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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following treatment with nitrosoguanidine, mutant derivatives of Rhizobium leguminosarum strain 3841 were isolated which failed to react with AFRC MAC 203. This monoclonal antibody normally recognizes a strain-specific lipopolysaccharide epitope which is developmentally regulated during legume nodule differentiation. Structural modification of lipopolysaccharide (LPS) was analysed by examining reactivity with a range of monoclonal antibodies with different epitope specificities, and also by analysis of LPS mobility changes after electrophoresis on polyacrylamide gels. One class of these LPS-defective mutants induced normal nitrogen-fixing (Fix+) nodules on peas (Pisum sativum), while another two classes of Fix- mutants were also identified, suggesting that a component of the LPS antigen that is part of the MAC 203 epitope is essential for normal nodule development leading to symbiotic nitrogen fixation. When grown under low-oxygen or low-pH culture conditions, one class of Fix- mutants completely lacked LPS-1 (the species that carries O antigen) and a second class showed a modified and truncated form of LPS-1. Mutants with defective LPS structure were also obtained after Tn5 mutagenesis of R. leguminosarum 3841 and all nine Fix- mutants were also found to lack the MAC 203 epitope. Three of these transposon-induced mutants synthesized a truncated form of LPS-1 that was structurally similar to that of the class of the NTG-induced mutants described above. These transposon-induced mutations, and the nitrosoguanidine-induced Fix- mutations, were closely linked and could be suppressed by the same cloned fragment of chromosomal DNA. The data presented here suggest that a precondition for normal nodule development of R. leguminosarum 3841 within pea nodules is the ability to synthesize relatively long-chain LPS-1 macromolecules under the physiological conditions encountered within the nodule. All mutants that lacked the ability to elongate LPS-1 macromolecules also failed to express the MAC 203 epitope.
Mol Microbiol 1992 Sep
PMID:Molecular dissection of structure and function in the lipopolysaccharide of Rhizobium leguminosarum strain 3841 using monoclonal antibodies and genetic analysis. 138 72

Vasoconstriction occurs frequently following coronary angioplasty and is implicated in the pathogenesis of abrupt closure and restenosis. Control of vasomotor tone is regulated in part directly by smooth muscle cells and indirectly through the endothelium. To study the mechanisms underlying vasoconstriction, the effect of angioplasty and endothelial denudation on endothelium-dependent and -independent relaxation was examined in 15 mongrel dogs. Percutaneous transluminal angioplasty and endothelial denudation of the right femoral artery were performed. Endothelial injury was assessed by adhesion of indium-111-labeled platelets. Endothelium-dependent and -independent relaxation were assessed using acetylcholine and nitroglycerin, respectively. Vessels precontracted with potassium chloride and exposed to acetylcholine showed impaired relaxation in both the angioplasty and denuded groups (angioplasty = 14 +/- 5%, denuded = 0 +/- 0%, normal = 73 +/- 12%; P less than 0.05 for both angioplasty and denuded compared to normal). Precontraction with phenylephrine yielded similar results (angioplasty = 16 +/- 8%, denuded = 4 +/- 2%, normal = 39 +/- 10%; P less than 0.05 only for denuded segment compared to normal). Segments precontracted with phenylephrine and exposed to nitroglycerin did not demonstrate impaired relaxation (angioplasty = 73 +/- 9%, denuded = 68 +/- 9%, normal = 71 +/- 7%, P = ns). Mean indium-111 counts were similar in both the angioplasty and denuded segments (2820 +/- 1481 and 2963 +/- 1228 counts/min/g, respectively) compared to a lower count in the normal segment (1514 +/- 956 counts/min/g). Thus, angioplasty produces significant vascular injury and impairment of vasodilator function, comparable to that caused by endothelial denudation alone. This implies that vasoconstriction seen following coronary angioplasty may be due to endothelial injury and the resultant loss of control of vasomotor tone.
Exp Mol Pathol 1992 Apr
PMID:Impaired vascular reactivity following angioplasty is mainly due to endothelial injury. 158 41

The ribosomal RNA genes of two species of Trypanosoma, Trypanosoma cruzi, the etiological agent of Chagas' disease, and Trypanosoma conorhini, a non-pathogenic rodent trypanosome, were cloned and partially characterized. The physical maps derived for their rRNA genes were similar throughout the region that encompasses the SSU-and LSU-rRNA coding sequences. However, the non-transcribed spacer DNA of both T. cruzi and T. conorhini was found to be polymorphic for several restriction enzyme sites. We show that strains of T. cruzi can be typed according to the characteristic restriction fragment length polymorphism of their NTS DNAs.
Mol Biochem Parasitol 1990 Aug
PMID:Restriction fragment length polymorphisms in the ribosomal gene spacers of Trypanosoma cruzi and Trypanosoma conorhini. 197 49

