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At least 307 records · Page 17Linked to original sources
PubMed1997

Do plaques grow upstream or downstream?: an angiographic study in the femoral artery.

Although the distribution of atherosclerosis has been described, little is known about the direction of growth of plaques. In this study, 237 patients with slight or moderate atherosclerosis underwent femoral angiography twice at a 3-year interval, and the films were studied with computerized image analysis. First, atherosclerosis was measured as edge roughness, and the change in roughness of each 1-cm segment over the 3-year period was related to the edge roughness of the segments immediately upstream and downstream. On the medial side of the artery, the change in edge roughness was found to be more strongly related to the roughness values upstream than to those downstream of the segment studied. This suggests that growth in the downstream direction is more common than growth in the upstream direction. On the lateral side, more equivocal results were obtained. Atherosclerosis was also assessed by study of the cross-sectional area of the artery as a function of distance along the vessel. A mathematical model of plaque growth was formulated as a nonlinear filtering of this curve. Growth in the downstream direction was significantly (P<.001) more frequent than growth in the upstream direction. The findings are compatible with an atherogenic effect of fluid mechanical disturbances, such as flow separation, that may occur downstream of a stenosis.

Adult↗
PubMed2006

Flanking HS-62.5 and 3' HS1, and regions upstream of the LCR, are not required for beta-globin transcription.

The locus control region (LCR) was thought to be necessary and sufficient for establishing and maintaining an open beta-globin locus chromatin domain in the repressive environment of the developing erythrocyte. However, deletion of the LCR from the endogenous locus had no significant effect on chromatin structure and did not silence transcription. Thus, the cis-regulatory elements that confer the open domain remain unidentified. The conserved DNaseI hypersensitivity sites (HSs) HS-62.5 and 3'HS1 that flank the locus, and the region upstream of the LCR have been implicated in globin gene regulation. The flanking HSs bind CCCTC binding factor (CTCF) and are thought to interact with the LCR to form a "chromatin hub" involved in beta-globin gene activation. Hispanic thalassemia, a deletion of the LCR and 27 kb upstream, leads to heterochromatinization and silencing of the locus. Thus, the region upstream of the LCR deleted in Hispanic thalassemia (upstream Hispanic region [UHR]) may be required for expression. To determine the importance of the UHR and flanking HSs for beta-globin expression, we generated and analyzed mice with targeted deletions of these elements. We demonstrate deletion of these regions alone, and in combination, do not affect transcription, bringing into question current models for the regulation of the beta-globin locus.

5' Flanking Region↗
PubMed2004

Computational identification of transcription factor binding sites by functional analysis of sets of genes sharing overrepresented upstream motifs.

BACKGROUND: Transcriptional regulation is a key mechanism in the functioning of the cell, and is mostly effected through transcription factors binding to specific recognition motifs located upstream of the coding region of the regulated gene. The computational identification of such motifs is made easier by the fact that they often appear several times in the upstream region of the regulated genes, so that the number of occurrences of relevant motifs is often significantly larger than expected by pure chance. RESULTS: To exploit this fact, we construct sets of genes characterized by the statistical overrepresentation of a certain motif in their upstream regions. Then we study the functional characterization of these sets by analyzing their annotation to Gene Ontology terms. For the sets showing a statistically significant specific functional characterization, we conjecture that the upstream motif characterizing the set is a binding site for a transcription factor involved in the regulation of the genes in the set. CONCLUSIONS: The method we propose is able to identify many known binding sites in S. cerevisiae and new candidate targets of regulation by known transcription factors. Its application to less well studied organisms is likely to be valuable in the exploration of their regulatory interaction network.

5' Flanking Region↗
PubMed2005

Genes involved in complex adaptive processes tend to have highly conserved upstream regions in mammalian genomes.

