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 RON receptor tyrosine kinase is a 180 kDa heterodimeric protein composed of a 40 kDa alpha chain and a 145 kDa beta chain with intrinsic tyrosine kinase activity. Activation of RON causes cell dissociation, motility and invasion of extracellular matrices, suggesting that RON might be involved in tumor metastasis. We report here the cloning of a novel splice variant of RON in human colorectal carcinoma cell line HT-29. This RON variant is first produced as a single chain precursor with a molecular mass of 160 kDa. Proteolytic cleavage results in a 40 kDa alpha chain and a short form of the beta chain with a molecular mass of 125 kDa. The altered receptor is synthesized from a transcript differing from the full-length RON mRNA by an in-frame deletion of 109 amino acids in the extracellular domain of the RON beta chain. The consequence of the deletion is constitutive activation of the protein with autophosphorylation. Expression of the RON variant in colon epithelial CoTr cells results in increased cell migration and invasion of extracellular matrices. These data suggest that generation of the activated splice variant of RON may contribute to the invasive phenotype of human colorectal carcinomas in vivo.
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PMID:Identification of a novel splicing product of the RON receptor tyrosine kinase in human colorectal carcinoma cells. 1091 Sep 51

We recently showed that macrophage-stimulating protein (MSP), a serum protein homologous to hepatocyte growth factor, promotes ciliary motility by activating its receptor, RON, on the airway ciliated epithelium. To investigate the functional involvement of MSP and RON in bronchiectasis, in which mucociliary clearance (MCC) is impaired, first we examined RON expression on the bronchial ciliated epithelium of patients with bronchiectasis. We confirmed RON expression at the apical surface of bronchial ciliated epithelium of patients with bronchiectasis as well as those of normal human bronchus. Next, we examined whether MSP is present in sputum of patients with bronchiectasis and normal control subjects. By Western blotting, we found that half of the MSP in sputum is present as a biologically active alpha/beta chain heterodimer (mature MSP). In addition, we found that the MSP concentrations in sputum were significantly elevated in patients with bronchiectasis (n=8; 16.8+/-3.0 ng ml(-1)) compared with normal controls (n=9; 8.4+/-2.4 ng ml(-1); P<0.05). In contrast, the difference in concentrations of serum MSP (pro-MSP) was not significant between the two groups. These results indicate that (i) MSP is supplied to the airways and converted to a biologically active form, (ii) MSP is increased in patients with bronchiectasis compared with normal controls. Taken together, our findings suggest that increased MSP may be involved in compensation for impaired MCC in bronchiectasis.
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PMID:Elevated levels of macrophage-stimulating protein in induced sputum of patients with bronchiectasis. 1095 55

The human RON gene (MST1R) maps to 3p21.3, a region frequently altered in lung cancer and other malignancies. It encodes a receptor tyrosine kinase (RTK) closely related to MET, whose mutations are associated with neoplasia. We investigated whether RON might be involved in the development or progression of lung cancer. We first determined the exon-intron structure of the gene by direct sequencing of RON cosmid DNA and PCR products containing intronic sequences, and then developed primers suitable for mutation analysis by the single-strand conformation polymorphism (SSCP) method. Twenty coding exons were characterized, all but the first one small (average size: 170 bp), a feature shared with other RTK genes. We performed SSCP analysis of RON in small and non-small cell lung cancer samples, upon detection of its expression in a sample of lung cancer cell lines. A mutation (T915C: L296P) was found in an adenocarcinoma specimen. Several single nucleotide polymorphisms were also found. The panel of intron-anchored primers developed in this work will be useful for mutation analysis of the RON gene in different types of human tumors.
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PMID:Gene structure of the human receptor tyrosine kinase RON and mutation analysis in lung cancer samples. 1095 94

