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At least 19 recordsLinked to original sources

PubMed1990

Protein recognition sites in polyomavirus enhancer: formation of a novel site for NF-1 factor in an enhancer mutant and characterization of a site in the enhancer D domain.

Polyomavirus mutants selected for modified host range exhibit DNA sequence alterations in the regulatory region, which consist mainly of duplications and/or deletions. Single base pair mutations have also been observed, which create or abolish DNA sequence motifs recognized by DNA-binding regulatory factors. The present work deals with the molecular characterization of a Polyoma mutant (PyNB11/1), selected for its high efficiency of growth in neuroblastoma cells. The enhancer region of PyNB11/1 displays a 91 bp tandem duplication harbouring a novel DNA sequence motif created at the boundary of the duplicated fragment. This motif is absent in the wild-type enhancer and is specifically recognized by a nuclear factor that belongs to the NF-1 family of transcription factors. We also report the characterization of an as yet unidentified DNA sequence motif in the D domain of the viral enhancer, that represents the binding site for a nuclear factor that is ubiquitous and comparably abundant in several murine cell types.

Animals↗

PubMed1990

Regulation of the human T-cell receptor alpha gene enhancer: multiple ubiquitous and T-cell-specific nuclear proteins interact with four hypomethylated enhancer elements.

Transcription of human T-cell receptor (TCR) alpha genes is regulated by a T-cell-specific transcriptional enhancer that is located 4.5 kilobases 3' of the C alpha gene segment. Previous studies have demonstrated that this enhancer contains at least five nuclear protein-binding sites called T alpha 1 to T alpha 5. In the studies described in this report, we have determined the molecular requirements for human TCR alpha enhancer function. In vitro mutagenesis and deletion analyses demonstrated that full enhancer activity is retained in a 116-base-pair fragment containing the T alpha 1 and T alpha 2 nuclear protein-binding sites and that both of these sites are required for full enhancer function. Functional enhancer activity requires that the T alpha 1 and T alpha 2 binding sites be separated by more than 15 and fewer than 85 base pairs. However, the sequence of this spacer region and the relative phase of the two binding sites on the DNA helix do not affect enhancer function. Deletion and mutation analyses demonstrated that the T alpha 3 and T alpha 4 nuclear protein-binding sites are not necessary or sufficient for TCR alpha enhancer activity. However, a fragment containing these two sites was able to compensate for T alpha 1 and T alpha 2 mutations that otherwise abolished enhancer activity. Electrophoretic mobility shift analyses of the TCR alpha enhancer binding proteins revealed that the T alpha 1, T alpha 3, and T alpha 4 binding proteins are expressed in a variety of T-cell and non-T-cell tumor cell lines. In contrast, one of the two T alpha 2 binding activities was detected only in T-cell nuclear extracts. The activity of the TCR alpha enhancer does not appear to be regulated solely at the level of DNA methylation on that the enhancer sequences were found to be identically hypomethylated in B and T cells as compared with fibroblasts. Taken together, these results suggest that TCR alpha enhancer activity is regulated by the interaction of multiple T-cell-specific and ubiquitous nuclear proteins with partially redundant cis-acting enhancer elements that are hypomethylated in cells of the lymphoid lineage.

Base Sequence↗

PubMed1990

The genome of hepatitis B virus contains a second enhancer: cooperation of two elements within this enhancer is required for its function.

Previous studies have identified an enhancer (enhancer I) at nucleotides (nt) 1074 to 1234 in the genome of the human hepatitis B virus (HBV), which locates immediately upstream from the X gene. By analysis of the expression of the chloramphenicol acetyltransferase gene driven by a heterologous simian virus 40 early promoter, we describe the identification of a second enhancer (enhancer II) at nt 1636 to 1741, which locates downstream of enhancer I and immediately upstream of the core gene. With various deletions at the 5' end of enhancer II, a positive regulatory element was identified at nt 1636 to 1690 (the II-A element), with the 5' boundary between nt 1636 and 1671. The II-A element alone did not have an enhancer function, but the enhancer activity was achieved by the concomitant presence of the sequence from nt 1704 to 1741 (the II-B element). The II-B element alone did not have enhancer activity. These results indicate that cooperation between the II-A and II-B elements is required to exhibit the enhancer activity of enhancer II. We also show that enhancer II stimulates the transcriptional activity of both the SPI and SPII promoters of the surface gene. Therefore, the SPI promoter activity is regulated by the proximal HNF-1 binding element and the distal enhancers I and II. These results indicate that multiple regulatory elements scattered over the whole viral genome are involved in the regulation of expression of each individual HBV gene and that the same regulatory element controls the expression of different HBV genes. The relative positions of these regulatory elements in the HBV genome suggest that they may control the expression of HBV genes in a coordinate and cooperative manner.

