Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012872 (DNA marker)
 929 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Upon superinfection of immune (lysogenic) cells with bacteriophage Mu, a form of Mu DNA accumulates that sediments about twice as fast as the linear phage DNA marker in neutral sucrose gradients. This form is also detected upon infection of sensitive cells with Mu. We have purified it and examined its physical nature. Under the electron microscope it appears circular and supertwisted. Upon treatment with Pronase, phenol or sodium dodecyl sulfate, however, it is converted to a linear Mu-length form, indicating that the circle is not covalently closed. The linear DNA still has heterogeneous host sequences at its termini. The circular DNA is resistant to the action of Escherichia coli exonuclease III and T7 exonuclease, but becomes sensitive to these nucleases after treatment with Pronase showing the presence of a protein that binds non-covalently to the ends of the DNA to circularize it as well as protect it from digestion with exonucleases. The complex is resistant to high salt (up to 6 M-NaCl) but can undergo transitions between forms that are partially open, open circular, linear and circular dimers and trimers. Examination of DNA from mature phage particles reveals that a circular DNA species is present in at least 0.1 to 1% of the population. The purified complex is extremely efficient in transfection of E. coli spheroplasts. We estimate the molecular weight of the protein in this DNA-protein complex to be approximately 64,000, and suggest that this complex might represent the integrative precursor of infecting Mu DNA.
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PMID:Infecting bacteriophage mu DNA forms a circular DNA-protein complex. 630 60

A computer program has been developed for computing DNA fragment size from its electrophoretic mobility using a graphical method. The program uses DNA marker data and selects the semilogarithmic linear range (sl-range), i.e., the linear portion of the semilogarithmic curve (mobility vs. log of DNA fragment length). Over this range a linear interpolation is derived for calculating the size of a DNA fragment whose mobility falls in the sl-range. The program also derives a hyperbolic interpolation formula that covers the entire range for determining the size of a DNA fragment whose mobility is beyond the semilogarithmic linear range. The method described in this paper is sensitive, accurate and reliable. This program can also be used to compute protein or polypeptide size from sodium dodecyl sulfate polyacrylamide gel electrophoresis data. The DOS version of the DNASIZE program is freely available from Netserver at EMBL or from BioTechNet by EMail.
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PMID:Improved estimation of DNA fragment length from gel electrophoresis data using a graphical method. 794 91

Adducin is a heterodymeric cytoskeleton protein, the 3 subunits of which are encoded by genes (ADD1, ADD2, ADD3) mapping to 3 different chromosomes. A long series of parallel studies in the Milan hypertensive rat strain model of hypertension and humans indicated that an altered adducin function may cause hypertension through an enhanced constitutive tubular sodium reabsorption. Six human linkage studies showed positive results when a DNA marker mapping to 30 kb from the ADD1 locus or single-nucleotide polymorphisms (SNPs) of 1 of the 3 adducin genes were considered either alone or in combination with each other or angiotensin-converting enzyme (ACE) D allele or salt intake. When DNA markers mapping at much larger distance from the ADD1 locus were used, negative results were found by 4 studies. Positive results were also obtained in 18 of 20 association studies that, in addition to blood pressure, investigated variables reflecting body sodium or the renin-angiotensin system. Mixed results regarded case-control studies or studies in predominantly normotensive populations that did not consider the above-mentioned variables. Four of 5 studies showed a selective beneficial effect of diuretics in carriers of the mutated ADD1. Twelve of 16 studies found that ADD1 polymorphism alone or in combination with that of ACE positively associates with stroke or coronary heart disease or renal or vascular dysfunctions. In conclusion, when context is taken into account, the impact of adducin in hypertension and its related disorders is clear.
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PMID:Adducin polymorphism: detection and impact on hypertension and related disorders. 1569 49

