Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A screening method, based upon resistance to a tetrazolium salt (TTC), is described which permitted the isolation in Paramecium of 28 mutants resistant to TTC. These mutants displayed various defects in mitochondrial functions (cytochromic content cyanide insensitive respiration). Some mutations seemed to affect directly the respiration chain while others seemed to cause indirect modifications, possibly altering mitochondrial protein synthesis. Genetic analysis of four mutants showed in all that the resistance to TTC was of nuclear origin.
Mol Gen Genet 1978 Jun 01
PMID:Selection and characterization of nuclear mutations affecting mitochondria in Paramecium. 20 8

Apolipoprotein B100 (apoB), the only protein of low-density lipoprotein, is produced primarily in the liver and serves as a ligand for the low-density lipoprotein receptor. Hepatic cell-specific expression of the human apoB gene is controlled by at least two cis-acting positive elements located between positions-128 and -70 (H. K. Das, T. Leff, and J.L. Breslow, J. Biol. Chem. 263:11452-11458, 1988). The distal element (-128 to -85) appears to be liver specific since it shows positive activity in HepG2 cells and negative activity in HeLa cells. The proximal element (-84 to -70) acts as a positive element in both these cell lines, and two rat liver nuclear proteins, BRF-1 and C/EBP, bind to two overlapping sites (-84 to -60 and -70 to -50, respectively). By gel mobility shift assay, we have identified a rat liver nuclear protein (BRF-2) which binds to the distal element (-128 to -85) of the apoB gene. This putative trans-acting factor has been purified to apparent homogeneity by DEAE-cellulose, heparin-agarose, and DNA-specific affinity chromatography. The purified BRF-2 has an apparent molecular mass of 120 kDa and was found to specifically recognize sequence -128 to -85; BRF-2 also produced a strong hypersensitive site at nucleotide position -95 with copper-orthophenanthroline reagent. A double-stranded oligonucleotide (-128 to -85) containing a 3-nucleotide (TTC) insertion between position -95 and -94 was found to abolish DNA binding by BRF-2. This result suggests that the region surrounding the hypersensitive site -95 is important for protein-DNA interaction. By using apoB promoter fragments containing various internal deletions as templates for gel mobility shift assay, the region between -104 and -85 was identified to be crucial for binding by BRF-2. We propose that BRF-2 may play an important role in the tissue-specific regulation of apoB gene transcription.
Mol Cell Biol 1992 Jul
PMID:Transcriptional regulation of the apolipoprotein B100 gene: purification and characterization of trans-acting factor BRF-2. 162 Jan 25

The ability of an iron chelator, desferrioxamine, to inhibit the infarct size in in vivo rat heart was assessed. Anaesthetised rats were subjected to coronary artery ligation (CAL) for 72 hr and infarct size was measured macroscopically using TTC staining. Systolic blood pressure and ECG were monitored. Desferrioxamine (10 mg/kg and 20 mg/kg i.v.) administered half an hour after CAL markedly reduced the infarct size. However, drug treatment did not alter the systolic blood pressure of animals. In addition, desferrioxamine in vitro and in vivo demonstrated an inhibition of rat PMN-evoked and luminol-enhanced chemiluminescence. The capacity of desferrioxamine to impair the generation or to scavenge directly oxygen free radicals may be responsible for its beneficial effect on myocardial infarct size in rats.
Mol Cell Biochem 1992 Jul 06
PMID:Decrease of myocardial infarct size with desferrioxamine: possible role of oxygen free radicals in its ameliorative effect. 164 Sep 38

We have determined the nucleotide sequence of the polC gene of Bacillus subtilis which codes for DNA polymerase III. Our recent analysis has revealed that the gene comprises 4311 nucleotides, from the start to the stop codon, 306 nucleotides more than we reported earlier. The plasmid reported by us and by N.C. Brown's laboratory contained a sequence at the end of the gene which is not related to the polC region of B. subtilis. We have isolated the rest of the gene, the sequence of which is presented in this paper. The new stop codon is followed by a hyphenated palindromic sequence of 13 nucleotides. The C-terminus of the coding region contains the novel mutation, dnaF, which results in a defect in the initiation of replication due to a change in the codon TCC to TTC (serine to phenylalanine). The hypermutator mutation mut-1 is due to two point mutations in the 3' to 5' exonuclease domain, the proof reading function. The codon changes are GGA to GAA (glycine to glutamic acid) and AGC to AAC (serine to asparagine). The elongation defective mutation, polC26, affecting the catalytic site that adds nucleotides to the growing chain, is due to a change in the codon GTC to GAC (valine to aspartic acid). It is separated from the mutation reported earlier, azp-12, by 306 nucleotides. Knowing the locations of the mutational sites allowed us to deduce the domains of the gene and the enzyme it encodes, and permitted us to present a precise map of the gene at the molecular level.
Mol Gen Genet 1991 May
PMID:Genetic structure and domains of DNA polymerase III of Bacillus subtilis. 184 Jun 38