Carcinoma, Hepatocellular↗

PubMed1992

Labyrinthine enhancement on gadolinium-enhanced magnetic resonance imaging in sudden deafness and vertigo: correlation with audiologic and electronystagmographic studies.

Sudden deafness with or without vertigo presents a difficult diagnostic problem. This article describes 12 patients with enhancement of the cochlea and/or vestibule on gadolinium-diethylenetriamine pentaacetic acid-enhanced magnetic resonance imaging (MRI), correlating the enhancement with the auditory and vestibular function. All patients were studied with T2-weighted axial images taken through the whole brain, enhanced 3-mm axial T1-weighted images taken through the temporal bone, and enhanced T1-weighted sagittal images taken through the whole brain. Cochlear enhancement on the side of hearing loss was found in all the patients. The vestibular enhancement correlated with both subjective vestibular symptoms and objective measures of vestibular function on electronystagmography. In 2 patients, the resolution of symptoms 4 to 6 months later correlated with resolution of the enhancement on MRI. No labyrinthine enhancement was seen in a series of 30 control patients studied with the same MRI protocol. Labyrinthine enhancement in patients with auditory and vestibular symptoms is a new finding and is indicative of labyrinthine disease. While abnormalities on electronystagmograms and audiograms are nonspecific and only indicate a sensorineural problem, enhanced MRI may separate patients with retrocochlear lesions, such as acoustic neuromas, from those in whom the abnormal process is in the labyrinth or the brain.

Adult↗

PubMed1991

Enhancement of propranolol hydrochloride and diazepam skin absorption in vitro: effect of enhancer lipophilicity.

The enhancement of model hydrophilic (propranolol hydrochloride) and lipophilic (diazepam) drug penetration across rat and hairless mouse skin in vitro has been studied. Preliminary experiments established that most n-alkanes having chain lengths of between 7 and 16 promote the flux of both drugs. For propranolol, enhancement varied parabolically with carbon number; for diazepam, heptane was ineffective and all others were essentially equipotent. Enhancement by n-nonane was then compared with that by n-nonanol. Propranolol flux was increased by both enhancers, whereas diazepam penetration was not affected by the less lipophilic alcohol. The enhancement of propranolol by n-nonane and n-nonanol was examined as a function of adjuvant concentration in the applied formulation. Maximum increases in maximum penetration rates of 6.5-fold (n-nonane) and 8.2-fold (n-nonanol) were determined. As expected, the enhancement was saturable, indicative of a maximally perturbed stratum corneum. Finally, the penetration enhancing abilities of six monoterpenes were assessed. The purely hydrocarbon analogues promoted both propranolol and diazepam transport to an extent similar to that of n-nonane. The terpenes with hydrogen-bonding ability, however, only enhanced propranolol flux (at a level comparable to n-nonanol). While the data reported do not directly reveal mechanistic information on percutaneous penetration enhancement, they do provide a starting point for the rational investigation of interrelationships between drug, enhancer, and skin. Such information is clearly essential for the optimization and exploitation of transdermal drug delivery.

Alkanes↗

PubMed1991

Normal abdominal enhancement patterns with dynamic gadolinium-enhanced MR imaging.

The objective of this study was to quantitatively and qualitatively determine contrast enhancement patterns of normal abdominal organs with dynamic gadolinium-enhanced magnetic resonance (MR) imaging. Dynamic gadolinium-enhanced, T1-weighted, spin-echo imaging was performed during a 23-second breath hold in 38 patients, with images acquired before, during, and at 1,2, and 5 minutes after bolus injection of gadopentetate dimeglumine. Enhancement patterns of normal liver, spleen, pancreas, adrenal gland, kidney, aorta, inferior vena cava, and fat were determined by visual evaluation and by performance of signal intensity measurements with an electronic cursor. Time-intensity curves demonstrated peak enhancement of all abdominal organs during or immediately after bolus injection of gadopentetate dimeglumine. MR enhancement patterns included visualization of renal cortical nephrogram and heterogeneous enhancement of the spleen during the bolus phase of contrast material administration. Peak enhancement of normal liver was 72%; spleen, 172%; pancreas, 82%; adrenal gland, 85%; and kidney, 291%. This study established reference data regarding abdominal organ enhancement that will be useful as dynamic gadolinium-enhanced MR imaging becomes clinically implemented.

