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Query: UNIPROT:P01034 (cystatin C)
 3,397 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The elongation rate of RNAs synthesized from AI promoters of T7 phage DNA and its deletion mutant delta DIII T7 DNA by E. coli RNA polymerase was analyzed. The distribution of incorporation rates of any definite nucleotides at any definite position along the two RNA chains was studied. The minimal structure which reproducibly forms pauses seems to be trinucleotide. Two main groups of trinucleotides could be distinguished: 1) those mostly associated with pauses and; 2) those usually found in pause free regions. The first group consists of AUG, AUA, AUC, AAU, GUG, GUA, CGU, CGC, UUA, UUU; the second one comprises AAA, CAA, CCC, UCC, CUA, CUG, CUC, GGG, ACU, GAG, GAA, GGA. A model accounting for intermittent elongation has been developed. It is based on the hypothesis that the kinetic constants of each nucleotide incorporation to and pyrophosphorolysis from the 3'-end of the growing RNA chain depend on the nature of the incoming nucleotide as well as on the nature of a nucleotide residue situated at the 3'-end of the growing RNA. A general equation describing the pause distribution along the RNA of a known nucleotide sequence is proposed.
Mol Biol (Mosk)
PMID:[Effect of the primary structure of RNA on the pulse character of RNA elongation in vitro by Escherichia coli RNA polymerase: a model]. 616 4

An Escherichia coli DNA fragment containing an Su+6 amber suppressor gene (supP) was cloned into a lambda gt lambda Ch vector by the shotgun method, selecting a Su+6 transducing phage lambda pSu+6. Through prophage integration followed by induction occurring at the transducing region of the lambda pSu+6 in Su- E. coli, a counterpart transducing phage carrying the wild-type allele (Su degrees 6) was isolated (lambda pSu degrees 6). The fingerprint of a tRNA encoded by lambda pSu degrees 6 was identical to that of an unidentified tRNAE previously reported (Ikemura & Ozeki, 1977). The cloverleaf structure of this tRNA was determined by combining the results of tRNA analysis and DNA sequencing of the gene. Judging from the anticodon of 5'-CAA-3', Su degrees 6 tRNA was identified as a new type of leucine isoacceptor in E. coli. Unlike other suppressors analyzed, Su+6 tRNA differed by two nucleotides from Su degrees 6 tRNA; one at the anticodon (CAA to CUA) and the other at the junction of D- and anticodon-stem (A27 to G27). DNA sequence analysis revealed that a single stretch of tRNA is flanked by the putative sequences of promoter and terminator. Thus a single copy of the Su degrees 6 tRNA gene constitutes a solitary tRNA transcription unit. Southern blotting showed only one copy of Su degrees 6 tRNA gene per haploid genome of E. coli. Since this single gene can mutate to the Su+6 suppressor, the Su degrees 6 leucine tRNA may be accounted as a dispensable species among the leucine isoacceptor tRNAs. Two possible open reading frames are found immediately following the Su degrees 6 tRNA gene.
J Mol Biol 1984 Aug 25
PMID:Identification of transfer RNA suppressors in Escherichia coli. IV. Amber suppressor Su+6 a double mutant of a new species of leucine tRNA. 620 2

Amber suppressors previously isolated from the yeast Saccharomyces cerevisiae and belonging to the same phenotypic class (Liebman et al., 1976) were assigned to nine different linkage groups named SUP52 through SUP60. One of these suppressors, SUP52, had been shown to cause the insertion of leucine and had been genetically mapped (Liebman et al., 1977). The following additional amber suppressors were mapped: SUP53 maps near the centromere of chromosome III closely linked to leu2; SUP54 maps on chromosome VII, 6 cM distal to trp5; SUP56 maps on chromosome I, 5.4 cM distal to ade1; SUP57 maps on chromosome VI, closely linked to met10; and SUP58 maps on the left arm of chromosome XI, loosely linked to met14. We show by protein analysis that like SUP52, the suppressors SUP53 through SUP56 are leucine-inserters. Furthermore, by hybridization with a cloned tRNA3Leu probe we demonstrate that at least SUP53, SUP54, SUP55 and SUP56 contain mutations in redundant tRNA3Leu genes because they each generate a new XbaI site in a DNA fragment encompassing a tRNA3Leu gene. These new XbaI sites are predicted by the known sequences of tRNA3Leu genes if the CAA anticodon mutates to the amber suppressing anticodon CTA. It is likely that each of the nine suppressors in this phenotypic class contain similar mutations in different tRNA3Leu genes since we find that there are approximately nine unlinked redundant copies of tRNA3Leu genes in haploid strains.
J Mol Biol 1984 Sep 15
PMID:Yeast amber suppressors corresponding to tRNA3Leu genes. 638 50

