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:2.7.10.1 (ERK)
95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The human c-MET oncogene encodes a transmembrane tyrosine kinase (p190c-met) with structural and functional features of a growth-factor receptor. Monoclonal antibodies (MAbs) have been used to investigate the distribution of the c-Met protein in human normal and neoplastic tissues. By immunofluorescence microscopy homogeneous expression was detected in normal hepatocytes as well as in epithelial cells lining the stomach, the small and the large intestine. Positive staining was also found in epithelial cells of the endometrium and ovary, and in basal keratinocytes of esophagus and skin. By Northern blot analysis, high levels of c-met messenger RNA were detected in specimens of liver, gastro-intestinal tract and kidney. c-met-specific mRNA was also found in thyroid, pancreas and placenta, in which organs c-Met protein was barely detectable by immunofluorescence. The antibodies revealed expression of c-MET protein in hepatomas (11/14), carcinomas of colon and rectum (19/21), stomach (11/22), kidney (16/19), ovary (9/17) and skin (7/17). Carcinomas of the lung (13/20), thyroid (11/13) and pancreas (5/7) were also positive. In these last cases (lung, thyroid and pancreas) tumor cells were homogeneously stained by the antibodies, whereas in their normal counterparts staining was barely detectable. These data suggest that the receptor encoded by c-MET plays a physiological role in epithelial cell growth and that its expression is altered in human carcinomas.
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PMID:The receptor encoded by the human c-MET oncogene is expressed in hepatocytes, epithelial cells and solid tumors. 191 29

Good exercise prescriptions provide work rates (WRs) that maintain heart rates (HR) in a target zone and at a percent of maximum metabolic equivalent (%METmax). HR and MET were evaluated from computer-controlled and set WR (constant speed) sessions (20 min at 65% METmax). Computer-controlled WR used a control algorithm to adjust speed and grade to maintain the target HR. The set WR (mean +/- S.D.) HR (139 +/- 8 bpm) was lower (p less than 0.05) than the target (147 +/- 3 bpm) and computer-controlled HRs (153 +/- 5 bpm). The set WR MET (8.6 +/- 2.2) was not different than the target (8.6 +/- 2.2), but both were lower than computer-controlled exercise (9.7 +/- 2.2). Computer-control time in target HR zone (16 +/- 5 min) was significantly (p less than 0.004) greater than set WR exercise (6 +/- 5 min). Computer-controlled WR was significantly better in maintaining target HR and the MET values were not physiologically different than target WRs.
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PMID:A comparison between computer-controlled and set work rate exercise based on target heart rate. 193 84

The urinary excretion and serum concentration of amino acids were studied in 62 healthy individuals aged 15 to 70 years. In elderly subjects (61-70 years), it was found that renal amino acid clearance per 100 ml GFR (fractional excretion, FE) rose significantly in the following amino acids: CYS, VAL, MET, ILE and LEU. Since the serum concentrations of these amino acids showed no significant changes, but the GFR was reduced, it can be concluded that the raised FE of these amino acids was due to a decrease in their effective tubular reabsorption. A significant correlation was found between FENa and FE of most amino acids including those mentioned above. The findings support the assumption that changes in tubular Na+ transport probably participate in the changes of tubular amino acid transport in elderly individuals.
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PMID:Renal amino acid excretion and aging. 193 19

Plasma met-enkephalin immunoreactivity (MET-ENKi) and catecholamine levels were measured in umbilibal cord blood from 46 healthy newborn infants. Clinical data including Apgar scores, birth weight, gestational age, route of delivery, fetal heart tracings and arterial blood gas values were also obtained. Thirty-nine infants were delivered by the vaginal route. All but 1 infant delivered by cesarian section had undergone a trial of labor. Plasma MET-ENKi in the newborn infants was markedly greater than levels found in healthy adult volunteers: 360 +/- 25 versus 25 +/- 2 pg/ml, respectively. MET-ENKi levels were similar in umbilical arterial and umbilical venous blood, and in infants delivered vaginally or by cesarian section.
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PMID:Plasma methionine enkephalin levels in the human newborn at birth. 193 84