Abdomen↗

PubMed1992

Sequence of enhancement of various portions of the pituitary gland on gadolinium-enhanced MR images: correlation with regional blood supply.

In an effort to study the blood supply of the pituitary gland, we determined the sequence in which various portions of the gland enhanced on MR images obtained after administration of gadopentetate dimeglumine in seven healthy volunteers. The pituitary gland has a unique blood supply: the pars nervosa is supplied by the inferior hypophyseal arteries; the infundibular stem is supplied by the superior hypophyseal arteries, which are more distal than the inferior hypophyseal arteries; and the pars distalis is supplied indirectly by portal systems from the infundibular stem. Therefore, the expected sequence of contrast enhancement of the pituitary gland is: the pars nervosa first, the infundibular stem second, and the pars distalis last. However, it is difficult to evaluate the temporal sequence of contrast enhancement with "slow" conventional MR techniques, such as routine enhanced images acquired minutes after contrast administration. Accordingly, we used rapid enhanced gradient-echo sequences (14 sec/image) and the region-of-interest method to determine contrast enhancement for various portions of the gland. Enhancement-time curves were then plotted for each portion and compared to determine the sequence of enhancement. Our results show that the timing of contrast enhancement of various parts of the pituitary gland as demonstrated on MR imaging correlates closely with the expected perfusion sequence based on knowledge of regional vascular anatomy. Normal enhancement-time curves of different portions of the pituitary gland were established. This technique and baseline data can be used to evaluate patients with hypopituitarism caused by ischemia.

Adult↗

PubMed1990

Detection of hepatic metastases: comparison of contrast-enhanced CT, unenhanced MR imaging, and iron oxide-enhanced MR imaging.

Diagnostic accuracy of contrast-enhanced CT, unenhanced MR imaging, and MR images enhanced with superparamagnetic iron oxide was evaluated in 10 patients with histologically proved hepatic metastases. First, diagnostic performance of the imaging technique with respect to the ability of radiologists to recognize the presence or absence of a metastasis was measured by using receiver-operating-characteristic (ROC) analysis of single images. Second, the total number of lesions (N = 108) detected by "complete" CT and MR examinations was counted. Finally, lesion-liver contrast-to-noise ratios (CNR) were measured in all MR sequences. The area under the ROC curve was .67 +/- .03 for contrast-enhanced CT, .81 +/- .07 for the unenhanced SE 260/14 sequence, and .92 +/- .01 for the iron oxide-enhanced SE 1500/40 sequence. The enhanced SE 1500/40 sequence yielded significantly (p less than .005) greater accuracy than did contrast-enhanced CT. The same sequence detected significantly (p less than .05) more lesions than all other imaging techniques (19% more than the best unenhanced MR sequence and 36% more than contrast-enhanced CT). The enhanced SE 1500/40 sequence also yielded the highest CNR value (19.5 +/- 10.2) of all MR sequences. These results indicate that iron oxide-enhanced MR imaging is a superior imaging technique for the detection of hepatic lesions.

Adult↗

PubMed2026

MYB activity drives emergent enhancer activation and enhancer-promoter interactions in acute lymphoblastic leukemia.

