ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    A DNA-Binding Zinc-Protein Increases the Immortalizing Activity of an Extrachromosomal DNA Sequence from Mouse L929 Cells (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 684 (1993), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1993.tb32281.x
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Engraftment of connexin 43-expressing cells prevents post-infarct arrhythmia (2007)
    [s.l.] : Nature Publishing Group
    Nature 450 (2007), S. 819-824 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Ventricular tachyarrhythmias are the main cause of sudden death in patients after myocardial infarction. Here we show that transplantation of embryonic cardiomyocytes (eCMs) in myocardial infarcts protects against the induction of ventricular tachycardia (VT) in mice. Engraftment of eCMs, but not ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nature06321
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Segment-specific expression of the gap junction gene connexin31 during hindbrain development (1997)
    Springer
    Development genes and evolution 207 (1997), S. 359-361 
    Details
    ISSN: 1432-041X
    Keywords: Key words Rhombomere ; connexin31 ; Gap junctions ; Communication compartment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract  During segmentation of the mouse hindbrain (d8.0–8.5 pc), expression of the gap junction gene connexin31 (cx31) is precisely restricted to rhombomeres (r) 3 and 5. Shortly afterwards, during the turning process, cx31 expression in rhombomere 3 decreases and is no longer detectable at d9.5 pc, whereas expression in rhombomere 5 is maintained until about d10.0 pc. So far, cx31 is the first gap junction gene found to be expressed in rhombomeres. Its precise segmental and temporal expression pattern may reflect a critical requirement of cx31 channels for these odd numbered rhombomeres to acquire distinct cell identities.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004270050123
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Acute-phase response and circadian expression of connexin26 are not altered in connexin32-deficient mouse liver (2000)
    Springer
    Cell & tissue research 300 (2000), S. 111-117 
    Details
    ISSN: 1432-0878
    Keywords: Liver gap junctions Experimental inflammation Cx32-deficient mice Circadian rhythm Mouse (BALB/c; C57BL/6)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. In mouse hepatocytes, the gap junctional proteins connexin32 (Cx32) and connexin26 (Cx26) are expressed in the same gap junctional plaque. Expression of the major Cx32 protein is downregulated during liver regeneration and cholestasis. Here we have analyzed the acute-phase response (after experimental inflammation) and circadian connexin expression in Cx32-deficient and wild-type mouse liver. Acute-phase response was triggered by intraperitoneal injection of lipopolysaccharide (LPS). Injection of recombinant mouse interleukin-1β (mIL-1β), mIL-6 or tumor necrosis factor α (mTNF-α) had no inflammatory effect. Northern blot analysis of positive and negative acute-phase transcripts following stimulation with cytokine or LPS revealed no difference between Cx32-deficient livers and wild-type controls, suggesting that loss of the Cx32 gene had no effect on experimental liver inflammation. Actin, β-fibrinogen and Cx26 transcripts were increased after endotoxin stimulation. Under conditions of hepatic acute-phase response, Cx32 transcripts were not detected in LPS-treated livers of wild-type mice. Immunoblot analysis of proteins from inflamed wild-type livers indicated a strongly diminished amount of Cx32 protein, whereas the level of Cx26 protein was increased. Although intraperitoneal injection of mIL-1, mIL-6 as well as mTNF-α did not induce an acute-phase response, Cx32 protein expression was diminished, suggesting that post-transcriptional downregulation of Cx32 preceded the acute-phase response. Northern blot hybridization of RNA from wild-type and Cx32-deficient mouse liver revealed a similar circadian regulation of Cx26 and GAPDH transcripts with maximal expression around 2 p.m. and a minimum after midnight.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004410000177
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    DNA-mediated transfer of the mouse gene for hypoxanthine phosphoribosyltransferase into cultured mouse cells: No integration of the transferred gene at its homologous site in the host genome (1981)
    Springer
    Molecular genetics and genomics 182 (1981), S. 70-76 
    Details
