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  • 1
    ISSN: 1573-5001
    Keywords: Heteronuclear NMR ; chemical shift ; DNA-binding domain ; protein-DNA interaction ; Mrf-2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Based on the published amino-acid sequence of H-2Kb, we synthesized a mixture of eight 16-base long oligodeoxyribonucleotides representing all possible coding sequences for residues 51–56 (Trp-Met-Glu-Gln-Glu-Gly). The hexadecanucleotide mixture was used as a probe to screen recombinant DNA clones constructed from cytoplasmic PolyA+ RNA isolated from the murine thymoma cell line EL4 (b haplotype). Of the 30 000 independent clones screened, one clone was found to hybridize with the probe. DNA sequence analysis showed that the cDNA clone was derived from a portion of an H-2Kb-related mRNA. The clone encodes a protein sequence identical with a region of H-2Kb in 42 consecutive residues (50 through 91). The sequence then diverges from the H-2Kb sequence and, after a single Glu codon, a termination codon is encountered. It is possible that this mRNA codes for a small 92 amino-acid protein with a sequence identical (except for a carboxy-terminal Glu residue) with the amino terminus of H-2Kb It is further speculated that this mRNA is coded for by the H-2K b gene and differs from the H-2Kb mRNA in the pattern of posttranscriptional splicing.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0730-2312
    Keywords: TGF-β1 ; retinoblastoma susceptibility protein ; cell cycle ; growth inhibitors ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: In the rat liver epithelial cell line, WB, the ability of TGF-β1 to inhibit DNA synthesis was shown to correlate with its ability inhibit phosphorylation of the protein product of the retinoblastoma susceptibility gene, pRb. When WB cells were serum-starved, then refed with serum-containing medium, a peak of DNA synthesis occurred at about 18 h. Autoradiographs showed that 43.6% of cell nuclei could be labeled with 3H-thymidine at this time. When TGF-β1 was added simultaneously with serum, it blocked DNA synthesis and reduced the number of labeled nucleii to 6.3%. Cells treated with serum alone for 18 h also showed a pronounced increase in the highly phosphorylated form of pRb, as shown by mobility shifts in immunoblots, and in active phosphorylation of pRb, as shown by 32P incorporation. Simultaneous addition of TGF-β1 with serum abolished both 32P incorporation into pRb and its mobility shift on immunoblots. The effect of TGF-β1 on DNA synthesis measured at 18 h was sharply reduced if the cells were incubated with serum for 8 h (and thus allowed to enter S) before the addition of TGF-β1. If TGF-β1 was added after 8 h of serum treatment, its ability to inhibit pRb phosphorylation at 18 h was unchanged. If TGF-β1 was added after 13 h of serum treatment, its effects on pRb phosphorylation were reduced. Thus, as the cell population moved into S, the ability of TGF-β1 to inhibit both pRb phosphorylation and DNA synthesis was lost. In higher passages of WB cells the dose-response for inhibition of DNA synthesis by TGF-β1 was shifted to the right. Inhibition of pRb phosphorylation by TGF-β1 was also lost in higher passage WB cells. Thus, the passage-dependent loss of sensitivity to inhibition of DNA synthesis accompained the loss of sensitivity to inhibition of pRb phosphorylation. Since the phosphorylation of pRb is believed to be required for the progression of cells from G1 to S, inhibition of pRb phosphorylation may be either a cause or a consequence of the G1 arrest of WB cells by TGF-β1.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 0730-2312
    Keywords: TGFβ gene ; hepatic regeneration ; hepatomas ; carcinogens ; growth inhibitor ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: TGFβ is a potent, nontoxic inhibitor of mitogen-induced DNA synthesis in primary cultures of adult rat hepatocytes. Using a cDNA probe, we investigated TGFβ gene expression in quiescent, regenerating, and neoplastic liver, and several hepatoma lines by Northern gel analysis. We found that regenerating liver had increased TGFβ gene transcripts beginning at about 8 h, with a broad peak of 48-120 h and return to normal after 9 days. Separation of the regenerating liver into its constituent cell types, followed by RNA extraction and reprobing, revealed that increased TGFβ gene transcripts were confined to the enriched endothelial-cell population and not the hepatocytes. Increased hepatic TGFβ expression was also found in fetal liver and in rats immediately after birth. Elevated TGFβ mRNA levels were also found in primary cultures of oval cells and an established bile ductular cell line, as well as in carcinogen-altered liver epithelial cell lines. Transcripts were undetectable in normal human liver but were abundant in the human hepatoma lines Hep G2, Hep 3B, PLC/PRF/5, and SK-Hep-1. Elevated levels were also found in the normal rat liver-derived lines BRL-3A and clone 9 and the H4IIE rat hepatoma, but not in the HTC, MH1C1, and MH7777 rat hepatomas. The hepatocarcinogen diethylnitrosamine induced high transcript levels after single injections in a time- and dose-dependent manner. These results suggest that the liver may be a paracrine organ with respect to TGFβ gene expression, which can be induced by carcinogens and by growth stimulation.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 0730-2312