BACKGROUND: Recent advances in genome sequencing suggest a remarkable conservation in gene content of mammalian organisms. The similarity in gene repertoire present in different organisms has increased interest in studying regulatory mechanisms of gene expression aimed at elucidating the differences in phenotypes. In particular, a proximal promoter region contains a large number of regulatory elements that control the expression of its downstream gene. Although many studies have focused on identification of these elements, a broader picture on the complexity of transcriptional regulation of different biological processes has not been addressed in mammals. The regulatory complexity may strongly correlate with gene function, as different evolutionary forces must act on the regulatory systems under different biological conditions. We investigate this hypothesis by comparing the conservation of promoters upstream of genes classified in different functional categories. RESULTS: By conducting a rank correlation analysis between functional annotation and upstream sequence alignment scores obtained by human-mouse and human-dog comparison, we found a significantly greater conservation of the upstream sequence of genes involved in development, cell communication, neural functions and signaling processes than those involved in more basic processes shared with unicellular organisms such as metabolism and ribosomal function. This observation persists after controlling for G+C content. Considering conservation as a functional signature, we hypothesize a higher density of cis-regulatory elements upstream of genes participating in complex and adaptive processes. CONCLUSION: We identified a class of functions that are associated with either high or low promoter conservation in mammals. We detected a significant tendency that points to complex and adaptive processes were associated with higher promoter conservation, despite the fact that they have emerged relatively recently during evolution. We described and contrasted several hypotheses that provide a deeper insight into how transcriptional complexity might have been emerged during evolution.

Animals↗
PubMed2007

Chicken ovalbumin upstream promoter transcription factor II regulates uncoupling protein 3 gene transcription in Phodopus sungorus.

BACKGROUND: Ucp3 is an integral protein of the inner mitochondrial membrane with a role in lipid metabolism preventing deleterious effects of fatty acids in states of high lipid oxidation. Ucp3 is expressed in brown adipose tissue and skeletal muscle and controlled by a transcription factor complex including PPARalpha, MyoD and the histone acetyltransferase p300. Several studies have demonstrated interaction of these factors with chicken ovalbumin upstream promoter transcription factor II (Coup-TFII). This nuclear receptor is involved in organogenesis and other developmental processes including skeletal muscle development, but also co-regulates a number of metabolic genes. In this study we in silico analyzed the upstream region of Ucp3 of the Djungarian hamster Phodopus sungorus and identified several putative response elements for Coup-TFII. We therefore investigated whether Coup-TFII is a further player in the transcriptional control of the Ucp3 gene in rodents. RESULTS: By quantitative PCR we demonstrated a positive correlation of Coup-TFII and Ucp3 mRNA expression in skeletal muscle and brown adipose tissue in response to food deprivation and cold exposure, respectively. In reporter gene assays Coup-TFII enhanced transactivation of the Ucp3 promoter conveyed by MyoD, PPARalpha, RXRalpha and/or p300. Using deletions and mutated constructs, we identified a Coup-TFII enhancer element 816-840 bp upstream of the transcriptional start site. Binding of Coup-TFII to this upstream enhancer was confirmed in electrophoretic mobility shift and supershift assays. CONCLUSION: Transcriptional regulation of the Coup-TFII gene in response to starvation and cold exposure seems to be the regulatory mechanism of Ucp3 mRNA expression in brown adipose and skeletal muscle tissue determining the final appropriate rate of transcript synthesis. These findings add a crucial component to the complex transcriptional machinery controlling expression of Ucp3. Given the substantial evidence for a function of Ucp3 in lipid metabolism, Coup-TFII may not only be a negative regulator of glucose responsive genes but also transactivate genes involved in lipid metabolism.

Animals↗
PubMed2005

Functional promoter upstream p53 regulatory sequence of IGFBP3 that is silenced by tumor specific methylation.

