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Biomedical subjects

B Durand

Publications and source records attributed to B Durand.

At least 91 records · Page 5Linked to original sources
PubMed1991

Cellular retinoic acid-binding protein type 2 mRNA is overexpressed in human psoriatic skin as shown by in situ hybridization.

In situ hybridization with full length mouse cellular retinoic acid-binding protein type 1 and cellular retinoic acid-binding protein type 2 cDNA derived RNA probes showed overexpression of cellular retinoic acid-binding protein type 2 mRNA in lesional hyperplastic psoriatic skin whereas cellular retinoic acid-binding protein type 1 mRNA was undetectable. This suggests that the previously reported increase of cellular retinoic acid-binding protein in psoriatic epidermis corresponds to increased translation of cellular retinoic acid-binding protein type 2 gene. Cellular retinoic acid-binding protein types 1 and 2 mRNAs were not detectable in normal epidermis; however, type 2 message was detected in non-hyperplastic, non-lesional skin of psoriatic patients thus before altered epidermal differentiation and hyperplasia are morphologically detectable.

Antisense Elements (Genetics)↗
PubMed1989

The Epstein-Barr virus (EBV) early protein EB2 is a posttranscriptional activator expressed under the control of EBV transcription factors EB1 and R.

From the cloning and characterization of cDNAs, we found that the Epstein-Barr virus (EBV) open reading frame (ORF) BMLF1-BSLF2 coding for the early protein EB2 is present in several mRNAs generated by alternative splicing and expressed in the leftward direction from two promoters PM and PM1. The PM promoter controls the expression of two abundant mRNA species of 1.9 and 2 kilobases (kb), whereas the PM1 promoter controls the expression of at least three mRNAs 3.6, 4.0, and 4.4 kb long. The PM promoter probably overlaps with the PS promoter which controls the transcription of a 3.6-kb mRNA expressed in the rightward direction and containing the ORF BSRF1. Although it increases the amount of chloramphenicol acetyltransferase enzyme expressed from the chimeric pMCAT gene, EB2 is not a promiscuous trans-activator of gene expression and does not positively regulate its own expression from promoter PM. The EB2 activation is not promoter dependent but could possibly act by stabilizing mRNAs and increasing their translation. The PM promoter is, however, activated by the two EBV transcription trans-acting factors, EB1 and R, encoded by the EBV ORFs BZLF1 and BRLF1, respectively. EB1 activates the PM promoter from a consensus AP-1 binding site, and R activates the PM promoter from an enhancer.

Base Sequence↗
PubMed1988

Compartmentalization of MHC class II gene expression in transgenic mice.

A set of transgenic mouse lines carrying Ek alpha genes with promoter region deletions was created in an attempt to compartmentalize MHC class II gene expression. Fine immunohistological analyses established that one transgenic line is essentially devoid of E complex in the thymic cortex, another displays almost no E in the thymic medulla or on peripheral macrophages, and two lines display no E on greater than 98% of B cells. We have assayed these mice for immune function: E-dependent tolerance, antigen presentation, T cell priming, and antibody response. Certain of the findings are difficult to reconcile with currently popular hypotheses, e.g., tolerance induction to E molecules in the virtual absence of E complex in the thymic medulla and efficient antibody responses to E-restricted antigens when almost all B cells are E-.

Animals↗
PubMed1987

Conserved major histocompatibility complex class II boxes--X and Y--are transcriptional control elements and specifically bind nuclear proteins.

A conserved sequence motif exists at the 5' end of all major histocompatibility complex class II genes. This motif consists of the 14-base X and Y boxes separated by a short stretch of variable sequence. In this report, we provide evidence that the X and Y boxes play an important role in controlling transcription of the murine class II gene E kappa alpha. We have developed transgenic mouse lines that carry E alpha genes cleanly deleted for either the X or Y box and have compared the expression of these mutant transgenes with that of a nondeleted control. Both the X and Y segments appear critical for accurate and efficient transcription of E kappa alpha. The most drastic effect is seen with gamma-interferon-treated macrophages, where deletion of the Y box completely abrogates transcription initiated by the normal promoter. In addition, we identify proteins from nuclear extracts that bind specifically to the X or Y box.

Animals↗
PubMed1984

Evidence for Host Genome Involvement in Cytokinin Metabolism by Male and Female Cells of Mercurialis annua Transformed by Strain 15,955 of Agrobacterium tumefaciens.

When male and female individuals of a dioecious species Mercurialis annua L. were inoculated with the same strain of Agrobacterium tumefaciens (15,955), the corresponding tumor tissues of each sex clearly differed in their endogenous cytokinin content; only the male tumors had a morphogenetic feminizing effect on male flowers.In male tumor tissues, zeatin (Z) in higher quantity than ribosyl-zeatin (RZ) became the major metabolite in contrast with the general situation for crown-galls; the female tumor tissues were characterized by an increase of total endogenous cytokinins and by the appearance of some specific metabolites such as a methyl-thio-Z and several glycosylated Z derivatives that had not been detected in healthy apices.In both male and female tumor tissues, the cis form of RZ, present in healthy apices as 30% of trans-RZ form, was no longer detectable.Quantitative and qualitative differences characterize male and female tumor tissues (host genes expression) but since differences also appeared between healthy male and female apices and their corresponding tumor tissues (TDNA gene expression), it can be tentatively concluded that a complex interaction between host cytokinin genes and those of TDNA control the endogenous metabolism of tumor tissues.

Journal Article↗