Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.7 (DNA polymerase)
 17,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The adaptive response was examining chromosomal aberrations and micronucleus in cultured fish cells, ULF-23 (mudminnow) and CAF-31 (gold fish). When cultured fish cells were first irradiated with small doses of X-rays, they became less sensitive to subsequent exposures to high doses. The effective adaptive dose was 4.8 cGy-9.5 cGy. Adaptive doses given cells in the G1 phase were more effective than when given in the S phase. The adaptive response was maximal at 5 hours and disappeared at 10 hours after the adaptive dose. The expression of the response was inhibited by treatment with 3-aminobenzamide, as reported for mammalian cells, and with arabinofuranoside cytosine, an inhibitor of DNA polymerase alpha. Caffeine, an inhibitor of post-replicational repair, had no effect on the response.
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PMID:Cytogenetic adaptive response of cultured fish cells to low doses of X-rays. 129 96

We have examined the killing effect of 4-S-cysteaminylphenol (4-S-CAP), a newly synthesised melanin precursor, on B16 melanoma cell lines possessing different melanin-producing activities and found it to be particularly effective in heavily melanised melanoma cells, but less so in moderately melanised melanoma cells, and having no effect on amelanotic melanoma cells and nonmelanoma cells. Thus, it was found that the killing effect of 4-S-CAP is highly dependent upon the synthesis of melanin and tyrosinase in melanoma cells, suggesting that 4-S-CAP may become toxic to melanoma cells only after oxidation by tyrosinase. The killing activity of 4-S-CAP also was found to be associated with a profound inhibition of the thymidine incorporation in pigmented melanoma cells, as compared to the uridine and leucine incorporation. Further, the inhibition of DNA synthesis was most pronounced in heavily melanised melanoma cells, less so in moderately melanised melanoma cells, and not seen in amelanotic melanoma cells. As a possible mechanism that might account for this action, it may be that 4-S-CAP is oxidised by tyrosinase to the o-quinone form via the catechol derivative and that some of the quinones then conjugate with sulfhydryl enzymes including DNA polymerase, thus exerting a killing activity for pigmented melanoma cells. Thus, 4-S-CAP appears to provide a new, effective cytotoxic agent for rational chemotherapy of malignant melanomas.
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PMID:The killing effect of 4-S-cysteaminylphenol, a newly synthesised melanin precursor, on B16 melanoma cell lines. 199 95

A family of plasmids containing short pieces of Escherichia coli lac promoter DNA has been constructed. DNA fragments from any source may be inserted directly into the unique EcoRI sites of some of these plasmids to achieve transcription under the control of the lacUV5 promoter. Alternatively, the plasmids serve as convenient sources of lac DNA fragments ('portable promoters') containing the 'up' promoter mutations UV5 or Ps (super promoter) as well as the wild-type promoter. pOP95-2, pOP95-5, pOP203-1, pOP203-2 and pOP203-3 are derivatives of pMB9 while pOP95-15 and pOP203-13 are derivatives of pBR322. The pOP95 plasmids contain the 95-bp AluI lac fragment. This fragment includes the UV5 promoter (minus the CAP binding site), the repressor binding site, and ends 2 bp before an ATG encoding the beta-Gal start codon. The pOP203 plasmids contain the 203-bp HaeIII lac fragment. This fragment contains the UV5 promoter (including the L8 mutation in the CAP binding site), the repressor binding site and sequences encoding the first 8 amino acids of beta-Gal. To shorten and introduce reading frame heterogeneity in the beta-Gal coding end of the pOP203 plasmids, the EcoRI site in pOP203-12 was moved upstream by digesting EcoRI cut plasmid DNA with T4 DNA polymerase and S1 nuclease followed by ligation in the presence of EcoRI linker. This produced the plasmids pOP203-24, pOP203-27, pOP203-28 and pOP203-29. pOP203-29 encodes essentially just that portion of the beta-Gal mRNA sequence which is protected from nuclease digestion by the bound ribosomal complex (Maizels, 1974).
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PMID:A family of cloning vectors containing the lacUV5 promoter. 629 48

Chromatin assembly factor-1 (CAF-1), a complex consisting of p150, p60, and p48 subunits, is highly conserved from yeast to humans and facilitates nucleosome assembly of newly replicated DNA in vitro. To investigate roles of CAF-1 in vertebrates, we generated two conditional DT40 mutants, respectively, devoid of CAF-1p150 and p60. Depletion of each of these CAF-1 subunits led to delayed S-phase progression concomitant with slow DNA synthesis, followed by accumulation in late S/G2 phase and aberrant mitosis associated with extra centrosomes, and then the final consequence was cell death. We demonstrated that CAF-1 is necessary for rapid nucleosome formation during DNA replication in vivo as well as in vitro. Loss of CAF-1 was not associated with the apparent induction of phosphorylations of S-checkpoint kinases Chk1 and Chk2. To elucidate the precise role of domain(s) in CAF-1p150, functional dissection analyses including rescue assays were preformed. Results showed that the binding abilities of CAF-1p150 with CAF-1p60 and DNA polymerase sliding clamp proliferating cell nuclear antigen (PCNA) but not with heterochromatin protein HP1-gamma are required for cell viability. These observations highlighted the essential role of CAF-1-dependent nucleosome assembly in DNA replication and cell proliferation through its interaction with PCNA.
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PMID:Essential role of chromatin assembly factor-1-mediated rapid nucleosome assembly for DNA replication and cell division in vertebrate cells. 1706 58