We tested the ability of a single dose of superoxide dismutase to induce salvage of reperfused rabbit myocardium. Infarct size was measured by tetrazolium method following 3, 24, or 72 h of reperfusion. In addition, the 24 h reperfused hearts were examined to determine if the drug induced salvage in those hearts was reflected in the histology. A coronary arterial branch was occluded for 45 min and then allowed to reperfuse for 3, 24 or 72 h. At the end of the reperfusion period the hearts were removed, perfusion stained with triphenyl tetrazolium, and fixed in buffered formalin. The hearts were sectioned and infarct size was determined in all groups. In addition, the 24 h heart slices were prepared for histology with H&E staining. The results revealed that 5 mg/kg hSOD treatment was associated with smaller infarcts in the 3 and 24 h groups but that differences were no longer apparent in the 72 h group. The 24 h control hearts showed good correlation between infarct size by TTC and that by conventional histology. In the 24 h treatment hearts, however, infarcts by TTC averaged only about 1/2 the size of those by conventional histology. We conclude that a single dose of hSOD fails to offer a sustained reduction of infarct size. Furthermore, histology from the 24 h reperfused group revealed that hSOD did not delay the onset of necrosis but rather simply caused dead tissue to retain its ability to reduce the tetrazolium salts.
J Mol Cell Cardiol 1989 Nov
PMID:Tetrazolium artifactually indicates superoxide dismutase-induced salvage in reperfused rabbit heart. 248 48

In soybean, the small heat shock proteins of 15 to 18 kDa are encoded in the nucleus by at least two different multigene families, designated class I and class VI. Genomic DNA sequences of two new heat shock genes and flanking regions were determined: Gmhsp18.5-C, a class I gene, and Gmhsp17.9-D, the first known class VI gene. Comparison of both genes revealed a moderate homology (approx. 38%) mainly within the 3' ends of their coding regions. Hydropathic characterizations and secondary-structure predictions of the deduced amino acid sequences revealed two conserved domains within the C-terminal halves of the polypeptides that are also present in related proteins of other organisms. The transcription of both genes is heat shock dependent and the mRNA start sites, as determined by S1 nuclease mapping, are located downstream from typical TATA box sequences and multiple heat shock promoter elements such as 5' CT-GAA--TTC-AG. The putative promoter regions of the genes are preceded by long tracts of repetitive sequences with a high A + T content of 79 to 89%, which are bordered by runs of "simple sequences" such as (A) 12/13, (T)10 and (TA)10. Similar characteristic features are present in the promoter and 5'-flanking regions of other soybean heat shock genes. The possible function of these distinct sequences is discussed.
J Mol Biol 1988 Feb 20
PMID:Nucleotide sequence analysis of soybean small heat shock protein genes belonging to two different multigene families. 335 43

The genetic and physiological properties of two nuclear mutants of Paramecium tetraurelia affecting mitochondrial properties, and first screened as resistant to tetrazolium (TTC) are described. The mutant TTC64-1R is strongly deficient in cytochrome c and the mutant TTC66pR is partially deficient in cytochrome aa3; both mutants display cyanide insensitive respiration in exponential growth phase. In the double mutant TTC64-1R -- TTC66pR/TTC64-1R -- TTC66pR the deficiency in cytochrome aa3 due to the TTC66pR mutation is suppressed. The mutation TTC64-1R does not suppress cytochrome aa3 deficiencies due to mitochondrial mutations, but does interact with another nuclear mutation, cl1, (compatible only with mitochondria deficient in cytochrome oxidase) in such a way that the double mutant TTC64-1R -- cl1/TTC64-1R -- cl1 displays a normal amount of cytochrome aa3. The possible mechanisms and physiological significance of these suppressive effects are discussed.
Mol Gen Genet 1980
PMID:Genetic interactions in the control of mitochondrial functions in Paramecium. I. Interactions between nuclear genes. 693 1