Progeny (n = 70) from unrelated, DNA tested, Rendement Napole carrier (RN-/rn+) Hampshire sires, and DNA tested, Rendement Napole normal (rn+/rn+) Yorkshire dams were genotyped for the segregating RN- allele via DNA marker-assisted methodology. Six slaughter groups ensued, with littermates all being represented within the same slaughter group. Boneless pork loins were removed from right carcass sides after a 48-h chill at 2 degrees C. The anterior portions of the loins were not enhanced, whereas the posterior sections were enhanced with a solution containing 0.5% sodium chloride and 0.5% sodium tripolyphosphate to 110% of their initial weight. Carcasses of carrier pigs had less (P < 0.05) 10th rib fat depth and a greater (P < 0.01) percentage carcass lean than carcasses of normal pigs. Postmortem LM pH of carrier pigs was lower (P < 0.002) at 3, 6, 12, and 24 h, and tended to be lower (P = 0.062) at 48 h compared with that of normal animals. Samples of LM from carrier pigs had greater (P < 0.01) glycolytic potential values, drip loss percentages, and a* values, and lower pH values at fabrication than LM from normal pigs. No genotype differences (P > 0.05) were found for LM lactate, L*, or b* values. Nonenhanced semimembranosus samples from carrier pigs exhibited greater (P < 0.05) purge loss percentages and L* values, and lower (P < 0.01) pH values than samples from normal pigs. Enhanced LM samples exhibited greater (P < 0.05) drip and purge loss percentages, greater pH, and lower L* values at fabrication, regardless of Napole status. These findings suggest that the Napole gene has a positive influence on carcass leanness but detrimental effects for lean quality, which were often further compounded when meat was subjected to enhancement treatment.
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PMID:Growth performance, carcass composition, quality, and enhancement treatment of fresh pork identified through deoxyribonucleic acid marker-assisted selection for the Rendement Napole gene. 1654 69

The present study tested the hypothesis that intracellular ANG II directly induces transcriptional effects by stimulating AT(1a) receptors in the nucleus of rat renal cortical cells. Intact nuclei were freshly isolated from the rat renal cortex, and transcriptional responses to ANG II were studied using in vitro RNA transcription assays and semiquantitative RT-PCR. High-power phase-contrast micrographs showed that isolated nuclei were encircled by an intact nuclear envelope and stained strongly by the DNA marker 4',6-diamidino-2-phenylindole, but not by the membrane or endosomal markers. Fluorescein isothiocyanate-labeled ANG II and [(125)I]Val(5)-ANG II binding confirmed the presence of ANG II receptors in the nuclei with a predominance of AT(1) receptors. RT-PCR showed that AT(1a) mRNA expression was threefold greater than AT(1b) receptor mRNAs in these nuclei. In freshly isolated nuclei, ANG II increased in vitro [alpha-(32)P]CTP incorporation in a concentration-dependent manner, and the effect was confirmed by autoradiography and RNA electrophoresis. ANG II markedly increased in vitro transcription of mRNAs for transforming growth factor-beta1 by 143% (P < 0.01), macrophage chemoattractant protein-1 by 89% (P < 0.01), and the sodium and hydrogen exchanger-3 by 110% (P < 0.01). These transcriptional effects of ANG II on the nuclei were completely blocked by the AT(1) receptor antagonist losartan (P < 0.01). By contrast, ANG II had no effects on transcription of angiotensinogen and glyceraldehyde-3-phosphate dehydrogenase mRNAs. Because these transcriptional effects of ANG II in isolated nuclei were induced by ANG II in the absence of cell surface receptor-mediated signaling and completely blocked by losartan, we concluded that ANG II may directly stimulate nuclear AT(1a) receptors to induce transcriptional responses that are associated with tubular epithelial sodium transport, cellular growth and hypertrophy, and proinflammatory cytokines.
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PMID:Intracellular ANG II directly induces in vitro transcription of TGF-beta1, MCP-1, and NHE-3 mRNAs in isolated rat renal cortical nuclei via activation of nuclear AT1a receptors. 1825 74

The aggregation behavior of the DNA marker dye thiazole orange (TO), has been investigated in two types of surfactant assemblies, namely, premicelles/micelles of sodium dodecyl sulfate (SDS) and pre reverse micelles/reverse micelles of sodium bis(2-ethylhexyl) sulfosuccinate (AOT). In the case of an SDS/water system, absorption spectral changes of TO signify the formation of H-aggregates and H-dimers of the dye at premicellar concentrations, which subsequently convert to the monomeric form beyond the critical micellar concentration (cmc). Interestingly, the observed changes in the absorption and emission characteristics due to the surfactant-induced formation of H-aggregates/dimers of TO are found to be useful to estimate the surfactant concentration parameters for premicellar aggregation of SDS. In the case of an AOT/n-heptane system, similarly, H-aggregates/dimers are observed at low AOT concentrations, below the cmc. However, in this case, the H-dimers persist even beyond the cmc. This is attributed to the strong tendency of TO for self-aggregation and its favorable electrostatic interactions with the AOT head groups. With increasing water content in the AOT reverse micelles, the hydration of the dye leads to the conversion of H-dimers to the monomeric form. The steady-state fluorescence results are nicely corroborated with those from time-resolved fluorescence studies and demonstrate the interesting behavior of the surfactant-induced aggregation of TO dye.
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PMID:Surfactant-induced aggregation patterns of thiazole orange: a photophysical study. 2190 67