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)

Chloramphenicol resistance (Cmlr) of Streptomyces coelicolor A3(2) behaves like a transposon locus, not being localisable in any region of the map and yet being transferable in crosses at a rate comparable to that of chromosomal markers. It can also be transposed onto a plasmid (SCP1) and back to the chromosome. Some traits, such as arginino-succinate synthase production (ArgG), aerial mycelium formation (AmyA), resistance to tetracycline and to rifamycin C appear to be joined to Cml in three processes: co-mutation, i.e. simultaneous loss, post-mutation, i.e. spontaneous loss at high frequency in subclones from Cmls strains, co-transfer, i.e. joint transfer with the cml locus in crosses or during infection by the aggregate SCP1::SCTn1 plasmid. All these processes have been consistently observed with special attention to the argG locus.
Mol Gen Genet 1983
PMID:Properties of transposon SCTn1 of Streptomyces coelicolor A3(2). 631 Mar 49

A conditional respiratory deficiency in yeast Saccharomyces cerevisiae is expressed as a result of a nuclear mutation in sup1 and sup2 genes (II and IV chromosomes, respectively), coding for a component of cytoplasmic ribosomes (Ter-Avanesyan et al. 1982). One such strain is studied here in detail. The strain is temperature-dependent and expresses a respiratory deficient phenotype at 20 degrees C but not at 30 degrees C. Moreover, the strain is simultaneously chloramphenicol-dependent and is able to grow on media containing glycerol or ethanol as a sole carbon source only in the presence of the drug. Chloramphenicol has a differential effect on protein synthesis in mitochondria of the parent strain and the mutant. Since chloramphenicol is a ribosome-targeting antibiotic we suggest that the differential effect of the drug on parent and mutant mitochondrial protein synthesis is due to the altered properties of mito-ribosomes of the mutant compared to those of the parent strain. Mitochondria of the mutant synthesize all the mitochondrially encoded polypeptides, however, in significantly lowered amounts. A suggestion is put forward for the existence of a common component (a ribosomal protein) for mito and cyto-ribosomes.
Mol Gen Genet 1983
PMID:Relationship between cytoplasmic and mitochondrial apparatus of protein synthesis in yeast Saccharomyces cerevisiae. 634 82

We analyzed the reversion of strains carrying alk208, a mutation in the alkBAC (alkane utilization) region of the Pseudomonas CAM-OCT plasmid. Reversion of alk208 was stimulated 25 to 75-fold by small doses of UV-irradiation. All alkane hydroxylase-positive (AlkB+) revertants proved to be aliphatic alcohol dehydrogenase-positive (AlkC+) as well, whereas AlkC+ revertants could be either AlkB+ or AlkB-. Most of the AlkB- AlkC+ partial revertants produced AlkC- segregants at measurable frequencies. UV-irradiation substantially increased the rate of AlkC- segregation. Most segregants reverted to AlkB+ or AlkC+ at frequencies similar to the original alk208 strain. Dot blot hybridization analyses using cloned probes from various regions of CAM-OCT revealed that the partial revertants contained specific amplications of alk DNA. The endpoints of these amplifications mapped in at least two regions. AlkC- segregants had lost the DNA amplifications.
Mol Gen Genet 1984
PMID:Reversal by DNA amplifications of an unusual mutation blocking alkane and alcohol utilization in Pseudomonas putida. 659 34

Two mitochondrially synthesized marker polypeptides, MV-1 and MV-2, were found in human HeLa and HT1080 cells. These were assigned to the mitochondrial DNA in HeLa-HT1080 cybrids and hybrids by demonstrating their linkage to cytoplasmic genetic markers. These markers include mitochondrial DNA restriction site polymorphisms and resistance to chloramphenicol, an inhibitor of mitochondrial protein synthesis. In the absence of chloramphenicol, the expression of MV-1 and MV-2 in cybrids and hybrids was found to be directly proportional to the ratio of the parental mitochondrial DNAs. In the presence of chloramphenicol, the marker polypeptide linked to the chloramphenicol-sensitive mitochondrial DNA continued to be expressed. This demonstrated that resistant and sensitive mitochondrial DNAs can cooperate within a cell for gene expression and that the CAP-resistant allele was dominant or codominant to sensitive. Such cooperation suggests that mitochondrial DNAs can be exchanged between mitochondria.
Mol Cell Biol 1982 Jan
PMID:Assignment of two mitochondrially synthesized polypeptides to human mitochondrial DNA and their use in the study of intracellular mitochondrial interaction. 695 89