RON is a receptor tyrosine kinase belonging to the MET proto-oncogene family. The purposes of this study are to determine the expression and activation of RON in a panel of human colon carcinoma cell lines. Western blotting showed that RON is barely detectable in normal and SV-40-transformed colon epithelial cells, but highly expressed and constitutively activated in several colon carcinoma cell lines including Colo201, HT-29, HCT116, and SW837. Moreover, a novel RON variant with a molecular mass of 160 kDa (RONDelta160) was identified from HT-29 cells. The cDNA encoding RONDelta160 has an in-frame deletion of 109 amino acids in the extracellular domain of the RON beta chain, which is caused by splicing out of two exons in the RON mRNA. No mutations were found in the kinase domain of the RON gene in five carcinoma cell lines screened. By expressing RON in colon epithelial cells, we found that RON activation increases cell motile-invasive activities and protects cells against apoptotic death. These data suggest that RON expression and activation are deregulated in colon carcinoma cell lines. By abnormal activation of RON, this receptor and its variant may regulate motile-invasive phenotypes of certain colon carcinoma cells in vivo.
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PMID:Overexpression and activation of the RON receptor tyrosine kinase in a panel of human colorectal carcinoma cell lines. 1108 93

Two clonally unrelated Pseudomonas aeruginosa clinical strains, RON-1 and RON-2, were isolated in 1997 and 1998 from patients hospitalized in a suburb of Paris, France. Both isolates expressed the class B carbapenem-hydrolyzing beta-lactamase VIM-2 previously identified in Marseilles in the French Riviera. In both isolates, the bla(VIM-2) cassette was part of a class 1 integron that also encoded aminoglycoside-modifying enzymes. In one case, two novel aminoglycoside resistance gene cassettes, aacA29a and aacA29b, were located at the 5' and 3' end of the bla(VIM-2) gene cassette, respectively. The aacA29a and aacA29b gene cassettes were fused upstream with a 101-bp part of the 5' end of the qacE cassette. The deduced amino acid sequence AAC(6')-29a protein shared 96% identity with AAC(6')-29b but only 34% identity with the aacA7-encoded AAC(6')-I1, the closest relative of the AAC(6')-I family enzymes. These aminoglycoside acetyltransferases had amino acid sequences much shorter (131 amino acids) than the other AAC(6')-I enzymes (144 to 153 amino acids). They conferred resistance to amikacin, isepamicin, kanamycin, and tobramycin but not to gentamicin, netilmicin, and sisomicin.
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PMID:Characterization of Class 1 integrons from Pseudomonas aeruginosa that contain the bla(VIM-2) carbapenem-hydrolyzing beta-lactamase gene and of two novel aminoglycoside resistance gene cassettes. 1115 53

Infrequent task-irrelevant deviations in the frequency of a tone may distract our attention away from the processing of task-relevant tone duration. The distraction obtained in the auditory paradigm is reflected in prolonged reaction times in duration discrimination and in P3a. The P3a is followed by a late negative component, which may be related to a re-orienting process following distraction (RON, re-orienting negativity). The present study aimed at comparing effects of the auditory and a corresponding visual distraction paradigm. Distraction elicited a deviance-related negativity which revealed a modality-specific distribution. It was followed by P3a (350-ms post-stimulus) and by RON (500-ms post-stimulus). RON did not occur with long-duration visual stimuli indicating a difference in visual and auditory distraction. Moreover, the results suggest that in both tasks irrelevant deviants were detected by modality-specific processes which caused an attention shift.
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PMID:A comparison of auditory and visual distraction effects: behavioral and event-related indices. 1116 50

A few of the known associations between paediatric cancer and congenital anomalies are attributable to contiguous-gene syndromes. Neuroblastoma (NB) has been linked with an excess of gastrointestinal malformations, but there is a significant scarcity of associated respiratory anomalies. We report on two children having an abdominal NB and a bronchogenic cyst diagnosed simultaneously and in different order of appearance. Both masses were removed in separated procedures, taking into account the priority and the time sequence of chemotherapy. Literature is reviewed, checking that the genetic basis for this association is supported by speculations about the oncogene RON.
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PMID:Neuroblastoma and bronchogenic cyst: a rare association. 1119 48