BACKGROUND: Insulin-like growth factor binding protein (IGFBP)-3 functions as a carrier of insulin-like growth factors (IGFs) in circulation and a mediator of the growth suppression signal in cells. There are two reported p53 regulatory regions in the IGFBP3 gene; one upstream of the promoter and one intronic. We previously reported a hot spot of promoter hypermethylation of IGFBP-3 in human hepatocellular carcinomas and derivative cell lines. As the hot spot locates at the putative upstream p53 consensus sequences, these p53 consensus sequences are really functional is a question to be answered. METHODS: In this study, we examined the p53 consensus sequences upstream of the IGFBP-3 promoter for the p53 induced expression of IGFBP-3. Deletion, mutagenesis, and methylation constructs of IGFBP-3 promoter were assessed in the human hepatoblastoma cell line HepG2 for promoter activity. RESULTS: Deletions and mutations of these sequences completely abolished the expression of IGFBP-3 in the presence of p53 overexpression. In vitro methylation of these p53 consensus sequences also suppressed IGFBP-3 expression. In contrast, the expression of IGFBP-3 was not affected in the absence of p53 overexpression. Further, we observed by electrophoresis mobility shift assay that p53 binding to the promoter region was diminished when methylated. CONCLUSION: From these observations, we conclude that four out of eleven p53 consensus sequences upstream of the IGFBP-3 promoter are essential for the p53 induced expression of IGFBP-3, and hypermethylation of these sequences selectively suppresses p53 induced IGFBP-3 expression in HepG2 cells.

Base Sequence↗
PubMed1998

Characterization of a region upstream of exon I.1 of the human CYP19 (aromatase) gene that mediates regulation by retinoids in human choriocarcinoma cells.

The biosynthesis of estrogens is catalyzed by aromatase P450 (P450arom), the product of the CYP19 gene. The tissue-specific expression of the CYP19 gene is regulated by means of tissue-specific promoters through the use of alternative splicing mechanisms. Thus, transcripts containing various 5'-untranslated termini are present in ovary, brain, adipose stromal cells, and placenta. Sequence corresponding to untranslated exon I.1 is present uniquely in 5'-termini of transcripts expressed in human placenta and choriocarcinoma cells, as a consequence of expression driven by a distal promoter, I.1. The goal of the present study was the identification of regulatory elements in this promoter region. Various deletion mutations of the upstream flanking region of exon I.1 were constructed using the PCR or restriction enzyme digestion. The genomic fragments were fused upstream of the luciferase reporter gene. These constructs were transfected into human choriocarcinoma (JEG3) cells. The longest construct employed, -924/+10 bp, expressed the highest luciferase reporter gene activity. The -64/+10 bp and -125/+10 bp constructs showed no reporter gene expression. Transfection of the -201/+10 bp construct resulted in reporter gene expression, but at a lower level than that of the -924/+10 bp construct, and this expression was induced by serum as well as by LG69 and TTNPB, ligands specific for RXR and RAR respectively, as well as by vitamin D. These results parallel the actions of the ligands on aromatase activity. Mutation or deletion of an imperfect palindromic sequence (AGGTCATGCCCC) located at -183 to -172 bp upstream of the transcriptional start site of exon I.1 resulted in loss of basal- and retinoid-induced reporter gene expression. Gel retardation analysis using nuclear extracts of JEG3 cells treated with retinoids and the imperfect palindromic sequence as probe, showed that proteins present in the nuclear extracts bound to this sequence in a specific fashion. The binding activities were elevated by incubation of the cells with LG69 and TTNPB, ligands specific for RXR and RAR respectively. Binding of nuclear proteins to the palindromic sequence was displaced either by anti-RXR alpha serum or by anti-VDR serum, suggesting the formation of a heterodimer of RXR alpha and VDR. These results suggest that the imperfect palindromic sequence upstream of exon I.1 plays an important but novel role in the regulated expression of the CYP19 gene in choriocarcinoma cells.

Aromatase↗
PubMed2002

Identification of an upstream pituitary-active promoter of human somatostatin receptor subtype 5.