Met-enkephalin immunoreactivity (MET-ENKi), total enkephalin immunoreactivity (TOTAL MET-ENKi) and catecholamines were measured in adrenal and extra-adrenal tissue of fetal, newborn and adult rabbits. Met-enkephalin peptides were detected in adrenal and extra-adrenal tissue by 29 days of gestation. There were progressive increases in TOTAL MET-ENKi in both the adrenal and extra-adrenal tissue during development. In 29-day-old fetuses, MET-ENKi represented 43 and 50% of the peptide content in adrenal and extra-adrenal tissues respectively. By 3 days after birth, MET-ENKi represented only 15 and 7% of the peptide content in the same tissues. In the adult adrenals, 10% of enkephalin peptides were found as MET-ENKi. There were progressive increases in adrenal and extra-adrenal catecholamine content in the fetal and newborn rabbits throughout development. The changes in the ratio of MET-ENKi to TOTAL MET-ENKi peptides suggest differences in posttranslational processing of proenkephalin peptide during maturation. We speculate that enkephalin peptides derived from proenkephalin A are important during fetal and early newborn life and that extra-adrenal tissue may be an important source of these peptides during development.
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PMID:Maturational changes in expression of enkephalin peptides in adrenal and extra-adrenal tissue of fetal and adult rabbits. 193 13

There is now convincing evidence for the imposition of self tolerance by means of the clonal deletion of self-reactive T cells operating within the thymus. Since not all self components may be encountered there, the question must be asked whether tolerance can occur post-thymically. To test this, we and other investigators have used transgenic technology to direct expression of a known "nonself" gene to a given extrathymic tissue. No lymphocytic infiltration was ever seen in transgene-expressing tissues, even if the mice were given normal syngeneic (nontransgenic) spleen cells intravenously or were stimulated with H-2Kb spleen cells. Infiltration did, however, occur in irradiated transgenic recipients of H-2Kb immune spleen cells. In MET-Kb mice, this infiltrate diminished with time, raising the possibility that peripheral tolerance may even have been induced in immune cells. H-2Kb-bearing skin was accepted in young RIP-Kb mice but rejected in older mice, which had lost more than 75% of their beta cells as a result of the overexpression of H-2Kb. This loss of tolerance thus occurred when the concentration of the tolerogen, H-2Kb, fell below some critical threshold. Following in vitro stimulation, spleen cells from young RIP-Kb mice could not kill H-2Kb-bearing targets, but could respond to third party targets. Thymus cells, on the other hand, could be stimulated to kill both targets, clearly indicating that tolerance was not imposed intrathymically. Spleen cells from older RIP-Kb mice (those that had lost most of their beta cells) killed both targets, which is in agreement with the in vivo data. Reactivity to H-2Kb was restored to young spleen cells by providing them with IL-2. Two hypotheses were proposed to account for the above findings: tolerance results either from the deletion or functional silencing of high-affinity effector cells or of regulatory, IL-2-producing helper T cells. As it is difficult to distinguish between these, we have produced a second series of transgenic mice (F3+) with rearranged TCR genes encoding an anti-H-2Kb TCR and derived "double-transgenic" (F3+RIP+) offspring by mating these mice with RIP-Kb mice. The transgenic TCR utilized the V beta 11 segment which can be detected by a monoclonal antibody. There were in the thymus very few CD4+ and very few CD4+8+ cells in both F3+ and F3+RIP+ mice and, in the double-transgenic mice, there was no evidence of deletion of CD8+V beta 11+ cells in the periphery although they showed tolerance to H-2Kb-bearing skin.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A transgenic approach to the study of peripheral T-cell tolerance. 193 38

The MET proto-oncogene encodes a transmembrane tyrosine kinase of 190 kDa (p190MET), which has recently been identified as the receptor for hepatocyte growth factor/scatter factor. p190MET is a heterodimer composed of two disulfide-linked chains of 50 kDa (p50 alpha) and 145 kDa (p145 beta). We have produced four different monoclonal antibodies that are specific for the extracellular domain of the Met receptor. These antibodies immunoprecipitate with p190MET two additional Met proteins of 140 and 130 kDa. The first protein (p140MET) is membrane bound and is composed of an alpha chain (p50 alpha) and an 85-kDa C-terminal truncated beta chain (p85 beta). The second protein (p130MET) is released in the culture supernatant and consists of an alpha chain (p50 alpha) and a 75-kDa C-terminal truncated beta chain (p75 beta). Both truncated forms lack the tyrosine kinase domain. p140MET and p130MET are consistently detected in vivo, together with p190MET, in different cell lines or their culture supernatants. p140MET is preferentially localized at the cell surface, where it is present in roughly half the amount of p190MET. The two C-terminal truncated forms of the Met receptor are also found in stable transfectants expressing the full-length MET cDNA, thus showing that they originate from posttranslational proteolysis. This process is regulated by protein kinase C activation. Together, these data suggest that the production of the C-terminal truncated Met forms may have a physiological role in modulating the Met receptor function.
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PMID:C-terminal truncated forms of Met, the hepatocyte growth factor receptor. 194 72

