SEARCH · PubMed Health

Results for “Enhancer mapping”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 595 records · Page 33Linked to original sources

PubMed2005

Association mapping of kernel size and milling quality in wheat (Triticum aestivum L.) cultivars.

Association mapping is a method for detection of gene effects based on linkage disequilibrium (LD) that complements QTL analysis in the development of tools for molecular plant breeding. In this study, association mapping was performed on a selected sample of 95 cultivars of soft winter wheat. Population structure was estimated on the basis of 36 unlinked simple-sequence repeat (SSR) markers. The extent of LD was estimated on chromosomes 2D and part of 5A, relative to the LD observed among unlinked markers. Consistent LD on chromosome 2D was <1 cM, whereas in the centromeric region of 5A, LD extended for approximately 5 cM. Association of 62 SSR loci on chromosomes 2D, 5A, and 5B with kernel morphology and milling quality was analyzed through a mixed-effects model, where subpopulation was considered as a random factor and the marker tested was considered as a fixed factor. Permutations were used to adjust the threshold of significance for multiple testing within chromosomes. In agreement with previous QTL analysis, significant markers for kernel size were detected on the three chromosomes tested, and alleles potentially useful for selection were identified. Our results demonstrated that association mapping could complement and enhance previous QTL information for marker-assisted selection.

Chromosome Mapping↗

PubMed1994

Ontogeny of enhanced striatal dopamine release in rats with methamphetamine-induced behavioral sensitization.

The behavioral sensitization has not been observed in rats under three weeks of age when administration of repeated psychostimulants is started. The aim of our study was to determine the effect of methamphetamine (MAP)-induced behavioral sensitization ontogeny on MAP challenge-induced changes of striatal extracellular concentrations of dopamine (DA) and its metabolites, using in vivo microdialysis. Experimental rats aged 7, 14, 21, 28, and 56 postnatal days (PNDs) were injected IP twice daily with 2 mg/kg MAP for three days, followed by 4 mg/kg for three days. Matched control rats were given equivalent volumes of saline according to the same schedule. Dialysis experiments were carried out 21 days after the last MAP or saline injection. All the rats were injected (IP) with a challenge dose of MAP (4 mg/kg). We reconfirmed that MAP-induced stereotyped behavior was enhanced significantly only when MAP pretreatment was started on PNDs 21, 28, and 56, but not PNDs 7 and 14. Correspondingly, the MAP challenge induced significantly greater increases in striatal extracellular DA concentrations in the MAP-pretreated rats compared with control rats only when MAP pretreatment was initiated on PNDs 21, 28, and 56, but not in younger rats.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

junB promoter regulation: Ras mediated transactivation by c-Ets-1 and c-Ets-2.

The Jun gene family encode components of the AP-1 transcription factor complex that regulate a variety of TRE-containing target promoters. Expression of family members is induced by a wide variety of extracellular stimuli and thought to be important in mediating cellular proliferation and differentiation. We have localized cis-acting DNA sequences in the murine junB promoter capable of mediating transcriptional activation by the proto-oncogene products c-Ets-1 and c-Ets-2. We show by promoter deletion analysis that multiple elements located between -848 and -574, and between -196 and -91 can mediate transactivation by ETS-family members in different cell types. In vitro DNA binding assays indicate that the elements identified can specifically interact with c-Ets-1 protein. Furthermore, we show that ETS-transactivation of a variety of reporter constructs is dramatically enhanced by introduction of oncogenic Ha-ras. The activation of Ras by extracellular stimuli invokes a phosphorylation cascade that includes the downstream mitogen-activated protein (MAP) kinase p44ERK-1. We further show that addition of activated p44ERK-1 MAP kinase can also enhance ETS-transactivation of junB promoter reporter constructs. Here we propose that ETS-family members play a role in the activation of junB transcription by a Ras-stimulated signal transducing pathway that includes MAP kinase(s).

Animals↗

PubMed1999

Effects of cAMP on ERK mitogen-activated protein kinase activity in hepatocytes do not parallel the bidirectional regulation of DNA synthesis.