When E. coli protein synthesis was blocked by chloramphenicol (100 micrograms/ml) or by essential amino acid deprivation, the transcription rates of rplKAJL genes (the ones for L11, L4, L10 and L7/L12 ribosomal proteins) and adjacent rpoBC genes (genes for RNA polymerase beta- and beta'-polypeptides) have been non-coordinately changed. The level of the gene transcription rate was obtained from RNA--DNA hybridization assays with E. coli pulse-labelled RNA and pJC703 or pJC720 plasmid DNA. The transcription of ribosomal protein genes has been found to be uncoupled with translation and controlled by the allelic state of relA gene. Conversely, the effective transcription of proBC gene was relA independent and coupled with translation of the mRNA. Chloramphenicol-induced transcription polarity within rplKAJL-rpoBC chromosome region can be suppressed by 10 micrograms/ml rifampicin.
Mol Biol (Mosk)
PMID:[Non-coordinated transcription of RNA polymerase beta,beta'-polypeptide genes and adjacent ribosomal protein genes in Escherichia coli cells]. 701 82

The effect of specific inhibitors of translation in chloroplasts (chloramphenicol) and in cytoplasm (cycloheximide) on the formation of pigment-protein-lipid complexes of photosynthetic membranes, on the chlorophyll state in chloroplasts and isolated membrane complexes had been studied. It is proved that the inhibition of translation blocks chlorophyll incorporation only into the complexes of reaction centres of photosystems without any change of the light-harvesting complex. The action of inhibitors leads to the disappearance of long-wave native forms of pigment in the complexes of reaction centres, which are characteristic for them. But the action of inhibitors does not effect the formation of non-specific short-wave forms which are present in all types of membrane complexes. Chloramphenicol proved to be more active in such processes than cycloheximide. On the basis of the data on localization of biosynthesis of polypeptide components of plastid membranes we suppose that during biogenesis of the photosynthetic apparatus the conditions for self-assembly of non-specific native forms of chlorophyll in light-harvesting complexes are made as the result of polymerazation of the main membrane polypeptides which are synthesized in the cytoplasms. Minor polypeptides of plastid (photosystems 1 and 2) and cytoplasmic (photosystem 1) orgin are necessary for self-assembly of the dense units of pigment in reaction centre complexes.
Mol Biol (Mosk)
PMID:[Study of the effect of specific translation inhibitors on formation of native forms of chlorophyll in pigment-protein-lipid complexes of pea chloroplasts]. 742 8

Epithelial damage in the airways is a feature often observed in patients with asthma and is probably caused by the interaction of epithelial cells with leukocytes. As adhesion molecules are thought to be important in this interaction, we analyzed the expression and modulation of adhesion molecules on primary cultured human bronchial epithelial cells and the bronchial epithelial cell lines BEAS-2B and NCI-H292. E-selectin, P-selectin, and VCAM-1 were absent under basal and stimulated conditions. The adhesion molecules ICAM-1 (CD54), LFA-3 (CD58), and CD44 (H-CAM) were expressed basally on primary cultured human bronchial epithelial cells and the BEAS-2B and NCI-H292 cell lines. CD44 and LFA-3 expression did not change after stimulation with IFN-gamma or TNF-alpha. In contrast, ICAM-1 expression on human bronchial epithelial cells and BEAS-2B cells could be increased by incubation with PMA, IFN-gamma, TNF-alpha, and especially with the combination of IFN-gamma and TNF-alpha. The maximal ICAM-1 expression on both epithelial cell types was obtained with the combination of TNF-alpha and IFN-gamma after 48 h of incubation. The NCI-H292 cell line was different in that it only showed increased ICAM-1 expression after stimulation with PMA and IFN-gamma and not by the combination of IFN-gamma and TNF-alpha or with TNF-alpha alone. In conclusion, the bronchial epithelial cells tested express several adhesion molecules, but only ICAM-1 expression was influenced by inflammatory cytokines.
Am J Respir Cell Mol Biol 1993 Dec
PMID:Expression and modulation of adhesion molecules on human bronchial epithelial cells. 750 27