Somatostatin receptor subtype 5 (sst5) has been linked to inhibition of PRL and insulin secretion. We characterized the genomic structure of the human sst5. The transcription start site was located 94 nucleotides upstream of the initiator ATG codon. Sequence analysis of 5'-inverse PCR products revealed the presence of a 6.1-kb intron in the 5'-untranslated region. RT-PCR analysis indicated tissue-specific activation of the newly identified upstream promoter in pituitary, but not in small intestine, lung, or placenta. A -1741 promoter directed significant levels of luciferase expression in GH(4) rat pituitary cells, Skut-1B endometrium cells, and JEG3 chorion carcinoma cells, which was absent in COS-7 monkey kidney cells. A minimal -101 promoter was sufficient to allow tissue-specific expression. Its activity in COS-7 cells was not enhanced by cotransfection of the pituitary-specific transcription factor Pit-1. Analysis of deletion constructs revealed a GC-rich region immediately upstream of the transcription start site, which is necessary for promoter activity. Somatostatin led to a significant inhibition, and forskolin and thyroid hormone to a significant stimulation of pituitary-specific promoter activity. Further mapping suggested a cAMP-responsive element located between -101 and the transcription start site, and thyroid hormone-responsive elements between -1741 and -1269 and between -317 and -101. These studies identified an upstream promoter of the sst5 gene with tissue-specific activity.

Animals↗
PubMed1997

An androgen response element in a far upstream enhancer region is essential for high, androgen-regulated activity of the prostate-specific antigen promoter.

Prostate-specific antigen (PSA) is expressed at a high level in the luminal epithelial cells of the prostate and is absent or expressed at very low levels in other tissues. PSA expression can be regulated by androgens. Previously, two functional androgen-response elements were identified in the proximal promoter of the PSA gene. To detect additional, more distal control elements, DNasel-hypersensitive sites (DHSs) upstream of the PSA gene were mapped in chromatin from the prostate-derived cell line LNCaP grown in the presence and absence of the synthetic androgen R1881. In a region 4.8 to 3.8 kb upstream of the transcription start site of the PSA gene, a cluster of three DHSs was detected. The middle DNAseI-hypersensitive site (DHSII, at approximately -4.2 kb) showed strong androgen responsiveness in LNCaP cells and was absent in chromatin from HeLa cells. Further analysis of the region encompassing DHSII provided evidence for the presence of a complex, androgen-responsive and cell-specific enhancer. In transient transfected LNCaP cells, PSA promoter constructs containing this upstream enhancer region showed approximately 3000-fold higher activity in the presence than in the absence of R1881. The core region of the enhancer could be mapped within a 440-bp fragment. The enhancer showed synergistic cooperation with the proximal PSA promoter and was found to be composed of at least three separate regulatory regions. In the center, a functionally active, high-affinity androgen receptor binding site (GGAACATATTGTATC) could be identified. Mutation of this element almost completely abolished PSA promoter activity. Transfection experiments in prostate and nonprostate cell lines showed largely LNCaP cell specificity of the upstream enhancer region, although some activity was found in the T47D mammary tumor cell line.

Androgens↗
PubMed1994

A distal tyrosinase upstream element stimulates gene expression in neural-crest-derived melanocytes of transgenic mice: position-independent and mosaic expression.

We have assessed the importance of a melanocyte-specific DNase I hypersensitive site and matrix attachment region situated 15 kb upstream of the mouse tyrosinase gene by analysis in transgenic mice. Transgenes containing all, part, or none of this region linked to the tyrosinase promoter and human tyrosinase cDNA were introduced into genetically albino mice, and pigmentation and transgene message levels were analyzed in the resulting transgenic lines. The effect of the upstream region was to enhance significantly gene expression in melanocytes, and to provide position-independent expression of the transgene. Two exceptions to complete position independence were seen; these lines displayed a mosaic expression pattern in which the transgene was expressed fully in some melanocyte clones but less so in others, resulting in transverse stripes of colours ranging from near white to dark grey. Unexpectedly, pigmentation in the eye of all transgenic lines containing the upstream region was nonuniform, in that the neural-crest-derived melanocytes of the choroid and anterior iris contained significantly more pigment than those derived from the optic cup (retinal pigment epithelium and posterior iris). Transgenes containing a small part or none of the upstream region were expressed poorly and in a position-dependent manner; of those lines that were visibly pigmented, expression was equal in the neural crest and optic-cup-derived cells of the eye.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Identification of upstream regulatory regions in the heart-expressed homeobox gene Nkx2-5.