Previous studies have indicated that cAMP has bidirectional effects on epidermal growth factor (EGF)-induced DNA synthesis in cultured hepatocytes, acting to stimulate soon after plating (early G(1)) and to inhibit at later stages (nearer the G(1)/S transition). In this study we examined the role of the extracellular signal-regulated kinase (ERK) subgroup (p42/p44) of the mitogen activated protein (MAP) kinases both at growth-stimulatory and growth-inhibitory conditions. When added at low concentrations early during culturing, glucagon and 8-chlorophenylthio-cAMP (8-CPT-cAMP) did not increase MAP kinase activity, but enhanced the subsequent DNA synthesis. However, when administered at 24 h, glucagon and 8-CPT-cAMP decreased basal and EGF-induced MAP kinase activity and also inhibited EGF-induced DNA synthesis. Thus, although MAP kinase might play a role in the growth-inhibitory effect, it does not seem to be involved in growth-promoting regulation by cAMP in hepatocytes.

Animals↗

PubMed2003

The telomeric region of BTA18 containing a potential QTL region for health in cattle exhibits high similarity to the HSA19q region in humans.

We have applied a targeted physical mapping approach, based on the isolation of bovine region-specific large-insert clones using homologous human sequences and chromosome microdissection, to enhance the physical gene map of the telomeric region of BTA18 and to prove its evolutionary conservation. The latter is a prerequisite to exploit the dense human gene map for future positional cloning approaches. Partial sequencing and homology search were used to characterize 20 BACs targeted to the BTA18q2.4-q2.6 region. We used fluorescence in situ hybridization (FISH) to create physical maps of 11 BACs containing 15 gene loci; these BACs served as anchor loci. Using these approaches, 12 new gene loci (CKM, STK13, PSCD2, IRF3, VASP, ACTN4, ITPKC, CYP2B6, FOSB, DMPK, MIA, SIX5) were assigned on BTA18 in the bovine cytogenetic map. A resolved physical map of BTA18q2.4-q2.6 was developed, which encompasses 28 marker loci and a comparative cytogenetic map that contains 15 genes. The mapping results demonstrate the high evolutionary conservation between the telomeric region of BTA18q and HSA19q.

Animals↗

PubMed1999

Endonuclease-mediated long PCR and its application to restriction mapping.

The polymerase chain reaction (PCR) is the most widely used technique for the study of DNA. Applications for PCR have been extended significantly by the development of "long" PCR, a technique that makes it possible to amplify DNA fragments up to 40 kb in length. This article describes two novel applications of the long PCR technique, one which simplifies restriction mapping and another which enhances amplification specificity and yield. The same primers used to perform the long PCR amplification can be used as probes to perform restriction mapping of the DNA fragment amplified. Restriction digestion performed prior to long PCR amplification can be used to selectively suppress the amplification of members of families of closely related DNA sequences, thereby making it possible to selectively amplify one of a group of highly homologous sequences. These two complimentary techniques, both involving use of the long PCR paired with restriction digestion, have potential application in any laboratory in which PCR is performed.

DNA Restriction Enzymes↗

PubMed1991

Genetic analysis of determinants of disease severity and virus concentration in cauliflower mosaic virus.

Cauliflower mosaic virus (CaMV) strains CM1841 and W260 produced markedly different symptoms when inoculated onto turnips (Brassica campestris L. 'Just Right'). The CM1841 strain induced a mild degree of stunting of infected plants while strain W260 caused moderate to severe stunting. Although CM1841 was significantly milder than W260, it accumulated to a significantly higher concentration than W260 in systemically infected leaves. We constructed a series of hybrid viruses in order to map regions of W260 responsible for enhanced disease severity relative to CM1841 and to map regions of CM1841 responsible for higher virus accumulation. We found that the characteristic degree of stunting caused by a CaMV isolate is determined in a complex manner by viral genes that influence viral gene expression and viral genes that disrupt host metabolism. Genes I and VI influenced both virus concentration and stunting severity, suggesting that these regions affected disease severity primarily through their effect on gene expression. In addition, an interaction between genes IV and VI was observed which further indicated that stunting severity was influenced by differential accumulation of virus. In contrast, three regions of W260 influenced the stunting phenotype but had no effect, or a negative effect, on virus concentration. The three regions contained (1) portions of genes II and III, (2) gene IV, independent of gene VI, and (3) the 3' half of gene V and the 19 S promoter. These regions may influence stunting severity primarily by disrupting host metabolism. Additionally, some of the chimeric viruses induced systemic necrosis on leaves, a symptom that is not characteristic of either CM1841 or W260. The necrotic flecking symptom was caused by an interaction between a W260 DNA segment containing gene I and the 5' half of gene II and a CM1841 DNA segment containing the 3' half of gene II, gene III, and gene IV.

Chimera↗

PubMed2005

Single linkage group per chromosome genetic linkage map for the horse, based on two three-generation, full-sibling, crossbred horse reference families.

