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E López-Bayghen

Publications and source records attributed to E López-Bayghen.

7 recordsLinked to original sources
PubMed2000

Glutamate regulates kainate-binding protein expression in cultured chick Bergmann glia through an activator protein-1 binding site.

The expression of the chick kainate-binding protein, a member of the ionotropic glutamate receptor family, is restricted to the cerebellum, specifically to Bergmann glia. Glutamate induces a membrane to nuclei signaling involved in gene expression regulation. Exposure of cultured chick Bergmann glia cells to glutamate leads to an increase in kainate binding protein and mRNA levels, suggesting a transcriptional level of regulation. The 5' proximal region of the chick kainate binding gene was cloned and transfected 4into Bergmann glia cells. Three main regulatory regions could be defined, a minimal promoter region, a negative regulatory region, and interestingly, a glutamate-responsive element. Deletion of this element abolishes the agonist effect. Moreover, electrophoretic mobility shift assays, cotransfection experiments, and site-directed mutagenesis clearly suggest that the glutamate effect is mediated through an AP-1 site by a Fos/Jun heterodimer. The present results favor the notion of a functional role of kainate-binding protein in glutamatergic cerebellar neurotransmission.

Animals↗
PubMed2000

GLAST: gene expression regulation by phorbol esters.

The gene expression regulation of the Na+-dependent high affinity glutamate/aspartate transporter GLAST expressed in cultured Bergmann glia cells from chick cerebellum was studied. A 679 bp fragment of the chick GLAST cDNA was cloned and sequenced. Specific PCR primers were used to quantify chick GLAST mRNA levels. Treatment of the cells with the Ca2+/diacylglycerol dependent protein kinase C (PKC) activator, phorbol 12-tetradecanoyl-13-acetate (TPA) produced a decrease in transporter mRNA levels, without an effect in its mRNA half life, suggesting a transcriptional down regulation. Activation of the cAMP pathway results in a transient decrease in GLAST mRNA levels, in contrast with the TPA effect. These findings suggest that GLAST expression is under control of distinct signaling pathways.

ATP-Binding Cassette Transporters↗
PubMed1998

Transcriptional analysis of the EhPgp1 promoter of Entamoeba histolytica multidrug-resistant mutant.

We present here the cloning and characterization of the EhPgp1 multidrug resistance gene promoter isolated from the Entamoeba histolytica drug-resistant mutant clone C2. The EhPgp1 promoter lacks the typical TATA box and the transcriptional initiation sequences described for other E. histolytica promoters. The major transcription initiation site of the EhPgp1 gene was located at the ATG start codon. The EhPgp1 core promoter located within the first 244 base pairs showed a higher chloramphenicol acetyltransferase expression in the transfected trophozoites of clone C2 than in those of the sensitive clone A. Gel shift assays revealed three specific DNA-protein complexes (Ia, IIa, and IIIc) using nuclear extracts from clone C2, whereas three main complexes (If, IIf, and IIg) were limited to clone A. Competition assays suggested the presence of C/EBP-like and OCT-like proteins in complexes Ia and IIa, respectively, probably involved in the expression of the EhPgp1 gene, whereas complex IIIc was competed by GATA-1, C/EBP, OCT, and HOX oligonucleotides. Thus, differential DNA-protein complexes may be formed by transcriptional factors involved in the regulation of the EhPgp1 gene expression.

Animals↗
PubMed1998

Transcriptional analysis of the EhPgp5 promoter of Entamoeba histolytica multidrug-resistant mutant.

We report here the cloning and transcriptional characterization of the EhPgp5 multidrug resistance gene promoter isolated from the drug-resistant clone C2 of Entamoeba histolytica. The EhPgp5 promoter has the TATA-like motif at -31 base pairs; transcription initiates three nucleotides upstream from the ATG in trophozoites grown in 225 microM emetine (clone C2(225)), whereas in those grown without the drug (clone C2) a product with no open reading frame was detected. The promoter was active in transfected clone C2 trophozoites, its activity increased when trophozoites were cultured in 40 microM emetine, while it was turned off in the drug-sensitive clone A. The first -235 base pair kept full promoter activity, suggesting that it has important drug responsive elements. Gel shift assays detected the complex Ib in clone C2, which was augmented in clone C2(225). Competition experiments suggested that complex Ib may be constituted by HOX and AP-1 like factors in clone C2, whereas in clone C2(225), complex Ib was only competed by the HOX sequence. Complexes Ie, detected in clones A and C2 but not in C2(225), and Ia, present in all clones, were competed by the TATA box oligonucleotide. Our results suggest that proteins forming complexes Ib and Ie may be participating in the regulation of the EhPgp5 gene expression.

Animals↗
PubMedDate not supplied

[Genetic regulation of human genital papillomaviruses].

Human papillomavirus (HPV) specifically infect stratified epithelial cells, causing benign and malignant neoplasia. Several elements directing this virus' genetic expression are present in a non-coding region called LCR. HPV infection starts in the basal cells of stratified epithelia, where a particular combination of cellular factors interacting with the LCR starts the transcription of the viral E6 and E7 oncogenes. The E6 and E7 genes alter the cell cycle because they interact and inactivate tumor suppressor proteins: E6 binds and degrades protein p53 and E7 associates with p105RB. E1 and E2 are the next synthesized proteins. E2 blocks the early transcription and permits E1 specific binding to the viral origin of replication located within the LCR, initiating the viral genome replication. Following the course of viral infection, the E2-induced E6 and E7 down-regulation releases p53 and p105RB proteins, and the differentiation process can continue. Then, a putative late promoter can activate the capsid genes L1 and L2. At this step, mature virions can be detected in the upper layers of the epithelium. Disruption in E2 gene transcription is usually associated to genital malignant neoplasia. In the absence of E2, E6 and E7 remain constitutively expressed, sustaining the immortality of the infected cell and blocking the epithelial differentiation program.

Condylomata Acuminata↗