Aberrant enhancer usage is a defining feature of oncogenic transcriptional reprogramming. Therapeutic strategies that disrupt enhancer-driven gene regulation may offer new treatment avenues. MYB is a key hematopoietic transcription factor that is frequently dysregulated in a broad range of cancers and plays a critical role in sustaining malignant cell states, including in aggressive leukemia subtypes such as KMT2A-rearranged leukemias. The molecular mechanisms by which it maintains oncogenic transcription remain incompletely understood. Here, we investigate the role of MYB in directing pathological enhancer activity to drive oncogene expression in leukemia. Using high-resolution Micro Capture-C, we show that upon MYB degradation, highly defined enhancer-promoter interactions at MYB binding sites are lost, correlating with the significant downregulation of target gene expression. When anchored to a gene desert region, the Myb transactivation domain (MybTA) is sufficient and necessary for the nucleation of an enhancer-like region. Critically, long-range chromatin interactions are established up to 400 kb away from where MybTA is anchored. This results in the activation of transcription from distal cryptic elements, which is reduced or abolished in the presence of point mutations that disrupt its interaction with the coactivators P300/CBP. All these results indicate that MYB activity alone is sufficient to generate an enhancer, inducing transcription through precise enhancer-promoter cross talk, and identify the MYB-P300/CBP axis as a therapeutically actionable vulnerability in enhancer-driven malignancies.

Promoter Regions, Genetic↗

PubMed1992

The Mu transpositional enhancer can function in trans: requirement of the enhancer for synapsis but not strand cleavage.

The phage Mu transpositional enhancer has been previously shown to stimulate the initial rate of the Mu DNA strand transfer reaction by a factor of 100. We now show that the Mu enhancer can function in trans on an unlinked DNA molecule. This activity is greatly facilitated by the presence of a free DNA end proximal to the enhancer element. Function of the enhancer in trans does not alter either the requirement for donor DNA supercoiling or for the two Mu ends to be in their proper orientation on the donor plasmid. An important consequence of these findings is that we have been able to evaluate directly the step in the transposition reaction for which the enhancer is required. We show that the role of the enhancer is limited to promoting productive synapsis; efficient strand cleavage can occur in the absence of the enhancer.

Bacteriophage mu↗

PubMed1991

Dynamic gadolinium-enhanced MR imaging of the spleen: normal enhancement patterns and evaluation of splenic lesions.

The authors studied the ability to improve detection of splenic lesions during suspended respiration with dynamic gadolinium-enhanced T1-weighted spin-echo magnetic resonance (MR) imaging. In the first phase of the study, normal splenic contrast material enhancement patterns were assessed in 10 control patients without splenic lesions. A heterogeneous signal intensity pattern was observed in 11 patients with splenic lesions during bolus injection of gadopentetate dimeglumine, with conversion to homogeneous enhancement 1 minute later. Mean splenic enhancement was 321% during bolus injection, with a rapid return toward baseline signal intensity thereafter. In the second phase, evaluation of 18 splenic lesions detected with contrast-enhanced computed tomography in 11 patients revealed that dynamic gadolinium-enhanced MR pulse sequences significantly improved lesion conspicuity and detectability compared with conventional T1-and T2-weighted pulse sequences. Contrast-to-artifact ratio measurements were 0.5, 3.7, and 9.3 for conventional T1-weighted, T2-weighted, and dynamic gadolinium-enhanced MR images, respectively.

Adult↗

PubMed1991

Every enhancer works with every promoter for all the combinations tested: could new regulatory pathways evolve by enhancer shuffling?

The promoters and enhancers of cell type-specific genes are often conserved in evolution, and hence one might expect that a given enhancer has evolved to work best with its own promoter. While this expectation may be realized in some cases, we have not found evidence for it. A total of 27 combinations of different promoters and enhancers were tested by transfection into cultured cells. We found that the relative efficiency of the enhancers is approximately the same, irrespective of the type of promoter used, i.e., there was no strong preference for any given enhancer/promoter combination. Notably, we do not see particularly strong transcription when the immunoglobulin kappa enhancer (or the immunoglobulin heavy chain enhancer) is used to activate a kappa gene promoter. We propose that a generally permissive enhancer/promoter interaction is of evolutionary benefit for higher eukaryotes: by enhancer shuffling, genes could be easily brought under a new type of inducibility/cell type specificity.

B-Lymphocytes↗

PubMed2022

Enhancer and super-enhancer landscape in polycystic kidney disease.