A genetic linkage map of the horse consisting of 742 markers, which comprises a single linkage group for each of the autosomes and the X chromosome, is presented. The map has been generated from two three-generation full-sibling reference families, sired by the same stallion, in which there are 61 individuals in the F2 generation. Each linkage group has been assigned to a chromosome and oriented with reference to markers mapped by fluorescence in situ hybridization. The average interval between markers is 3.7 cM and the linkage groups collectively span 2772 cM. The 742 markers comprise 734 microsatellite and 8 gene-based markers. The utility of the microsatellite markers for comparative mapping has been significantly enhanced by comparing their flanking sequences with the human genome sequence; this enabled conserved segments between human and horse to be identified. The new map provides a valuable resource for genetically mapping traits of interest in the horse.

Animals↗

PubMed1998

Vulnerability of synaptic plasticity in the striatum of methamphetamine-sensitized rats.

We examined the influence of ischemia on methamphetamine (MAP)-induced behavioral sensitization and enhancement of dopamine (DA) release. After the recovery period of the ischemia operation, rats were treated with MAP (1 mg/kg, i.p.) once daily for 6 consecutive days. Re-administration of MAP (0.5 mg/kg, i.p.) potentiated the increase of locomotor activity after a 3-day withdrawal and the enhancement of DA release from striatal slices after a 6-day withdrawal. The MAP-induced sensitization was impaired by 5 min ischemia. On the other hand, the increase of locomotor activity induced by single MAP (1 mg/kg, i.p.) administration was impaired by 20 min of ischemia. Moreover, in saline-treated rats the increase of DA release from striatal slices induced by MAP (10 microM) application was also impaired by 20 min of ischemia. These results indicate that the neuronal plastic change may be very vulnerable to ischemia in MAP-induced sensitization.

Animals↗

PubMed1983

Long-lasting hypersensitivity to methamphetamine following amygdaloid kindling in cats: the relationship between limbic epilepsy and the psychotic state.

This study attempts to analyze the biological mechanisms involved in the association of a psychotic state with temporal lobe epilepsy, and the inverse relation between the epilepsy and this psychotic state. Responses to a test dose of methamphetamine (MAP) were examined in amygdaloid-kindled cats. It was found that (i) MAP-induced stereotyped behavior was enhanced after amygdaloid kindling, and this hypersensitivity lasted for at least 10 days after the final convulsion, (ii) autonomic responses to MAP including piloerection, salivation, heart rate, and respiration rate were also enhanced by the kindling, (iii) kindled generalized convulsions were suppressed during MAP-induced stereotyped behavior in some cats, and (iv) this suppression was blocked by pretreatment with pimozide. Engel and Ackermann proposed that inhibitory events precipitated by each kindling stimulus could produce changes in the catecholaminergic system similar to the reverse tolerance seen with dopamine agonists, and that inhibitory hypersensitivity could parallel the development of kindled excitation. This was partially confirmed by the present study, and leads to the hypothesis that excitation of seizure-inhibiting activity, including activity of the dopamine system, may be related to the emergence of a psychotic state, and to the inverse relationship between epilepsy and the psychotic state in temporal lobe epilepsy.

Amygdala↗

PubMed2005

Using concept maps to optimize the composition of collaborative student groups: a pilot study.

AIM: The aim of this paper is to stimulate interest in the practical classroom application of concept mapping strategies as an approach that teachers can easily use to enhance collaborative learning. BACKGROUND: Concept mapping has been developed as a tool to support meaningful learning. However, much of the research literature fails to explain how concept maps might be most gainfully employed within the classroom. As a result, concept mapping is a tool that is under-used. METHODS: Students on a postgraduate teacher preparation programme for nurses were arranged in triads on the basis of the morphology of individually-produced concept maps for the topics of 'genetics' and 'pathogenic microbes'. They were arranged in heterogeneous triads to produce a consensus map for 'pathogenic microbes', and then in homogeneous triads to produce a consensus map for 'genetics'. The number of acceptable propositions found in their individual maps was compared with the number found in the consensus group maps, and gain scores were calculated for each participant. FINDINGS: Participants arranged in triads of individuals having very different knowledge structures were found to make a greater improvement than those arranged in triads composed of individuals with qualitatively similar knowledge structures. CONCLUSIONS: The study was undertaken with a very small sample and only looked at two topic areas. However, the findings support the idea that collaborative groups work most effectively when individuals within the group bring different perspectives to a problem, and that this perspective can be usefully identified within the classroom environment as variations in concept map morphology.