Nkx2-5 marks the earliest recognizable cardiac progenitor cells, and is activated in response to inductive signals involved in lineage specification. Nkx2-5 is also expressed in the developing foregut, thyroid, spleen, stomach and tongue. One approach to elucidate the signals involved in cardiogenesis was to examine the transcriptional regulation of early lineage markers such as Nkx2-5. We generated F0 transgenic mice, which carry Nkx2-5 flanking sequences linked to a lacZ reporter gene. We identified multiple regulatory regions located within the proximal 10.7 kb of the Nkx2-5 gene. In addition to a proximal promoter, we identified a second promoter and a novel upstream exon that could participate in the regulation of Nkx2-5 transcription. Although used rarely in normal development, this novel exon could be spliced into the Nkx2-5 coding region in several ways, thereby potentially creating novel Nkx2-5 protein isoforms, whose transcriptional activity is greatly diminished as compared to wild-type Nkx2-5. An enhancer that directs expression in pharynx, spleen, thyroid and stomach was identified within 3.5 kb of exon 1 between the coding exon 1 and the novel upstream exon 1a. Two or more enhancers upstream of exon 1a were capable of driving expression in the cardiac crescent, throughout the myocardium of the early heart tube, then in the outflow tract and right ventricle of the looped heart tube. A negative element was also located upstream of exon1a, which interacted in complex ways with enhancers to direct correct spatial expression. In addition, potential autoregulatory elements can be cooperatively stimulated by Nkx2-5 and GATA-4. Our results demonstrate that a complex suite of interacting regulatory domains regulate Nkx2-5 transcription. Dissection of these elements should reveal essential features of cardiac induction and positive and negative signaling within the cardiac field.

Animals↗
PubMed2003

BETA2 activates transcription from the upstream glucokinase gene promoter in islet beta-cells and gut endocrine cells.

Glucokinase (GK) gene transcription initiates in the islet (beta-cell), gut, and brain from promoter sequences residing approximately 35 kbp upstream from those used in liver. Expression of betaGK is controlled in beta-cells by cell-enriched (i.e. pancreatic duodenal homeobox 1 [PDX-1]) and ubiquitously (i.e., Pal) distributed factors that bind to and activate from conserved sequence motifs within the upstream promoter region (termed betaGK). Here, we show that a conserved E-box element also contributes to control in the islet and gut. betaGK promoter-driven reporter gene activity was diminished by mutating the specific sequences involved in E-box-mediated basic helix-loop-helix factor activator binding in islet beta-cells and enteroendocrine cells. Gel shift assays demonstrated that the betaGK and insulin gene E-box elements formed the same cell-enriched (BETA2:E47) and generally distributed (upstream stimulatory factor [USF]) protein-DNA complexes. betaGK E-box-driven activity was stimulated in cotransfection assays performed in baby hamster kidney (BHK) cells with BETA2 and E47, but not USF. Chromatin immunoprecipitation assays performed with BETA2 antisera showed that BETA2 occupies the upstream promoter region of the endogenous betaGK gene in beta-cells. We propose that BETA2 (also termed NeuroD1) regulates betaGK promoter activity.

Animals↗
PubMed1990

Sequence signals in eukaryotic upstream regions.

Two DNA sequence elements are known to recur frequently upstream of eukaryotic polymerase II-transcribed genes. The TATAAA, at position -40, specifies the transcription initiation site. The GGCCAATCT is less frequent around -80. Sequence analysis of upstream regions reveals that the underlined yeast UAS2 consensus sequence, TGATTGGT, is also very frequent at -80 in higher polymerase II-transcribed animal sequences. The underlined CCAAT box and yeast UAS sequences are complementary. Structural analysis suggests some symmetry in their DNA structures. Upstream of the TATAAT-rich region there is an abundance of GC sequences. Analysis of nucleotide tracts indicates that these are preferentially flanked by their complementary nucleotides with a pyrimidine-purine junction, i.e., TTAN, CCGn, CnGG, TnAA. Here, I discuss DNA structural consideration in upstream regions along with protein readout of the major and minor groove information content. These sequence-structure aspects are put in the general context of protein (factors)-DNA (elements) recognition and regulation.