    Keywords: growth factor receptors ; heparin binding proteins ; cell adherence ; hepatoma cells ; affinity cross-linking ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: A low molecular weight inhibitor of TGF-β1 binding was detected in partially purified human platelet extracts by using Hep 3B hepatoma cells in the binding assays. The inhibitory protein was purified to homogeneity and was identified as platelet factor 4 on the basis of its amino acid sequence. TGF-β1 binding to Hep 3B cells was almost completely inhibited by 100 nM concentrations of platelet factor 4, but TGF-β1 binding to NRK 49F fibroblasts was inhibited only slightly. Affinity cross-linking experiments revealed that these differences in the inhibition of TGF-β1 binding by platelet factor 4 were due to differences in the complements of TGF-β1 binding proteins present on these two cell types. In Hep 3B cells the majority of bound TGF-β1 was cross-linked to a complex which had an apparent molecular weight of 70 kDa. TGF-β1 binding to this protein was the most sensitive to inhibition by platelet factor 4. Based on its size and TGF-β1 binding properties, we believe this protein is the type I TGF-β1 receptor. Hep 3B cells also had a high-affinity TGF-β1 binding protein which appeared as an 80 kDa complex, and which we believe to be the type II TGF-β1 receptor. TGF-β1 binding to this protein was not inhibited by platelet factor 4. TGF-β1 was also cross-linked to complexes of higher molecular weights in Hep 3B cells, but it was not clear whether any of them represented the type III TGF-β1 receptor. In NRK 49F cells, the majority of bound TGF-β1 was cross-linked to a high molecular weight complex which probably represented the type III TGF-β1 receptor. NRK 49F cells also had type I TGF-β1 receptors and platelet factor 4 inhibited binding to these receptors in the NRK cells. Since the type I receptor contributed only a small percentage of total TGF-β1 binding, however, the overall effects of platelet factor 4 on TGF-β1 binding to NRK 49F cells were negligible. We were unable to demonstrate specific or saturable binding of platelet factor 4 to Hep 3B cells using either direct binding or affinity cross-linking assays. Thus, it is not clear whether platelet factor 4 inhibits TGF-β1 binding by competition for binding to the type I receptor.Modest concentrations of TGF-β1 reduced the adherence of Hep 3B cells to tissue culture dishes. Platelet factor 4 did not mimic this effect of TGF-β1, nor did it inhibit the effect, even at concentrations which were sufficient to completely inhibit binding to the type I TGF-β1 binding protein/receptor. This suggests that the type I binding protein does not mediate the effect of TGF-β1 on Hep 3B cell adhesion.
    Additional Material: 8 Ill.
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  • 6
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Transcription factors carry functional domains, which are often physically distinct, for sequence-specific DNA binding, transcriptional activation and regulatory functions. The transcription factor ATF-2 is a DNA-binding protein that binds to cyclic AMP-response elements (CREs), forms a ...
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  • 7
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] A deficiency in the plasma protease inhibitor α1-antitrypsin can cause chronic obstructive emphysema or infantile liver cirrhosis. This deficiency results from a single amino acid substitution created by a G to A transition in the gene for α1-antitrypsin. ...
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  • 8
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Sir A trial is under way in San Francisco, California, involving a patent dispute between Genentech, Inc. and the University of California at San Francisco (see page 289 of this issue and ref. 1). During this trial, Peter Seeburg of the Max Planck Institute ...
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  • 9
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 286 (1980), S. 567-573 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The DNA tetramer d(CpGpCpG) or CGCG crystallizes from high-salt solution as a left-handed double helix, the Z′ helix. Its structure differs from that of the other known left-handed helix, Z-DNA, by a Cl′-exo sugar pucker at deoxyguanosines rather than C3′-endo, and these represent ...
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  • 10
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Blunt end ligation with an EcoRI/ octanucleotide “linker” was used to construct a plasmid containing chemically synthesized lac operator DNA. This plasmid renders the host bacterium constitutive for ...
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