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary An established Chinese hamster cell line was fused with microcells isolated from phenotypically stable transferent mouse cells which contained a mouse transgenome coding for an abnormal form of mouse hypoxanthine phosphoribosyltransferase (HPRT, EC. No. 2.4.2.8) (Willecke et al. 1979). Two hybrids were isolated which expressed the abnormal form of mouse HPRT but no mouse α-galactosidase (GALA, EC. No. 3.2.1.22). In one of these microcell hybrids the abnormal HPRT activity segregated under counter-selective conditions with mouse chromosome 3. No mouse chromosome or additional mouse gene marker was found in the second microcell hybrid, possibly because of breakage and/or rearrangement of the integrated transgenome during the isolation of this hybrid. We conclude from these results that the transferred mouse HPRT gene in a phenotypically stable clone is not integrated at its homologous site on the host X chromosome. Rather, the transgenome is probably integrated into mouse chromosome 3, possibly due to homologies in repeated DNA sequences which may occur in the transgenome and which are interspersed at many sites in the host genome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00422769
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Intraspecies transfer via total cellular DNA of the gene for hypoxanthine phosphoribosyltransferase into cultured mouse cells (1979)
    Springer
    Molecular genetics and genomics 170 (1979), S. 179-185 
    Details
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Under selective growth conditions a revertant of mouse cells, defective in hypoxanthine phosphoribosyltransferase activity (HPRT, EC-No. 2.4.2.8), was isolated, which contained an electrophoretically abnormal form of HPRT activity. The specific HPRT activity in crude extracts of the revertant cells is about 30% of the level determined in normal wild type cells. The variant HPRT reacts with antiserum against normal mouse HPRT but the rate of heat inactivation of the variant activity is different from the wild type form. By isozyme and karyotype analyses of somatic cell hybrids between the revertant mouse cells and Chinese hamster cells we found that the abnormal HPRT activity is coded for by the mouse X-chromosome as expected for a mutation in the structural HPRT gene. DNA has been purified from the abnormal HPRT revertant cells and incubated with mouse A9 cells (HPRT-). After growth in selective medium one clone was isolated which expressed the electrophoretically abnormal form of HPRT. Six clones showed the normal form of HPRT due to reversion of the defective HRRT locus in A9 cells. This result indicates DNA-mediated transfer of the mouse HPRT gene at a frequency of about 0.5×10-7. A similar frequency has been found for transfer of the variant HPRT locus via isolated metaphase chromosomes to A9 recipient cells. When placed in non-selective media the DNA-mediated transferent cells gradually lost their ability to express the HPRT transgenome at a rate of about 6% per average cell generation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00337794
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Segregation of human hypoxanthine phosphoribosyltransferase activity from somatic cell hybrids isolated after fusion of mouse gene transfer cells with Chinese hamster cells (1977)
    Springer
    Molecular genetics and genomics 154 (1977), S. 191-197 
    Details
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Four independent mouse gene transfer clones, i.e. mouse cells which had taken up a human chromosomal fragment carrying the human gene for hypoxanthine phosphoribosyltransferase (HPRT), were characterized with the following results: 1. None of the clones expressed human α-galactosidase activity whose structural gene has been previously located on the human X-chromosome in the neighbourhood of the gene coding for HPRT. Thus the human chromosomal fragment in these mouse cells is presumably so small that it does not carry the gene for human α-galactosidase A. 2. All the gene transfer clones when maintained in logarithmic growth for at least 100 generations in selective medium became phenotypically stable, i.e. they no longer segregated the transferred human HPRT activity after being shifted to non-selective growth conditions. 3. Somatic cell hybrids were isolated after fusion of phenotypically stable mouse gene transfer cells, expressing human HPRT, with chinese hamster cells, mouse cells which were derived from the same parental line as the gene transfer cells but which expressed reverted mouse HPRT were also fused with these chinese hamster cells. All isolated hybrid cell clones were counter-selected for the absence of functional HPRT. In two hybrids the reverted mouse HPRT activity and mouse α-galactosidase activity segregated together. This suggested that the normal linkage between the genes of mouse HPRT and mouse α-galactosidase was still maintained in this aneuploid cell line. In two other hybrids derived from a gene transfer clone human HPRT and mouse α-galactosidase segregated independently from each other. Therefore the transferred human HPRT gene is most likely not integrated at the position of the defective mouse HPRT gene in the X-chromosome of a phenotypically stable gene transfer clone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00330836
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Chromosomal gene transfer of human cytosol thymidine kinase into mouse cells (1978)