Animals↗
PubMed1996

A herpes simplex virus type 1 mutant with a deletion immediately upstream of the LAT locus establishes latency and reactivates from latently infected mice with normal kinetics.

The latency associated transcripts (LATs) are the only abundant viral gene products detected during latent herpes simplex virus (HSV) infection of peripheral nerves in animals and people. A LAT promoter has been identified and mutant viruses with lesions removing the promoter and surrounding region have been observed to reactivate slowly from trigeminal ganglia (TG) explanted from latently infected mice. Previous work has shown that most mutants with lesions limited to regions downstream of the LAT promoter reactivate normally. Therefore, to help map the boundaries of the slow reactivation phenotype, a mutant virus with lesions located immediately upstream of the LAT promoter was constructed and called 17 delta S/N. 17 delta S/N contains a 437 nucleotide (nt) deletion 332 nts upstream of the TATAA box of the LAT promoter. In productively infected cells, 17 delta S/N failed to synthesize detectable amounts of the 1.1 and 1.8 kb transcripts which are produced during wild-type infections and are specified by a region just upstream of the LAT promoter. However, 17 delta S/N did produce normal amounts of LAT in tissue culture as well as in neurons derived from latently infected cells, as ascertained by Northern blot and in situ hybridization analysis. Moreover, in latently infected mice, 17 delta S/N established and maintained infection in as many neurons as did wild type virus, as determined by in situ polymerase chain reaction (PCR) to detect viral DNA. Finally, the virus reactivated from TG derived from latently infected mice with kinetics indistinguishable from those of wild-type virus. Therefore, reactivation from latency, in this model system, does not appear to require function from the viral genomic region located immediately upstream of the LAT promoter.

Animals↗
PubMed2001

Expression of the INO2 regulatory gene of Saccharomyces cerevisiae is controlled by positive and negative promoter elements and an upstream open reading frame.

The INO2 gene encodes a transcriptional activator of the phospholipid biosynthetic genes of Saccharomyces cerevisiae. Complete derepression of phospholipid biosynthetic gene expression in response to inositol/choline deprivation requires both INO2 and INO4. Ino2p dimerizes with Ino4p to bind the upstream activating sequence (UAS)INO element found in the promoters of the target genes. We have demonstrated previously that transcription from the INO2 promoter is autoregulated 12-fold in a manner identical to that of the target genes. Here, we show that this regulation occurs at the levels of transcription and translation. Transcription accounts for fourfold regulation, whereas translation accounts for an additional threefold regulation. Regulation of transcription requires a UAS(INO) element. Additional promoter elements include an upstream essential sequence (UES) located upstream of the UAS(INO) element and a negative regulatory element in the vicinity of the UAS(INO) element. Regulation of translation is dependent on an upstream open reading frame (uORF) in the INO2 leader. These data support the model that regulatory gene promoters may display unusual organizations and may be subject to multiple levels of regulation. We have shown previously that the UME6 gene positively regulates INO2 expression. Here, we limit the UME6-responsive region of the INO2 promoter to nucleotides -217 to -56.

Amino Acid Sequence↗
PubMed2004

[Interaction of p53 with p53 response element like binding sequence at upstream of hepatitis B virus enhancer I].

