Search PubMed⌕ Search

Biomedical subjects

J Charron

Publications and source records attributed to J Charron.

32 records · Page 2Linked to original sources
PubMed1986

Glucocorticoid inhibition of transcription from episomal proopiomelanocortin gene promoter.

Glucocorticoid hormones alter transcription of specific genes. Glucocorticoid-stimulated genes have been especially useful in unraveling molecular events responsible for positive gene regulation in mammals. The gene encoding proopiomelanocortin (POMC), which is under feedback inhibition by glucocorticoids, provides a model system to study negative gene regulation. Using an episomal bovine papilloma virus vector, we now demonstrate that a 769-base-pair fragment containing the rat POMC promoter is sufficient to confer glucocorticoid inhibition. Transcription from the episomal POMC promoter starts at the same site and is inhibited by glucocorticoids to the same extent as POMC transcription in the anterior pituitary. Glucocorticoid inhibition is specific for POMC transcripts; neither bovine papilloma virus nor cellular actin mRNAs are affected by glucocorticoids. Thus, the episomal bovine papilloma virus/POMC system can be used to study the relationship between negative regulation of POMC transcription and chromatin structure.

Animals↗
PubMed1985

Structure of the rat pro-opiomelanocortin (POMC) gene.

The gene encoding pro-opiomelanocortin (POMC) presents unique regulatory features. In particular, glucocorticoids inhibit transcription of the POMC gene in the anterior pituitary, but not in the intermediate pituitary. In order to study the mechanism leading to transcriptional inhibition of POMC by glucocorticoid and the interaction of the glucocorticoid receptor complex with specific DNA sequences along the POMC gene, we have cloned the rat POMC gene and determined its structure. The gene is composed of three exons and appears to be present at a single copy per haploid genome. Besides the usual regulatory signals like 'TATA' and 'CCAAT' boxes, the upstream region contains sequences homologous to known enhancer sequences and to the glucocorticoid receptor binding site observed in glucocorticoid-responsive genes.

Animals↗
PubMed1985

Herpes simplex virus ribonucleotide reductase induced in infected BHK-21/C13 cells: biochemical evidence for the existence of two non-identical subunits, H1 and H2.

In nearly all systems studied, ribonucleotide reductase consists of two non-identical subunits. We present here the results of our study on herpes simplex virus (HSV) ribonucleotide reductase in favour of the existence of two subunits, H1 and H2, different from the mammalian subunits, M1 and M2. First, although the viral subunits could not be separated by Blue Sepharose chromatography (unlike mammalian subunits), they seemed to dissociate at very low protein concentration as suggested by the non-linear relationship between activity and low protein concentration. Second, pyridoxal phosphate (Pyr.P)-NaBH4 treatment and 4-methyl-5-amino-1-formylisoquinoline thiosemicarbazone (MAIQ) treatment of partially purified extract of mammalian ribonucleotide reductase which inactivated M1 and M2 respectively also inhibited the HSV ribonucleotide reductase. This activity could be restored by mixing Pyr.P-NaBH4-treated extracts with MAIQ-treated extracts of viral ribonucleotide reductase, suggesting that each treated extract contains one active subunit. Moreover, the addition of exogenous M1 or M2 subunits to one or the other of these two treated extracts did not produce any detectable reductase activity. Our interpretation of these results is that the two subunits H1 and H2 which could dissociate upon treatment did not form enzymically active hybrids with the mammalian subunits. Also, the higher degree of resistance to heat inactivation and to hydroxyurea of the viral reductase as compared to the mammalian enzyme suggests that H1 differs from M1 and H2 from M2.

Animals↗
PubMed1983

Fertilizing capacity and sperm antibodies in vasovasostomized men.

In order to explain the discrepancy between the patency rate (80%) and the pregnancy rate (46%) in a series of vasovasostomies, attention was focused on a group of patients who became normospermic. The mean age at vasectomy, the duration of vasobstruction, and the parameters of semen analysis were not different for those couples who achieved a pregnancy (n = 8), compared with those couples without pregnancy (n = 7). In the group with pregnancy, six of the eight patients had low titers of serum agglutinins (absent to 1:32), and the fertilizing capacity of their spermatozoa was normal. None had immobilizing antibodies. In the group without pregnancy, six of the seven patients had elevated serum agglutinins (greater than 1:256), and four had agglutinating antibodies in their seminal plasma as well as serum immobilizing antibodies. The spermatozoa of seven patients failed to fertilize zona-free hamster ova. It is concluded that a loss of fertilizing ability of the spermatozoa due to sperm antibodies is an important cause of infertility in vasovasostomized men.

Adult↗
PubMed1982

Bromodeoxyuridine resistance in CHO cells occurs in three discrete steps.

Four independent mutants were isolated from mutagenized cultures of CHO cells by sib selection on the basis of resistance to a low concentration (2.6 x 10(-5) M) of BrdU. All four lines were stable, but all had about 100% of the wild-type (WT) specific activity of thymidine kinase (TK). None of the four yielded derivatives resistant to a high level of BrdU (2 x 10(-4) M) in one step even after mutagenesis, but variants resistant to 4-6 x 10(-5) M BrdU could be isolated at frequencies of about 2 x 10(-5)/cell. At frequencies of 10(-4)-10(-5), the second-step mutants gave colonies resistant to 2 x 10(-4) M BrdU. The second and third steps of resistance were correlated with partial and complete reduction, respectively, in the specific activity of TK, suggesting that the variants may be genotypically heterozygous and homozygous-negative at the tk locus. The first step of BrdU resistance was dominant and appeared to result from a mutation in the gene from ribonucleotide reductase, since in vitro assays on partially purified preparations showed that the reductase activity in mutant cells was less sensitive to BrdUTP than in WT cells.

Animals↗
PubMed1982

Carcinoma of the sigmoid: a complication of ureterosigmoidostomy.

The case of a 58-year-old man who had carcinomatous change in the sigmoid colon many years after ureterosigmoidostomy prompted the authors to review the French and English literature on the subject. They found 47 cases in addition to their own, and noted a dramatic increase in the last 10 years, even though ureterosigmoidostomy is now seldom used. The latency of this complication makes it pertinent today. In the hope of determining the etiology of the complication, the authors studied the relation between the initial lesion for which the diversion was carried out and the nature of the colonic tumour that ensued, and have attempted to draw some conclusions. None of the current theories of pathogenesis seem satisfactory. By underlying the early clinical manifestations, the authors attempt to promote earlier diagnosis and better chances of survival for patients with carcinoma of the colon after ureterosigmoidostomy.

Adenocarcinoma↗
PubMed1981

Analysis of deoxycytidine (dC) deaminase activity in herpes simplex virus-infected or HSV TK-transformed cells: association with mycoplasma contamination but not with virus infection.

Deoxycytidine (dC) deaminase activity has been previously reported to be induced in herpes simplex virus (HSV)-infected cells (Chan, 1977). In contrast, we report here that HSV infection of either hamster cells naturally deficient in this enzyme activity or mouse cells containing a low level of activity never resulted in appearance of stimulation of dC deaminase, whereas thymidine kinase (TK) was always induced. Surprisingly, dC deaminase activity, which differed by electrophoretic mobility from the mouse or human cell enzyme, was discovered in some cells selected for the presence of HSV TK after infection with u.v.-irradiated HSV. Evidence is presented which suggests that the appearance of this new enzyme was not due to the presence of virus genes but rather to mycoplasma contamination.

Animals↗