Amplification is one of the mechanisms whereby the expression of genes can be specifically reinforced. Ribosomal gene amplification in amphibian and insect oocytes is a particularly well documented case. We studied heterogeneity, amplification and size of Acheta domesticus (insects; Orthoptera) ribosomal DNA and characteristics of male and female somatic or germ line rDNAs by analysis of genomic clones from a conventional and a microclone library. The length of the Acheta rDNA repeat unit (transcription unit and non-transcribed spacer (NTS] varied from 47 x 10(3) to 60 x 10(3) base-pairs, with highest variability within the NTS region. Deletions, fragment length heterogeneity and size variability in small steps of individual NTS segments are responsible for the observed size variation. The number of rDNA repeat units per haploid genome of Acheta was determined as 190(+/- 10%). The rDNA is amplified 14(+/- 10%)-fold in the oocyte, producing about 10,000 gene copies per cell. Our results show that the amplification mechanism does not favor individual fragments within the repeat unit. Thus, it can be concluded that amplification does not change the chromosomal characteristics of the rDNA pool. Two fragments specific for oocyte rDNA suggest that the rearrangements accompanying amplification are preferentially located in one distinct EcoRI fragment. Certain regions of Acheta rDNA contain cell-type-specific fragments: it was thus possible to characterize one purely male fragment and a second one specific for male and female soma but not for germ line rDNA. We show that Acheta rDNA reveals a combination of many features reported from different organisms and novel tissue-specific alterations on an extremely large repeat unit. The tissue-specific alterations indicate sexual and soma/germ line differentiation events that are derived by as yet unknown mechanisms.
J Mol Biol 1990 Dec 05
PMID:Structural organization of Acheta rDNA. Evidence for differential amplification of soma and germ-line-specific rDNA sequences. 225 30

Neuronal cell degeneration was studied in vitro in primary rat brain neuronal cultures grown in serum-free, chemically defined, CDM R12 medium, by measuring lactate dehydrogenase (LDH) released in the culture medium. A Ca2+-dependent neuronal cell degeneration was observed after prolonged and transient exposure 30 microM veratridine. The release of LDH occurred gradually and could be completely prevented by 2 mM ethylene glycol bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, 0.1 microM tetrodotoxin, and 1 microM flunarizine. Flunarizine was without effect on neuronal cell loss induced by 1 mM glutamate, 1 mM kainic acid, and 5 mM KCN. The lack of effect on neurotoxicity induced by 1 mM glutamate differentiates flunarizine from N-methyl-D-aspartate antagonists such as MK-801. The latter protected at nanomolar concentrations against glutamate-induced neuronal cell death but had a maximal effect only at 0.1 mM on the veratridine-induced released LDH. It is suggested that, besides the excitatory amino acid receptor pathway, prolonged opening of the veratridine-sensitive Na+ channel can be neurotoxic. The latter can be prevented by flunarizine. The role of Na+ channel blockers as therapeutic agents in cerebral ischemia is discussed.
Mol Pharmacol 1989 Oct
PMID:Ca2+-mediated neuronal death in rat brain neuronal cultures by veratridine: protection by flunarizine. 255 10

Since the diminished vasodilatation characterizing tolerance to organic nitrates is associated with lower rises in 3', 5'-cyclic guanosine monophosphate (cGMP) levels, the possibility that nitrovasodilators desensitized guanylate cyclase (GC) when pre-incubated with coronary supernatants was studied. In the absence of cysteine, pre-incubation with nitroglycerin (NG) decreased GC-activity during subsequent incubation to 24 +/- 7% of control values, whereas six other nitrovasodilators had much smaller effects. When cysteine was present during pre-incubation, NG-stimulation of GC remained significantly higher (59 +/- 3%; P less than 0.05), whereas the effects of other nitrovasodilators were not significantly changed. We also found that GC-activity, when reduced by pre-incubation with NG could only be restored by readdition of native coronary supernatant, suggesting that the enzyme became inactivated. NG pre-incubation of GC (in contrast to coronary strips) almost completely abolished the direct and thiol-independent stimulatory effect of 3-morpholinosydnonimine (SIN-1) down to 4.5 +/- 0.2%, whereas pre-incubation with other nitrovasodilators reduced the stimulatory response to SIN-1 to only 59 to 98%. Increasing concentrations of NG during pre-incubation dose-dependently (IC50 = 0.13 mM) reduced the activating effect of SIN-1 during incubation. There was also a time dependence in NG-induced inactivation of GC which followed first order kinetics with a calculated half life of 2.5 min in the absence of a thiol. The latter was increased to 4.0 or 19.2 min, respectively, when glutathione or cysteine-methylester were present during pre-incubation.(ABSTRACT TRUNCATED AT 250 WORDS)
J Mol Cell Cardiol 1989 Jan
PMID:Tolerance to nitroglycerin is caused by reduced guanylate cyclase activation. 256 81