Three oligonucleotide probes, complementary to tetM sequences, were labelled non-radiometrically using the DIG-oligonucleotide tailing kit and evaluated for their specificity for the detection of plasmid mediated tetracycline resistance in Neisseria gonorrhoeae. Only Probe 3, 5'-GCT CAA CAA TTC TGT TCC AGC-3', was specific for tetM. It hybridized with the tetM-containing 25.2-MDa plasmids from all of the 232 TRNG and the 130 PP/TRNG isolates used in the study. Its sensitivity, determined by dot-blot hybridization, was 0.1 pg of pJ13 plasmid DNA or 10(4) cells. It did not hybridize with the DNA from non-PPNG, CMRNG and tetracycline susceptible isolates from seven other Neisseria species (N. meningitidis, N. subflava, N. cinerea, N. lactamica, N. sicca, N. mucosa, and N. flavescens), Moraxella spp. and Haemophilus influenzae. Probe 3 also hybridized to DNA of three tetracycline resistant P. magnus (MIC = 16 micrograms ml-1) isolates which presumptively carried the tetM determinant. Therefore, probe 3 can be used by reference laboratories as a confirmatory test for TRNG, as well as isolates from other genera containing the tetM determinant.
Mol Cell Probes 1994 Jun
PMID:Detection of the tetM determinant in Neisseria gonorrhoeae using a non-radioactively labelled oligonucleotide probe. 796 93

Overexpression and point mutation of the p53 protein/gene was investigated in a series of chondrosarcoma by an immunohistochemical approach, and direct sequencing of the genomic DNA, respectively. In 2 of the 16 cases studied, both of which were high grade chondrosarcomas (grade III), immunodetectable p53 was identified. Histologically, one was ordinary type and the other a clear cell variant. However, no positivity was observed in the other cases including nine of low grade, ordinary type, three of low grade, clear cell type, and two of extraskeletal myxoid chondrosarcoma. Direct sequencing, following polymerase chain reaction amplification of exons 5-9 of the p53 gene in 14 cases, in which fresh materials were available, successfully demonstrated base substitution mutations in only two cases with detectable p53 overexpression on immunohistochemistry. Their details were GTC (valine) to TTC (phenylalanine) at codon 157 in exon 5, and CGT (arginine) to CAT (histidine) at codon 273 in exon 8. No mutation was detected in the other 12 cases which were negative for p53 immunostaining. These findings strongly suggest that p53 mutation plays a crucial role in the biologically aggressive subtype, and possibly in the process of tumor progression in human chondrosarcoma.
Diagn Mol Pathol 1993 Dec
PMID:Possible association of p53 overexpression and mutation with high-grade chondrosarcoma. 811 3

Studies to test whether superoxide dismutase (SOD), with or without catalase, limits myocardial infarct size have produced conflicting results. Positive results following short periods of reperfusion vs negative results following longer periods of reperfusion could be explained if either: (1) myocytes, initially salvaged by SOD, are killed by continued production of free radicals after the administered SOD have been excreted, or (2) false positive results occur because SOD transiently preserves the TTC reaction, despite loss of cellular viability. To evaluate these two possibilities, we measured infarct size after 90 min of ischemia and 4 h of reperfusion in SOD+catalase treated and untreated dogs. Treated dogs received a 60 min intra-arterial infusion of SOD (15,000 U/kg) plus catalase (CAT) (55,000 U/kg) beginning 25 min before reperfusion. Infarct size was measured using triphenyl tetrazolium (TTC) macrochemistry and was compared with the extent of necrosis assessed semi-quantitatively by light microscopy. Mean infarct size was similar in the control and treated groups. In addition, there was a positive linear correlation (r = 0.95) between the extent of necrosis estimated by microscopy and that estimated by TTC in both groups, and treatment did not alter the regression line. These current results were compared with results from the control dogs from our previous study (Richard et al., 1988) in which 90 min of ischemia was followed by 4 days of reperfusion. TTC-based infarct size at 4 days of reperfusion was similar to that observed in both groups at 4 h. These data indicate that oxygen free radicals, accessible to intravascular SOD and catalase, are not a cause of myocyte death detectable by measurement of infarct size after 4 h of reperfusion. Moreover, neither an "early protection, delayed death" hypothesis nor a specific preservation of the TTC reaction explain the positive results of other studies. TTC macrochemistry provides reliable estimates of myocardial infarct size, provided that sufficient magnification is used to permit resolution of interdigitating peninsulas of viable and necrotic tissue.
J Mol Cell Cardiol 1993 Apr
PMID:Superoxide dismutase plus catalase therapy delays neither cell death nor the loss of the TTC reaction in experimental myocardial infarction in dogs. 834 Sep 30


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