for detecting amplification. Cells could be directly screened by the assay without prior isolation of RNA. A 205-base-pair DNA fragment characteristic of the TPR-MET rearrangement was detected in cell lines previously known to contain this altered sequence. The rearrangement was also detected at very low levels in the parental (nontransformed) cell line, HOS TE-85. A preliminary survey of cell lines derived from a variety of human tumors indicates that TPR-MET rearrangement occurred and was expressed at very low frequencies by cells from 7 of 14 tumors of nonhematopoietic origin.
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PMID:TPR-MET oncogenic rearrangement: detection by polymerase chain reaction amplification of the transcript and expression in human tumor cell lines. 230 May 59

The MET oncogene, present in the MNNG-HOS chemically transformed human cell line, is activated by a gene fusion involving sequences from chromosome 1 and chromosome 7. Activated MET can act as a dominant selectable marker for chromosome-mediated gene transfer, and several transfectant cell lines have been established using this technique. Analysis of the transgenomes within these cell lines indicates that MET activation is not simply due to a chromosome translocation, but may involve an interstitial insertion of DNA from chromosome 1, into chromosome 7, probably associated with other rearrangements. Pulse field gel analysis of two transfectants indicates that, despite the presence of complex rearrangements close to MET, chromosome 7 sequences are grossly intact over a 1-Mb region thought to contain the gene defective in cystic fibrosis.
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PMID:Analysis of the transgenome of MET transfectant cell lines reveals that MET activation is accompanied by an interstitial insertion. 230 48

The Hodgkin's lymphoma-derived cell line L540, which exhibits multiple marker chromosomes and a genotype characteristic of T-cell origin, showed expression of MET oncogene. L540 was studied by in situ hybridization for chromosomal rearrangements concerning the regions where genes for TCRA and TCRB chains, for MET oncogene, and for rRNA are located. All four genes were demonstrated to be involved in the formation of marker chromosomes. Especially remarkable was the participation of rDNA-bearing regions in two different translocations.
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PMID:Chromosomal in situ hybridization of a Hodgkin's disease-derived cell line (L540) using DNA probes for TCRA, TCRB, MET, and rRNA. 232 75

Intestinal absorption of crystalline DL-methionine (DL-MET) and DL-methionine hydroxy analog calcium (DL-HMA) were determined in a true-digestibility-balance assay using cecectomized (CEC) and sham-operated conventional (CONV) cockerels. The treatments consisted of fasted birds and birds crop-intubated (CI) with 30 g of a corn-soybean meal basal diet (16% CP) supplemented with 0, .2, or .4% of DL-MET or equimolar levels of DL-HMA. There was no detectable free D-MET or L-MET or HMA in the excreta of fasted birds or of those fed the unsupplemented basal diet. The intestinal absorption of DL-HMA was 95.9 +/- .8% (means +/- SE) for CEC and 98.8 +/- .8% for the CONV cockerels. The absorption of DL-MET was approximately 99.7 +/- .2% for the CEC and the CONV cockerels. In a second experiment procedures were developed for a bioavailability assessment by comparing the growth responses to CI and intraperitoneal-injected (IP) DL-MET or DL-HMA in chicks fed a crystalline-amino-acid diet deficient in methionine. Graded increments of pH-adjusted DL-MET or DL-HMA (in water solutions) were administered twice daily in a 7-day growth assay. Slope-ratio analysis indicated that bioavailability (+/- SE) of CI DL-HMA was 91.3 +/- 11.8% relative to the CI DL-MET on an equimolar basis. The bioavailability of CI DL-HMA was similar to that of IP DL-HMA, indicating that the intestinal absorption of DL-HMA was highly efficient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Absorption and bioavailability of DL-methionine hydroxy analog compared to DL-methionine. 233 Mar 31

In this communication we show that T cell locomotion is affected by direct interaction with neurohormones. Opioid peptides, including beta-END, MET-ENK, LEU-ENK, and related enkephalin analogues enhanced migration of human peripheral blood T lymphocytes. Activity was dependent on the peptide NH2-terminal sequence, stimulated by enkephalin analogues with specificity for classical delta or mu types of opiate receptor, and inhibited by the opiate receptor antagonist naloxone. Our studies suggest that such neuropeptides stimulate T cell chemotaxis by interaction with sites analogues to classical opiate receptors. We propose that the endogenous opioids beta-END, MET-ENK, and LEU-ENK are potent immunomodulating signals that regulate the trafficking of immune response cells.
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PMID:Neurohormones regulate T cell function. 233 33


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