Expression of human prostatic acid phosphatase (ACPP) and prostate specific antigen (PSA) genes in prostatic carcinoma (CAP) and benign prostatic hyperplasia (BPH) was investigated by northern blot analyses. The expressions of ACPP and PSA, as well as the glycolytic enzymes glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and lactate dehydrogenase-muscle (LDH-A), were elevated significantly in prostatic carcinoma when compared with the expressions of these genes in benign prostatic hyperplasia in the same patient. The expression of the actin gene in both neoplastic and benign hyperplasia remained the same.
Biochem Mol Biol Int 1994 Jun
PMID:Expression of human prostatic acid phosphatase and prostate specific antigen genes in neoplastic and benign tissues. 752 3

In Streptococcus equisimilis H46A, a hypersymmetrical transcription terminator with bidirectional activity was localized between the translational termination codons of the streptokinase gene, skc, and the rel-orf1 genes. These two transcription units are oriented towards each other, and under normal conditions the skc mRNA level exceeds that of the rel-orf1 genes by a factor of at least 1000. Reporter vectors based on the promoterless cat gene were constructed by transcriptional fusion of skc to cat, such that the region between the two genes contained the terminator in skc orientation or in rel-orf1 orientation. Additionally, skc and cat were fused directly, with deletion of the terminator. The reporter vectors were designed to be capable of being studied either as multicopy plasmids in Escherichia coli or in single copy following integration, via skc, into the S. equisimilis chromosome. Chloramphenicol acetyl transferase (CAT) activity assays in conjunction with determination of chloramphenicol resistance levels and Northern hybridization analysis showed that the terminator is active in either host and orientation. However, termination efficiency was host dependent, with high terminator strength being observed in the homologous streptococcal background and appreciable readthrough occurring in E. coli. The extent of transcriptional readthrough was dependent upon terminator orientation, with termination being more efficient in rel-orf1 polarity. The results suggest that, in S. equisimilis, transcription of both skc and rel-orf1 is efficiently terminated by a common signal, and that these genes are largely protected from convergent transcription, which otherwise would seem to be particularly detrimental to the weakly expressed rel-orf1 genes.
Mol Gen Genet 1995 Feb 06
PMID:Transcription termination of the streptokinase gene of Streptococcus equisimilis H46A: bidirectionality and efficiency in homologous and heterologous hosts. 753 15

A mutation shown to cause resistance to chloramphenicol in Saccharomyces cerevisiae was mapped to the central loop in domain V of the yeast mitochondrial 21S rRNA. The mutant 21S rRNA has a base pair exchange from U2677 (corresponding to U2504 in Escherichia coli) to C2677, which significantly reduces rightward frameshifting at a UU UUU UCC A site in a +1 U mutant. There is evidence to suggest that this reduction also applies to leftward frameshifting at the same site in a -1 U mutant. The mutation did not increase the rate of misreading of a number of mitochondrial missense, nonsense or frameshift (of both signs) mutations, and did not adversely affect the synthesis of wild-type mitochondrial gene products. It is suggested here that ribosomes bearing either the C2677 mutation or its wild-type allele may behave identically during normal decoding and only differ at sites where a ribosomal stall, by permitting non-standard decoding, differentially affects the normal interaction of tRNAs with the chloramphenicol resistant domain V. Chloramphenicol-resistant mutations mapping at two other sites in domain V are described. These mutations had no effect on frameshifting.
Mol Gen Genet 1995 Jul 28
PMID:Mutation of a highly conserved base in the yeast mitochondrial 21S rRNA restricts ribosomal frameshifting. 754 31


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