Genetic analysis of histidine independent (His+) revertants induced by ultraviolet light in the his-4 E. coli strain AB1157 was carried out: 93% carried ochre (UAA) suppressor mutations and 17% carried back mutations to his+ or (intragenic?) suppressors not detectably separable from his-4. Using the specialized transducing lambda psu 2int- phage, which carries supE-supB, it was determined that 87% of the ochre suppressors mapped in the supE-supB region. We were able to deduce that 56% of these affected tRNA1Gln by a CAA leads to TAA change in the tRNA gene while 31% affected tRNA2Gln by TAG- leads to TAA change. Although we were unable to deduce the base substitution of the remaining 13%, the results indicate that most of the suppressor mutations are caused by G:C to A:T transition. These results suggest that the high incidence of supE-supB region suppressor mutation in E. coli by UV would be a reflection of the general feature of UV mutagenesis; i.e. preferential induction of G:C to A:T transition in repairing nonpairing DNA lesions. AI 05371
Mol Gen Genet 1980
PMID:Analysis of ultraviolet light-induced suppressor mutations in the strain of Escherichia coli K-12 AB1157: an implication for molecular mechanisms of UV mutagenesis. 645 Aug 70

The cerebrospinal fluid (CSF) contains the same proteins as blood plasma, but with a different pattern of concentrations. Protein concentrations in CSF are much lower than those in blood. CSF proteins are derived from blood or synthesized within the brain. The choroid plexus is an important source of CSF proteins. Transthyretin is the protein most abundantly synthesized and secreted by choroid plexus. It determines the distribution of thyroxine in the cerebral compartment. Synthesis of transthyretin first evolved in the brain, then later it became a plasma protein synthesized in the liver. Other proteins secreted by choroid plexus are serum retinol-binding protein, transferrin, caeruloplasmin, insulin-like growth factors, insulin-like growth factor binding proteins, cystatin C, alpha 1-antichymotrypsin, alpha 2-macroglobulin, prothrombin, beta 2-microglobulin and prostaglandin D synthetase. Species differences in expression of the genes for these proteins are outlined, and their developmental pattern, regulation and roles in the cerebral extracellular compartment are discussed.
Comp Biochem Physiol B Biochem Mol Biol 1995 May
PMID:The cerebral expression of plasma protein genes in different species. 774 30

Plasmids containing derivatives of the Saccharomyces cerevisiae leucyl-tRNA (tRNA(3Leu)) gene that vary in anticodon sequence were constructed and transformed into the pathogen Candida albicans and S. cerevisiae. C. albicans could readily be transformed with plasmids encoding leucyl-tRNA genes with the anticodons CAA and UAA (recognizing the codons UUG and UUA) and expression of the heterologous tRNALeu could be demonstrated by Northern RNA blotting. In contrast, no transformants were obtained if the anticodons were UAG (codons recognized CUN, UUR) and CAG (codon CUG), indicating that the insertion of leucine at CUG codons is toxic for C. albicans. All tRNALeu-encoding plasmids transformed S. cerevisiae with equally high efficiencies. These results provide in vivo evidence that non-standard decoding of CUG codons is essential for the viability of C. albicans.
Mol Gen Genet 1994 Oct 28
PMID:Toxicity of a heterologous leucyl-tRNA (anticodon CAG) in the pathogen Candida albicans: in vivo evidence for non-standard decoding of CUG codons. 781 29