Concept Formation↗

PubMed2002

p38 mitogen-activated protein kinase regulates growth factor-induced mitogenesis of rat pulmonary myofibroblasts.

Myofibroblast proliferation is a central feature of pulmonary fibrogenesis. Several growth factors, including platelet-derived growth factor (PDGF) and epidermal growth factor (EGF), stimulate myofibroblast growth by activating extracellular signal regulated kinases 1 and 2 (ERK1/2). In this report, we demonstrate that PDGF-BB and EGF also activate the p38 mitogen-activated protein (MAP) kinase. Inhibition of p38 activity with the pyridinylimidazole compound SB203580 enhanced both PDGF-BB and EGF-stimulated DNA synthesis in rat lung myofibroblasts. ERK1/2 phosphorylation in response to either PDGF-BB or EGF treatment was significantly increased by pretreatment of cells with SB203580. We also demonstrated that ERK1/2-induced phosphorylation of PHAS-1 substrate was enhanced by inhibition of p38 MAP kinase with SB203580. However, SB203580 did not significantly increase growth factor-induced activation of MEK, the upstream kinase that phosphorylates ERK1/2. p38 MAP kinase was co-immunoprecipitated with ERK-1/2 following growth factor stimulation. Collectively, these data demonstrate that p38 MAP kinase activation negatively regulates PDGF- and EGF-mediated growth responses by directly interacting with ERK1/2 and suppressing its phosphorylation.

Animals↗

PubMed1982

The interaction of actin filaments with microtubules and microtubule-associated proteins.

Purified actin and microtubule proteins polymerized together form a gel, while mixtures of actin with tubulin polymers lacking microtubule-associated proteins (MAPs) have low viscosities close to the sum of the viscosities of the constituents. Mixtures of actin and MAPs also have high viscosities. Our interpretation of these observations was that there is interaction of actin filaments and microtubules which is mediated by MAPs (Griffith, L. M., and Pollard, T. D. (1978) J. Cell Biol. 78, 958-965). We report here further evidence for this interaction. 1) Actin filaments and microtubules can form gels at physiological ionic strength providing the anion is glutamate rather than chloride. Both glutamate and chloride inhibit actin-MAPs interaction, but this is compensated for in glutamate where the microtubules are longer than in chloride. 2) The low shear viscosity of mixtures of isolated MAPs and actin filaments is enhanced by acidic pH and inhibited by high ionic strength. 3) MAPs can be fractionated to yield four different fractions with actin cross-linking activity: a subset of high molecular weight MAPs, purified "MAP-2" and two different fractions of tau polypeptides. 4) We have reconstituted a gel from actin, purified tubulin, and whole MAPs, but have not yet been successful with actin, purified tubulin, and any single purified MAP.

Actins↗

PubMed2004

Interleukin (IL)-17 enhances tumor necrosis factor-alpha-stimulated IL-6 synthesis via p38 mitogen-activated protein kinase in osteoblasts.

Inflammatory cytokines are well known to play crucial roles in the pathogenesis of rheumatoid arthritis. Among them, interleukin (IL)-17 is a cytokine that is mainly synthesized by activated T cells and its receptors are present in osteoblasts. The synthesis of IL-6, known to stimulate osteoclastic bone resorption, is reportedly responded to bone resorptive agents such as tumor necrosis factor-alpha (TNF-alpha) in osteoblasts. It has been reported that IL-17 enhances TNF-alpha-stimulated IL-6 synthesis in osteoblast-like MC3T3-E1 cells. We previously showed that sphingosine 1-phosphate (S1-P) mediates TNF-alpha-stimulated IL-6 synthesis in these cells. In the present study, we investigated the mechanism of IL-17 underlying enhancement of IL-6 synthesis in MC3T3-E1 cells. IL-17 induced phosphorylation of p38 mitogen-activated protein (MAP) kinase. SB203580 and PD169316, specific inhibitors of p38 MAP kinase, significantly reduced the enhancement by IL-17 of TNF-alpha-stimulated IL-6 synthesis. IL-17 also amplified S1-P-stimulated IL-6 synthesis, and the amplification by IL-17 was suppressed by SB203580. Anisomycin, an activator of p38 MAP kinase, which alone had no effect on IL-6 level, enhanced the IL-6 synthesis stimulated by TNF-alpha. SB203580 and PD169316 inhibited the amplification by anisomycin of the TNF-alpha-induced IL-6 synthesis. Taken together, our results strongly suggest that IL-17 enhances TNF-alpha-stimulated IL-6 synthesis via p38 MAP kinase activation in osteoblasts.