Palladium in gasoline was determined by means of neutron activation analysis (NAA) and selective sorbent extraction. Unleaded gasoline consistent with DIN EN 228, RON 95 was irradiated at a thermal neutron flux of phith = 1.68 x 10(13)s(-1)cm(-2) and an epithermal neutron flux of 3.32 x 10(11)s(-1)cm(-2) for t(irr) = 12 h. The irradiated gasoline was digested with nitric acid and palladium was then separated as N,N-diethyl-N'-benzoylthiourea complex by an automated column pre-concentration procedure. The eluate of 50 microL was dried on a filter paper and the 88.03 keV photons resulting from the decay of 109Pd were detected in a low level HPGe spectrometer with an efficiency of 35.5%. Severe interferences with other matrix constituents, especially 82Br could be overcome and the detection limit for palladium was improved to 3.4 ng/L at a confidence level of 90%. Although the analytical procedure applied yielded the lowest detection limit for palladium obtained in gasoline up to now, no indications for the presence of palladium were found.
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PMID:Determination of palladium in gasoline by neutron activation analysis and automated column extraction. 1122 May 86

The immunohistochemical distribution of RON receptor tyrosine kinase in digestive organs of both human fetus and adult, including the esophagus, stomach, duodenum, small intestine, colon, rectum, liver, gallbladder, pancreas, and spleen, was investigated semiquantitively using an affinity-purified rabbit polyclonal antibody. RON was observed to be widely distributed throughout various digestive organs and cell types in humans. The immunoreactivity for RON was observed in the epithelium of the esophagus, small intestine, colon, hepatocytes, Kupffer cells, and splenic macrophages both in the adult and the fetus, suggesting that the MSP/RON signaling pathway possesses the proper biological properties to possibly be involved in morphogenesis or differentiation of cells in these organs and cell types. Several organs differed in immunoreactivity between adult and fetus. No immunoreactive cells were found in the pancreas of adults; however, immunoreactivity was observed in acinar cells and in some of the duct or ductular cells and endocrine cells of the islet of the fetus. Similarly, immunoreactivity was not observed in gastric mucosa except in the intestinal metaplastic cells in adults; however, immunoreactivity was found in the foveolar epithelium of the stomach of the fetus. Although the biological significance of RON in malignancy is unclear, the presence of RON immunoreactivity in the fetus and it lack in the adult may indicate that RON is a oncofetal substance in human pancreas and stomach.
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PMID:Immunohistochemical analysis of distribution of RON receptor tyrosine kinase in human digestive organs. 1128 Nov 94

RON is a transmembrane receptor tyrosine kinase that mediates biological activities of Macrophage Stimulating Protein (MSP). MSP is a multifunctional factor regulating cell adhesion, motility, growth and survival. MSP binding to RON causes receptor tyrosine phosphorylation leading to up-regulation of RON catalytic activity and subsequent activation of downstream signaling molecules. Recent studies show that RON is spatially and functionally associated with other transmembrane molecules including adhesion receptors integrins and cadherins, and cytokine and growth factor receptors IL-3 betac, EPOR and MET. For example, MSP-induced cell shape change is mediated via RON-activated IL-3 betac receptor. Activation of integrins causes MSP-independent RON phosphorylation, and the integrin/RON collaboration regulates cell survival. Thus, RON can be activated without MSP by ligand stimulation of RON-associated receptors, and MSP-activated RON can cause ligand-independent activation of RON-associated receptors. As a result of the receptor cross-activation RON-specific pathways become a part of a signal transduction network of other receptors, and conversely signaling pathways activated by other receptors can be used by RON. This receptor collaboration extends the spectrum of cellular responses generated by MSP and by putative ligands of RON-associated receptors. However signaling pathways involved in the receptor cross-talk and underlying activation mechanisms remain to be investigated. The purpose of this review is to summarize data and to discuss a role of cross-talk between RON and other transmembrane receptors.
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PMID:Cross-talk between RON receptor tyrosine kinase and other transmembrane receptors. 1133 18


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