    Springer
    Molecular genetics and genomics 161 (1978), S. 49-57 
    Details
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary If a chromosomal fragment transferred into recipient cells were integrated or strongly associated with a specific recipient chromosome it should segregate with this chromosome in hybrid cells. In order to corroborate this prediction we studied two independent mouse cell clones (“transferent clones”) which had taken up by chromosomal gene transfer a human chromosomal fragment carrying the gene for cytosol thymidine kinase (TKs, E.C.No.2.7.1.75). The following results were obtained. 1. Ten somatic cell hybrids isolated after fusion of transferent mouse clones and chinese hamster cells expressed functional human TKs and mouse galactokinase (GALK, E.C.No.2.7.1.6) activity. Counterselected derivatives of all clones had lost human TKs but still expressed mouse GALK. Recently both mouse genes for TKs and GALK have been assigned to mouse chromosome 11 (Kozak and Ruddle, 1977a, McBreen et al., 1977). Therefore our results argue against integration or association of the human gene for TKs at the site of the homologous defective mouse TKs-GALK-region in the genome of transferent clones. 2. In three somatic cell hybrids isolated after fusion of microcells from two different transferent mouse clones with established chinese hamster cells only human TKs but not mouse GALK was expressed. Karyotypic analysis of one hybrid suggested the presence of at least one copy of mouse chromosome 9 per hybrid cell. Chromosome 9 and the mouse isozyme activity of mannose phosphate isomerase which had been previously assigned to a gene locus on mouse chromosome 9 were missing in a subclone counter-selected against the presence of TKs activity. These findings suggested that the transferred human gene for TKs may be integrated or strongly associated with mouse chromosome 9 in this transferent mouse clone. 3. Two other somatic cell hybrids were analyzed which were derived from a different phenotypically stable transferent mouse clone by similar microcell fusion with the chinese hamster cells. Although these hybrids expressed human TKs activity, no mouse chromosome could be detected in these clones. Possibly after fusion of microcells derived from certain transferent mouse clones the transferred human chromosomal fragment could become translocated from a mouse chromosome to the chinese hamster genome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00266614
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Connexin expression systems: To what extent do they reflect the situation in the animal? (1996)
    Springer
    Journal of bioenergetics and biomembranes 28 (1996), S. 319-326 
    Details
    ISSN: 1573-6881
    Keywords: Gap junctions ; lipid bilayers ; Xenopus oocytes ; established cell lines ; primary cells ; connexin-deficient mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Physics
    Notes: Abstract Intercellular communication is mediated by specialized cell-cell contact areas known as gap junctions. Connexins are the constitutive proteins of gap junction intercellular channels. Various cell expression systems are used to express connexins and, in turn, these expression systems can then be tested for their ability to form functional cell-cell channels. In this review, expression of murine endogenous connexins in primary cells and established cell lines is compared with results obtained by expression of exogenous connexins inXenopus oocytes and cultured mammalian cells. In addition, first reports on characterization of connexin-deficient mice are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02110108
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Chromosomal assignments of mouse connexin genes, coding for gap junctional proteins, by somatic cell hybridization (1992)
    Springer
    Somatic cell and molecular genetics 18 (1992), S. 351-359 
    Details
    ISSN: 1572-9931
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The connexin genes Cx31 and Cx45 coding for proteins of gap junctional subunits have been assigned to mouse chromosomes 4 and 11 by Southern blot hybridization of specific gene probes to DNA from mouse × Chinese hamster somatic cell hybrids. In addition, our results confirm the recent assignment of mouse connexin genes Cx26, Cx32, Cx37, Cx40, Cx43, and Cx46 to mouse chromosomes 14, X, 4, 3, 10, and 14, respectively, by analysis of interspecific backcrosses and by somatic cell hybridization. Our assignment of the Cx31 gene to mouse chromosome 4 locates the fourth connexin gene on this mouse chromosome to which the genes for Cx31.1, Cx37, and Cx30.3 have previously been assigned. Interestingly three of them (coding for Cx31, Cx31.1, and Cx30.3) are preferentially expressed in skin. Possibly some of the connexin genes clustered on mouse chromosome 4 may be regulated coordinately.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01235758
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...