Hemocyanin of the horseshoe crab Limulus polyphemus is composed of 48 oxygen-binding subunits, which are arranged in eight hexameric building blocks. Allosteric interactions in this oligomeric protein have been examined by measurement of high-precision oxygen-equilibrium curves, using an automated Imai cell. Several models were compared in numerical analysis of the data. A number of conclusions can be drawn with confidence. (1) Oxygen binding by Limulus hemocyanin cannot satisfactorily be described by the two-state MWC model [Monod, J., Wyman, J., & Changeux, J.P. (1965) J. Mol. Biol. 12, 88-118] for allosteric transitions with either the hexamer or dodecamer as the allosteric unit. (2) Of the models tested, the data sets can be best described by an extended MWC model that allows for an equilibrium, within the 48-subunit ensemble, between cooperative hexamers and cooperative dodecamers. The model invokes T and R states for both hexamers (T6 and R6) and dodecamers (T12 and R12). Allosteric effectors modulate oxygen affinity and cooperativity by affecting the R to T equilibria within hexamers and dodecamers and by shifting the equilibria between hexamers and dodecamers. (3) The fitted model parameters show that under most conditions the intersubunit contacts within T-state hexamers are more constrained than those within T-state dodecamers. (4) The oxygen affinities of the hexameric and dodecameric R states are the same, but under all conditions examined the conformation of the fully oxygenated molecule is that of the dodecameric R state. (5) Between pH 7.4 and pH 8.5 the dodecameric T state has a higher affinity for oxygen than the hexameric T state, allowing for "T-state cooperativity".(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Allosteric control in Limulus polyphemus hemocyanin: functional relevance of interactions between hexamers. 260 23

The histologic examination and planimetric evaluation of tissue slices has been so far the only available technique for studying the extent of experimental myocardial infarcts in long-term studies; however, this approach is rather time-consuming when the sample size is large. This study describes a new biochemical method for the quantitation of myocardial scarring, based on the determination of left ventricular hydroxyproline, and collagen content at the end of the healing process. Accordingly, several modifications were introduced into previously existing methods for the assay of hydroxyproline: our method allows a linear estimation of hydroxyproline in the range from 0.5 to 5 micrograms, with a precision of +/- 6.1% and a day-to-day variation of +/- 10.5%. The reliability of this approach for studying infarct size has been verified in rats with coronary artery occlusion divided into a control group and in a treated group receiving nitroglycerin. The animals were killed 21 days after coronary ligation and randomly assigned for infarct size evaluation either to the histologic or the collagen method. By histology infarct size averaged 30.6 +/- 4.8% (mean +/- S.E.M.) of left ventricle (LV) in control rats and 16.2 +/- 5.8% of LV in nitroglycerin-treated animals; by the proposed alternative method left ventricular collagen content was 26.8 +/- 1.0 micrograms/mg of dry weight in control rats and 19.5 +/- 1.2 micrograms/mg of dry weight in nitroglycerin-treated animals; infarct size calculated from collagen content by a simple formula, was 37.4 +/- 2.6% of LV and 22.3 +/- 2.6% of LV, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
J Mol Cell Cardiol 1986 Mar
PMID:A biochemical method for the quantitation of myocardial scarring after experimental coronary artery occlusion. 308 10

We studied the rDNA spacer length polymorphism in a sample of 121 individuals belonging to families of 2-3 generations. Our data, obtained by restriction pattern analysis of genomic DNA, confirmed the limited and discrete nature of this polymorphism. Using the pattern as a genetic marker, we analyzed the segregation of length variants in the different families and we investigated the possible occurrence of unequal crossing-over events among homologous and nonhomologous rDNA clusters. No direct evidence of recombination in the spacer region that we analyzed emerged from our study. All the differences in the restriction patterns observed among individuals from the same family could be explained as resulting from meiotic segregation. Family data showed a multichromosomal distribution of NTS length variants and demonstrated a direct correspondence between the frequency of a variant in the population and its degree of spreading on the different rDNA clusters.
Mol Gen Genet 1984
PMID:Inheritance of rDNA spacer length variants in man. 609 Aug 64

Chromatin structure of ribosomal genes from nuclei of Drosophila melanogaster embryos was studied by using micrococcal nuclease cleavage. End-directed labelling with short cloned fragments of the ribosomal repeat was carried out. It shows, that the micrococcal nuclease prefers specific sites in naked DNA, and the pattern of DNA cleavage is essentially conserved when the nuclei are digested. Only minor differences are visible. Hence, there are no specific positions of nucleosomes on the ribosomal repeat. The DNA fragments from the nuclei treated with micrococcal nuclease were electrophoresed, transferred to DBM-paper and hybridized with different probes subcloned from the ribosomal repeat. The non-transcribed spacer and the region of the beginning of transcription are hydrolysed significantly faster than the coding region or inactive ribosomal insertion. The region of NTS and the beginning of transcription do not give normal nucleosomal fragment in the range of 145-185 bp; instead they produce a heterogeneous band 200-280 bp in length even after prolonged digestion. Dinucleosomal fragments are also slightly longer and more heterogeneous than in other parts of the ribosomal repeat. Higher oligomers are similar throughout the ribosomal repeat. We suggest that a hypothetical transcription factor interacts in a way with histones and protects unusual fragments of DNA from digestion.
Mol Biol (Mosk)
PMID:[Chromatin structure of ribosomal genes of Drosophila melanogaster. Random location of nucleosomes in DNA and characteristics of organization of non-transcribed spacer]. 609 27


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