BACKGROUND & OBJECTIVE: A p53 response element like binding sequence, 5'-TGCC(G)T-TGCCT-3' was found at upstream of hepatitis B virus (HBV) enhancer I from 1047 to 1059 nucleotides after analyzing the HBV genome by a computer program in our previous work. It indicated that the sequence could specifically bind P53 protein in vitro by electrophoretic mobility shift assay (EMSA) and electrophoretic mobility supershift assay (EMSSA). This study was designed to further investigate the interaction between P53 and p53 response element like binding sequence at upstream of HBV enhancer I. METHODS: HBV x gene enhancer and promoter which contains p53 response element like binding sequence TGCGT-TGCCT was in upstream of CAT enzyme in pX-CAT reporter plasmid. Firstly, we designed a point mutation in pX-CAT which change TGCGT TGCCT into TGTAT. TGTAT by polymerase chain reaction (PCR) in order to damage the p53 response element like sequence. After pX-CAT or mutation pX-CAT (mpX-CAT) transfected alone or cotransfected with pCMVp53 into HepG2 hepatoma cell, CAT activity was assayed to confirm the correlation of p53 protein with this DNA sequence. In addition, an antisense sequence corresponding to the p53 response element like sequence in HBV was reconstructed into the pZeoSV2 vector (alpha pZeoXP) and transfected into HepG2.2.15 cell line to block the binding of P53 with this sequence, the stable transfected HepG2.2.15 cell was observed about P53/P21 expression, cell cycle distribution and apoptosis rates. RESULTS: CAT enzyme of HepG2 had an higher expression in cotransfection with pCMVp53 and pX-CAT than alone pX-CAT (1.353 VS 0.738,P< 0.05), but it was lower in mpX-CAT(0.304) and pCMVp53 (0.402). Compared with the control group, P53/P21 expression and cell apoptosis rate decreased greatly in the stable transfected alpha pZeoXP HepG2.2.15 cell line (0.95% VS 7.84%), the cell number in S phase increased in the same cell line (16.37% VS 9.48%). CONCLUSION: Reporter gene expression of pX-CAT in intracellular could be promoted by P53, which further suggest that P53 could bind TGCC(G)T-TGCCT in upstream of HBV enhancer I and induce a prolonged P53 half life. Subsequently, P53 and p21 protein (downstream gene of P53) would have a higher expression and stronger activity.

Apoptosis↗
PubMed2004

[Cloning and sequencing of the upstream of mouse dentin sialophosphoprotein promoter].

OBJECTIVE: To clone and sequence the upstream of mouse dentin sialophosphoprotein promoter. METHODS: Genomic DNA was obtained from Balb/c mouse blood. The upstream of mouse dentin sialophosphoprotein promoter segments was obtained by PCR. Then the segments were inserted into T-vector. The plasmids were identified by digestion with the restriction enzyme analysis. The positive clone was sequenced and compared with Genebank. RESULTS: The upstream of mouse dentin sialophosphoprotein promoter was divided into three sequences and three different target segments with 997 bp, 1004 bp and 674 bp in length were obtained. After identified, sequenced and compared with Genebank, the sequences of the segments were consistent with those displayed on Genebank by 99%. CONCLUSION: The clone of the upstream of mouse dentin sialophosphoprotein promoter was successful. This work will help to study the regulation of DSPP expression.

Animals↗
PubMed1991

Upstream elements of the MHC class II E beta gene active in B cells.

The MHC class II (Ia) molecules are heterodimeric cell surface glycoproteins that have a limited tissue distribution and are essential for an Ir. These proteins are known to both display a limited tissue distribution and be responsive to up-regulation by cytokines such as IL-4. To begin to identify the molecular basis for both of these phenomena in B cells, we performed a deletional analysis of the upstream region of the murine E beta gene. We show that there are several cooperating positive as well as negative control elements in the E beta upstream region. The sequence between -2679 and -66 is a strong transcriptional element containing several sequences that act synergistically as positive elements. The negative elements are located more proximal to the transcription start site. Furthermore, two consensus motifs, termed X and Y, which are located in the proximal upstream region of all class II genes, are necessary for the transcriptional activity of more distal elements. Additionally, we identify an IL-4-responsive element located within 666 bp upstream of the transcription initiation site.

Animals↗