Widespread aberrant gene expression is a pathological hallmark of polycystic kidney disease (PKD). Numerous pathogenic signaling cascades, including c-Myc, Fos, and Jun, are transactivated. However, the underlying epigenetic regulators are poorly defined. Here we show that H3K27ac, an acetylated modification of DNA packing protein histone H3 that marks active enhancers, is elevated in mouse and human samples of autosomal dominant PKD. Using comparative H3K27ac ChIP-Seq analysis, we mapped over 16000 active intronic and intergenic enhancer elements in Pkd1-mutant mouse kidneys. We found that the cystic kidney epigenetic landscape resembles that of a developing kidney, and over 90% of upregulated genes in Pkd1-mutant kidneys are co-housed with activated enhancers in the same topologically associated domains. Furthermore, we identified an evolutionarily conserved enhancer cluster downstream of the c-Myc gene and super-enhancers flanking both Jun and Fos loci in mouse and human models of autosomal dominant PKD. Deleting these regulatory elements reduced c-Myc, Jun, or Fos abundance and suppressed proliferation and 3D cyst growth of Pkd1-mutant cells. Finally, inhibiting glycolysis and glutaminolysis or activating Ppara in Pkd1-mutant cells lowerd global H3K27ac levels and its abundance on c-Myc enhancers. Thus, our work suggests that epigenetic rewiring mediates the transcriptomic dysregulation in PKD, and the regulatory elements can be targeted to slow cyst growth.

Animals↗

PubMed1992

Enhancement of systemic delivery of met-enkephalin and leu-enkephalin eyedrops with permeation enhancers.

It was found that methionine enkephalin (Met-Enk) and leucine-enkephalin (Leu-Enk) can be delivered efficiently into the systemic circulation through the outer route in rabbits. When 50 mcl of 1% Met-Enk eyedrops without absorption enhancers were instilled into eyes, the rabbits' blood concentration rose from 92 pg/ml to 153 pg/ml in 10 min. When either of two permeation enhancers (BL-9 or Brij-78) was added at a 0.5% concentration to the ophthalmic solution, the systemic absorption of 1% Met-Enk was markedly improved. Its blood level was increased to approximately 3.4 times that without the enhancer. When the eyedrops of 0.3% Met-Enk plus 0.5% absorption enhancer were administered, the blood concentration reached higher than that reached by 1% Met-Enk without permeation enhancers. Similar results were obtained with Leu-Enk except the systemic absorption was enhanced by BL-9 and Brij-78 even further to 10-fold and 8.3-fold, respectively. These results indicate that the systemic delivery of Met-Enk and Leu-Enk through eyes, especially with the addition of permeation enhancers, is a feasible alternative route to parenteral injection.

Absorption↗

PubMed2026

ATRX Condensates as Candidate Organizers of Enhancer-Centered Nuclear Microenvironments in Neural Progenitors: A Hypothesis for Enhancer-Associated ATRX Function in Neural Progenitors.

Neural progenitor cells (NPCs) must preserve lineage identity while remaining responsive to developmental cues. Here, we discuss the hypothesis that ATRX condensates help organize enhancer-centered nuclear microenvironments in NPCs. ATRX has long been studied in heterochromatin maintenance, histone variant deposition, and chromatin remodeling; earlier work has also shown that ATRX can occupy euchromatic and active regulatory regions and contribute to transcriptional regulation. Recent evidence in human NPCs indicates that ATRX forms nuclear puncta with condensate-like properties, associates with neurogenic enhancer-rich regions, and incorporates regulatory factors such as CHD7 and p300. Perturbation of ATRX condensate formation is associated with changes in enhancer-associated ATRX occupancy, neural gene-expression programs, and neuroepithelial organization, suggesting a regulatory mode that may complement canonical heterochromatin-associated functions. We propose a dual-mode model in which folded domains contribute to chromatin anchoring at repressive regions, whereas intrinsically disordered regions support condensate-associated organization at active developmental enhancers. We emphasize that whether ATRX condensates activate enhancers de novo, stabilize pre-existing enhancer states, buffer transcriptional variability, or primarily organize cofactor localization remains unresolved. We also discuss limitations of the current evidence and outline acute, locus-specific experiments needed to test the model.

X-linked Nuclear Protein↗

PubMed2026

Hi-Enhancer: a two-stage framework for prediction and localization of enhancers based on Blending-KAN and Stacking-Auto models.