Animals↗

PubMed1996

[Comparison of the effects of nicotine and methamphetamine on extracellular dopamine in the nucleus accumbens of behaviorally sensitized rats].

Repeated administration of nicotine (NCT) and methamphetamine (MAP) produced a progressive enhancement (sensitization) in the increasing effects on spontaneous motor activity in rats. The purpose of this study was to compare the effects of NCT and MAP on the extracellular levels of dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) in the nucleus accumbens of behaviorally sensitized rats by in vivo microdialysis. NCT 0.5 mg/kg, sc did not change the DA and DOPAC levels in drug-naive rats, but it showed an increase in the DA levels in rats sensitized to NCT. MAP 0.5 mg/kg, sc increased DA levels and decreased DOPAC levels in drug-naive rats, but it showed a smaller increase in DA levels in rats sensitized to MAP than in drug-naive rats. On the other hand, the basal levels of DA were increased in sensitized rats produced by MAP, but not in those produced by NCT. The present results suggest that NCT and MAP produce behavioral sensitization through the action on the mesolimbic dopaminergic system, but the manner of action of these drugs is different.

Animals↗

PubMed2005

Imagery-induced cortical excitability changes in stroke: a transcranial magnetic stimulation study.

Focal transcranial magnetic stimulation (TMS) was employed in a population of hemiparetic stroke patients in a post-acute stage to map out the abductor digiti minimi (ADM) muscle cortical representation of the affected (AH) and unaffected (UH) hemisphere at rest, during motor imagery and during voluntary contraction. Imagery induced an enhancement of the ADM map area and volume in both hemispheres in a way which partly corrected the abnormal asymmetry between AH and UH motor output seen in rest condition. The voluntary contraction was the task provoking maximal facilitation in the UH, whereas a similar degree of facilitation was obtained during voluntary contraction and motor imagery in the AH. We argued that motor imagery could induce a pronounced motor output enhancement in the hemisphere affected by stroke. Further, we demonstrated that imagery-induced excitability changes were specific for the muscle 'prime mover' for the imagined movement, while no differences were observed with respect to the stroke lesion locations. Present findings demonstrated that motor imagery significantly enhanced the cortical excitability of the hemisphere affected by stroke in a post-acute stage. Further studies are needed to correlate these cortical excitability changes with short-term plasticity therefore prompting motor imagery as a 'cortical reservoir' in post-stroke motor rehabilitation.

Brain Mapping↗

PubMed1997

Phosphocholine and sphingosine-1-phosphate synergistically stimulate DNA synthesis by a MAP kinase-dependent mechanism.

We have previously shown that in NIH 3T3 fibroblasts phosphocholine (PCho) potentiates sphingosine-1-phosphate (S1P)-induced mitogenesis. Here we report that PCho and S1P also synergistically stimulate DNA synthesis in mouse Swiss 3T3 fibroblasts and in mouse JB6 epidermal cells. The combined actions of PCho and S1P on DNA synthesis were associated with synergistic activation of the p42/p44 mitogen-activated protein (MAP) kinases. Ethanolamine (50-100 microM) further enhanced the synergistic effects of PCho and SIP on DNA synthesis but not on MAP kinase activity. The results indicate that the synergistic mitogenic effects of PCho and S1P (i) are not restricted to NIH 3T3 fibroblasts, (ii) are predominantly mediated by the MAP kinase-dependent signal transduction pathway, and (iii) are enhanced by ethanolamine via a MAP kinase-independent mechanism.

3T3 Cells↗

PubMed2000

A site specific increase in recombination in Drosophila ananassae.

The e65 pi; bri ru stock of Drosophila ananassae produced an extremely high rate of recombination in males when made heterozygous with any one of the wild type stocks. We analyzed and characterized the genetic factors which caused this phenomenon. We show that the second chromosome of the e65 pi; bri ru stock carries an enhancer of male recombination. The enhancer, En(2)-ep, is located between Om(2C) and Arc. The enhancement of meiotic recombination both in males and females was also observed at the specific region between Om(2C) and Arc on 2L. The magnitude of increased recombination was 30-40 fold in males and 13-30 fold in females. The relation between the hotspot of recombination in both sexes and the enhancer of male recombination is discussed.

Animals↗