Search PubMed⌕ Search

Biomedical subjects

G Thomas

Publications and source records attributed to G Thomas.

At least 667 records · Page 37Linked to original sources
PubMed1988

Recurrent t(11;22) breakpoint mapping by chromosome flow sorting and spot-blot hybridization.

The breakpoint of the recurrent t(11;22) translocation, one of the most frequent chromosome anomalies encountered in human population, always involves bands 11q23.2 and 22q11.2. The involvement of the C lambda locus of the immunoglobulin lambda gene cluster on chromosome 22 has been suggested: however, in situ hybridization experiments have yielded conflicting results. In order to solve these discrepancies by another approach, we have used bivariate flow sorting to separate the chromosomes of interest and to map the specific breakpoints by direct spot-blot hybridization with the gene-specific radiolabelled DNA probes, Alu, V lambda, ets. The results showed unambiguously that in the t(11;22) patient analysed, a set of C lambda and V lambda genes was translocated to the der(11) chromosome. Since V lambda genes are situated proximally to C lambda genes, we demonstrate that, in the case studied here, the chromosome 22 breakpoint is not located within or even immediately close to the C lambda region.

Cell Line↗
PubMed1988

Molecular characterization of different ataxia telangiectasia T-cell clones. I. A common breakpoint at the 14q11.2 band splits the T-cell receptor alpha-chain gene.

Using in situ chromosomal hybridization we have mapped the gene for the T-cell receptor alpha-chain in three different non-malignant T-cell clones occurring in ataxia telangiectasia. The constant region was translocated in each of the three clones. The variable region remained in its original position in two cases and was deleted in one clone which lost the derivative chromosome 14. We have therefore demonstrated that the T-cell receptor alpha-gene is split in at least two of these translocations. To our knowledge, this is the first direct evidence of the involvement of a gene from the immunoglobulin superfamily in chromosomal rearrangements in ataxia telangiectasia.

Ataxia Telangiectasia↗
PubMed1988

Molecular characterization of ataxia telangiectasia T cell clones. II. The clonal inv(14) in ataxia telangiectasia differs from the inv(14) in T cell lymphoma.

We compared inversions of chromosome 14 in an ataxia telangiectasia clone and in a malignant T cell line (SUP-T1). The R-banding chromosome analysis showed a clear difference between the distal breakpoint of the two inversions. Fine mapping of the distal breakpoint in the ataxia telangiectasia inv(14) was performed by in situ hybridization. We conclude that this breakpoint is centromeric to the immunoglobulin heavy chain locus and to the D14S1 anonymous locus. Our results favor the existence of an unknown oncogene in band 14q32.1.

Ataxia Telangiectasia↗
PubMed1988

Cell-type specific processing of neuroendocrine precursor proteins using vaccinia recombinants.

The cell-type specific processing of human pro-enkephalin was determined using a vaccinia recombinant (VV:hPE). The results show that all cell types infected with VV:hPE efficiently synthesize pro-enkephalin following cleavage of the signal peptide after Ala24. In addition, pro-enkephalin is shown to undergo N-linked glycosylation as well as other post-translational modifications. However, only one cell line. AtT-20, was able to efficiently cleave pro-enkephalin to smaller peptides including Met-enkephalin. Some results have been previously reported (Science 232, 1641-1643).

Amino Acid Sequence↗
PubMed1988

Differential regulation of S6 phosphorylation by insulin and epidermal growth factor in Swiss mouse 3T3 cells: insulin activation of type 1 phosphatase.

Insulin and epidermal growth factor (EGF) induce distinct kinetics of S6 kinase activation and S6 phosphorylation in Swiss 3T3 cells. Both events are differentially regulated by specific phosphatases. The major S6 phosphatase in cell extracts was identified as a type 1 enzyme by its chromatographic properties, its sensitivity to inhibitor 2, and its substrate specificity. This enzyme is different from the major S6 kinase phosphatase, which is a type 2A enzyme. Insulin at physiological concentrations causes up to a 2-fold activation of a type 1 S6 phosphatase, whereas at higher concentrations this effect is significantly diminished. EGF alone has little effect on this enzyme, and with both agents together the total phosphatase activity remains basal. The results are consistent with the phosphorylation state of S6 observed in vivo and suggest a role of phosphatase type 1 in the regulation of protein synthesis.

Animals↗
PubMed1988

S6 kinase in quiescent Swiss mouse 3T3 cells is activated by phosphorylation in response to serum treatment.

To investigate the role of phosphorylation in the activation of S6 kinase, the enzyme was isolated from 32P-labeled Swiss mouse 3T3 cells before and after stimulation with serum. The kinase activity was followed through several purification steps, and a radioactive protein of Mr 70,000 was obtained from the stimulated cells. This band was not detected in resting cells. The Mr 70,000 protein exhibited the same size upon NaDodSO4/PAGE as the homogeneous kinase, and it comigrated with the in vitro autophosphorylated form of the enzyme. Treatment of the in vivo-labeled material with phosphatase 2A led to a loss of kinase activity concomitant with a release of 32Pi from the Mr 70,000 protein. The partially dephosphorylated protein migrated faster during PAGE, displaying distinct species of Mr 69,000 and 68,000. Most importantly, phospho amino acid analysis of the labeled S6 kinase showed only phosphoserine and phosphothreonine. These results argue that the S6 kinase is phosphorylated at multiple sites in vivo and that it is activated by serine/threonine phosphorylation.