While there is still much debate in the literature regarding the specific MET levels at which there are differences in survival, the following points have become clear with the growing body of reports in the literature. Exercise capacity seems to be an independent predictor of mortality, and when it is combined with other clinical, exercise, or angiographic data, it becomes very powerful in this regard. This relates to both overall mortality and to that from cardiovascular disease. There is still a need for the establishment of mortality data related to MET levels adjusted for age and activity status. A low exercise capacity of less than 6 METs indicates a higher mortality group, probably regardless of the underlying extent of coronary disease or left ventricular function. Analysis of the CASS data has indicated that these patients benefit from coronary artery bypass surgery with respect to survival. An exercise capacity of greater than 10 METs designates an excellent survival group, again despite the extent of coronary artery disease or left ventricular function. If 10 METs truly exerts a "protective effect" that obviates any survival benefit from coronary artery bypass surgery, this has enormous implications for cost containment and medical care. It is nonetheless important to remember that this level of exercise capacity does not imply the absence of either coronary disease or triple-vessel coronary disease. Exercise capacity is related to more than just cardiovascular fitness and integrity. It is dependent upon a combination of other physiologic components as well, including pulmonary function, health status of other organ systems, nitrogen balance, nutritional status, medications, orthopedic limitations, and others.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The prognostic value of exercise capacity: a review of the literature. 195 Oct 7

Metastatic colonization of a secondary organ site is initiated by the attachment of blood-borne tumor cells to organ-specific adhesion molecules expressed on the surface of microvascular endothelial cells. Using digital video imaging microscopy and fluorescence activated cell sorting techniques, we show here that highly metastatic cells (B16-F10 murine melanoma and R3230AC-MET rat mammary adenocarcinoma cells) previously labeled with the fluorescent dye BCECF begin to transfer dye to endothelial cell monolayers shortly after adhesion is established. The extent of BCECF transfer to endothelial cell monolayers is dependent upon the number of BCECF-labeled tumor cells seeded onto the endothelial cell monolayer and the time of coculture of the two cell types, as visualized by an increase in the number of BCECF-positive cells among cells stained with an endothelial cell-specific mAb. Dye transfer to BAEC monolayers proceeds with a progressive loss of fluorescence intensity in the BCECF-labeled tumor cell population with time of coculture. The transfer of dye is bidirectional and sensitive to inhibition by 1-heptanol. In contrast, poorly metastatic B16-F0 melanoma cells and non-metastatic R3230AC-LR mammary adenocarcinoma cells do not efficiently couple with vascular endothelial cells. It is inferred from these experiments and from the amounts of connexin43 mRNA expressed by tumor cells that tumor cell/endothelial cell communication is mediated by gap junctional channels and that this interaction may play a critical role in tumor cell extravasation at secondary sites.
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PMID:Cytoplasmic dye transfer between metastatic tumor cells and vascular endothelium. 195 78

In 84 families with 101 children with cystic fibrosis (CF) and 103 unaffected siblings, the haplotype of CF chromosomes was determined with six restriction fragment length polymorphism (RFLP) markers that span the CF gene locus. Patient groups with different genotypes in the more distant flanking marker loci MET D, MET H, and D7S8 differed significantly from each other with respect to percentile height and weight, and percentage of weight for height. Patients homozygous 1-1 in met D (TaqI) and met H (TaqI) were thin and tall when homozygous 1-1 in J3.11 (MspI), and small when homozygous 2-2 in J3.11. Heterozygosity in 3.11 and met H and homozygosity 1-1 in met D segregated with the most severe growth retardation. In contrast, growth was normal in patients who were heterozygous in met D and/or had an uncommon KM.19/XV-2c haplotype. Most patients with pancreatic sufficiency and/or borderline sweat test values were carrying rare haplotypes on their CF chromosomes. Adult patients clustered in genotype groups with normal height percentile distributions. This association between haplotype and clinical severity of CF in the German population provides evidence for genetic microheterogeneity of the CF locus, either because of the existence of multiple alleles of the CF gene itself and/or because of the existence of closely linked polymorphic genes that control growth and development and hence modulate the clinical course and prognosis of CF.
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PMID:Marker haplotype association with growth in German cystic fibrosis patients. 196 35


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