Male F344 rats were fed N[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) for up to 4 wk, then given the basal diet with or without 5% sodium saccharin for up to 100 wk. In a previous study, we demonstrated point mutations in codons 12 and 61 of Ha-ras gene among eleven transitional cell carcinomas (TCC), one undifferentiated carcinoma, and two sarcomas of the urinary bladder (Mol Carcinogen 3:210-215, 1990). In this study, Ha-ras, Ki-ras, and N-ras sequences were examined by polymerase chain reaction (PCR) and direct DNA sequencing. The results confirm the point mutation in codon 61 (CAA to CGA in 5 TCCs and to CTA in one TCC) of the Ha-ras gene. Mutation at codon 12 was not confirmed. No mutation was found in the Ki-ras gene. Sequences of the N-ras gene exons 1 and 2 were determined, and no mutations was detected. These results suggest the involvement of activated Ha-ras gene, but not Ki-N or N-ras gene, in rat urinary bladder carcinogenesis induced by FANFT. Subsequent sodium saccharin administration did not affect the changes in Ha-ras gene.
 ...
PMID:Sequencing analysis of Ha-, Ki-, and N-ras genes in rat urinary bladder tumors induced by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) and sodium saccharin. 790 76

Although globin mRNAs are considered prototypes of highly stable messages, the mechanisms responsible for their longevity remain largely undefined. As an initial step in identifying potential cis-acting elements or structures which contribute to their stability, we analyzed the defect in expression of a naturally occurring alpha 2-globin mutant, alpha Constant Spring (CS). The CS mutation is a single-base change in the translation termination codon (UAA-->CAA) that allows the ribosome to read through into the 3' nontranslated region (NTR). The presence of CS mRNA in transcriptionally active erythroid precursors and its absence (relative to normal alpha-globin mRNA) in the more differentiated transcriptionally silent erythrocytes suggest that this mutation disrupts some feature of the alpha-globin mRNA required for its stability. Using a transient transfection system, we demonstrate that in murine erythroleukemia cells the CS mRNA is unstable compared with the normal alpha 2-globin mRNA. The analyses of several other naturally occurring and site-directed mutant alpha-globin genes in murine erythroleukemia cells indicate that entry of a translating ribosome into the 3' NTR targets the message for accelerated degradation in erythroid cells. In contrast, both the CS and alpha 2-globin mRNAs are stable in several nonerythroid cell lines. These results suggest that translational readthrough disrupts a determinant associated with the alpha 2-globin 3' NTR which is required for mRNA stability in erythroid cells.
Mol Cell Biol 1994 Dec
PMID:Erythroid cell-specific determinants of alpha-globin mRNA stability. 796 50

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

In order to study the conversion of UV lesions into frameshift and base substitution mutations, M13mp2 phage DNA was altered by the addition of extra pyrimidines, or by construction of a nonsense codon preceded by a run of pyrimidines within the beta-galactosidase complementing region. The normal sequence 5' GTC GTT TTA CAA 3' was changed to GTC GTT T TTA CAA (MIDT) or GTC GTT C TTA CAA (MIDC) to study frameshifts and to GTC GTT CTT TAA (OCHRE) to study reversion of the ochre (TAA) codon. Escherichia coli pol I Kf and T7 DNA polymerase mutant enzymes devoid of 3'-->5' exonuclease activity produced UV-induced revertants at higher frequency than did their exonuclease proficient counterparts. Removal of cyclobutane dimers with photolyase before in vitro synthesis did not greatly affect mutant frequency although such treatment led to significantly increased DNA synthesis by the wild-type T7 DNA polymerase on UV-irradiated substrate. Reversions of the in frame ochre sequence GTT CTT TAA produced by the delta 28 T7 DNA polymerase were mainly by base substitution in the TAA codon. About half of the E. coli Kf exo- enzyme ochre revertants had a TTA deletion. Five mutant T7 DNA polymerases with varying exonuclease activity gave revertant frequencies that correlated better with published values of enzyme velocity than with exonuclease activity or with measured bypass synthesis. Our data indicate that loss of proofreading activity increases the frequency of UV-induced frameshifts, but lack of such activity is not sufficient for their production. We suggest that frameshifts occur more frequently when nucleotide addition opposite the lesion is slow. The same lesion can give rise to a different spectrum of mutations depending on the polymerase.
J Mol Biol 1994 Jul 15
PMID:Production of UV-induced frameshift mutations in vitro by DNA polymerases deficient in 3'-->5' exonuclease activity. 802 6


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