Animals↗
PubMed1988

Identification and characterization of a mitogen-activated S6 kinase.

Treatment of Swiss mouse 3T3 cells with epidermal growth factor, orthovanadate, or serum results in the activation of a kinase that phosphorylates protein S6 of the 40S ribosomal subunit in vitro. This kinase is eluted as a single peak of activity from either a Mono Q anion-exchange column at 0.34 M NaCl or a Mono S cation-exchange column at 0.20 M NaCl. Treatment of the peak fraction from the Mono S column with phosphatase 2A completely abolishes the activity of the enzyme. The kinase appears to be distinct from protein kinase C, cAMP-dependent protein kinase, and two protease-activated kinases, PAK II and H4P. The kinase has been purified to apparent homogeneity and migrates as a single band at Mr 70,000 in NaDodSO4/polyacrylamide gels. The kinase exhibits the ability to autophosphorylate, and this activity directly parallels S6 phosphorylation activity on the final step of purification. In vitro, the kinase incorporates up to 5 mol of phosphate into S6, and the tryptic phosphopeptide maps obtained are equivalent to those from S6 phosphorylated in vivo. Most important, treatment of the purified kinase with phosphatase 2A results in complete inactivation of the enzyme, arguing that the activity of the kinase is directly controlled by phosphorylation.

Animals↗
PubMed1988

Inactive X chromosome has the highest concentration of unmethylated Hha I sites.

A procedure enabling the highly sensitive detection of accessible restriction endonuclease sites on metaphase chromosomes is described. The procedure is based on the following: (i) a terminal deoxynucleotidyltransferase is used to add a biotinylated nucleotide (Bio-11-dUTP) tail to the 3' hydroxyl terminus generated by the action of a restriction enzyme and (ii) the biotinylated oligonucleotide is detected by a peroxidase-based immunocytochemical method. When used with the 5-methylcytosine-sensitive enzyme Hha I, it gives rise to a pattern close to R and T banding on autosomes. In addition, the staining of one X chromosome in females appears very unusual by its pattern and its strong intensity. This procedure, as applied on a case with a polysomy X chromosome, provides direct evidence of an overall hypomethylation of the inactive X chromosomes.

Cells, Cultured↗
PubMed1988

Antidiarrhoeal activity of bisnordihydrotoxiferine isolated from the root bark of Strychnos trinervis (Vell.) Mart. (Loganiaceae).

Bisnordihydrotoxiferine, a dimeric tertiary indole alkaloid obtained from the root bark of Strychnos trinervis (Vell.) Mart. (Loganiaceae), inhibited normal defaecation and castor oil, arachidonic acid, and magnesium sulphate-induced diarrhoea on intraperitoneal administration in mice. The effect may be related to the ability of the compound to decrease normal and castor oil-stimulated gastric emptying, small intestinal transit and water and electrolyte accumulation, and inhibition of normal colonic transit. As prostaglandins are involved in gastrointestinal functions, inhibition of their synthesis is likely to contribute to the anticathartic activity, which has never been reported before for an indole alkaloid.

Animals↗
PubMed1988

Trapping of giant basilar trunk aneurysms. Report of two cases.

Two cases of successful trapping of giant basilar trunk aneurysms are presented. The aneurysms were trapped by clipping the basilar artery distal to the anterior inferior cerebellar arteries and proximal to the superior cerebellar arteries. The outcome was excellent in both cases. In the treatment of giant basilar trunk aneurysms, trapping the involved segment of the basilar artery is an effective way to obliterate and decompress the aneurysm. Preoperative assessment of potential collateral vascular supply, operative technique, and the efficacy of intraoperative monitoring are discussed.

Adult↗
PubMed1988

Endothelial potentiation of relaxation response to phentolamine in rat thoracic aorta.

In this study the role of the endothelium was evaluated in the relaxation of rat aortic rings induced by a number of alpha adrenergic antagonists. Phentolamine, a nonselective alpha adrenergic antagonist, relaxed rat aortic rings that were previously contracted with an EC80 dose of phenylephrine, in a concentration-dependent manner. Removal of the endothelium significantly reduced the sensitivity but not the amplitude of the response. The presence of endothelium also enhanced the vascular relaxation induced by yohimbine, a specific alpha-2 adrenergic antagonist (10(-8)-10(-6) M), and by prazosin, a specific alpha-1 adrenergic antagonist (10(-11)-10(-9) M). Both methylene blue (10(-5) M), an inhibitor of soluble guanylate cyclase, and eicosatetraynoic acid (3.2 X 10(-5) M) blocked the endothelial augmentation of vascular relaxation to phentolamine. Vessels precontracted with potassium chloride were slightly relaxed by phentolamine (10(-8)-10(-6) M) only with the endothelium was intact. Both methylene blue and eicosatetraynoic acid also inhibited the response to phentolamine in the intact vessels precontracted with potassium chloride. Prazosin (10(-9)-10(-7) M) and yohimbine (10(-8)-10(-6) M), unlike phentolamine, failed to induce relaxation in potassium chloride-precontracted vessels. When the vessels were precontracted with the thromboxane analog U46619 none of the three alpha antagonists induced vascular relaxation. These results indicate that the endothelium has a significant role in promoting relaxation induced by the three alpha adrenergic antagonists tested.

5,8,11,14-Eicosatetraynoic Acid↗