MOTIVATION: Gene expression plays a crucial role in cell function, and enhancers can regulate gene expression precisely. Therefore, accurate prediction of enhancers is particularly critical. However, existing prediction methods have low accuracy or rely on fixed multiple epigenetic signals, which may not always be available. RESULTS: We propose a two-stage framework that accurately predicts enhancers by flexibly combining multiple epigenetic signals. In the first stage, we designed a Blending-KAN model, which integrates the results of various base classifiers and employs Kolmogorov-Arnold Networks (KAN) as a meta-classifier to predict enhancers based on flexible combinations of multiple epigenetic signals. In the second stage, we developed a Stacking-Auto model, which extracted sequence features using DNABERT-2 and located the enhancers based on the Stacking strategy and AutoGluon framework. The accuracy of the Blending-KAN model reached 99.69 ± 0.11% when five epigenetic signals were used. In cross-cell line prediction, the accuracy was more significant than or equal to 93.72%. With Gaussian noise, it still maintains an accuracy of 98.74 ± 0.03%. In the second stage, the accuracy of the Stacking-Auto model is 80.50%, which is better than the existing 17 methods. The results show that our models can be flexibly used to predict and locate enhancers utilizing a combination of multiple epigenetic signals. AVAILABILITY AND IMPLEMENTATION: The source code is available at https://github.com/emanlee/Hi-Enhancer and https://doi.org/10.6084/m9.figshare.29262158.v1.

Enhancer Elements, Genetic↗

PubMed1989

Determinant differences between the rabbit and mouse immunoglobulin kappa enhancers impair the activity of the rabbit enhancer in mouse myeloma cells.

Enhancer activity of the rabbit immunoglobulin kappa light chain gene intron conserved region (KICR) was examined in mouse myeloma cells using transient expression experiments. Compared to the homologous region of the mouse kappa light chain gene, the rabbit KICR shows nearly no stimulatory effect on expression of the indicator gene, cat. Experiments with mouse-rabbit chimeric KICRs indicated that differences in the region around the NF-kappa B binding site are responsible for the impaired activity of the rabbit KICR whereas mouse sequences covering the kappa E2 and kappa E3 motifs can be replaced by the equivalent rabbit fragment without affecting enhancer function. Creation of a perfect mouse NF-kappa B target sequence in the rabbit gene only partially restores enhancer activity. Furthermore, mouse and rabbit DNA fragments encompassing the NF-kappa B target sequence behave in an identical manner in an electrophoretic mobility shift assay. The results indicate species-related functional differences in the immunoglobulin kappa light chain gene enhancer and suggest that although the NF-kappa B binding site plays a crucial role in enhancer activity surrounding gene elements are also necessary for full enhancer effect.

Animals↗

PubMed1990

The state of cellular differentiation determines the activity of the adenovirus E1A enhancer element: evidence for negative regulation of enhancer function.

Most of the eucaryotic enhancer elements so far described consist of multiple DNA binding sites for proteins that act either synergistically or antagonistically to modulate the rate of transcription. In this report, we show that the activity of the adenovirus E1A enhancer element is suppressed in virus-infected undifferentiated rodent fetal fibroblast cells (CREF and F111 cells) and primary rat liver hepatocytes that have lost their fully differentiated phenotype (dedifferentiated). This contrasts with the results obtained for virus-infected differentiated or partially dedifferentiated rodent hepatocytes or hepatoma cell lines and human HeLa cells, in which deletion of the E1A enhancer domain greatly reduces the rate of E1A gene transcription. An in vitro quantitation of the nuclear proteins (from HeLa and CREF cells) that interact with and modulate the activity of the E1A enhancer revealed similar binding activities for the E2f and ATF proteins. However, an AP3-like (phi AP3) activity was present at a 10- to 20-fold higher concentration in CREF cells than in HeLa cells, and removal of this phi AP3-binding site on the viral genome resulted in an increase in the rate of E1A gene transcription in virus-infected CREF cells. Together, these results demonstrated that the factors which positively regulate enhancer function were present in CREF cells and that the phi AP3 factor was acting to suppress the activity of the E1A enhancer. Furthermore, the level of this factor was found to increase to even higher levels in CREF cells treated with 12-O-tetradecanoylphorbol-13-acetate, and this induction resulted in a further suppression in the rate of E1A gene transcription. On the basis of these observations, we propose that E1A expression is negatively regulated by the phi AP3 factor in undifferentiated rodent fetal fibroblast cells and that this could be an important mechanism that distinguishes between establishment of the differentiated cell versus transformed cell phenotypes.

Adenovirus Early Proteins↗