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  • 1
    Electronic Resource
    Electronic Resource
    Cardiac Conduction Abnormalities in Mice Lacking the Gap Junction Protein Connexin40 (1999)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 10 (1999), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Cardiac Conduction in C×40−/− Mice. Introduction: The gap junction protein connexin40 (C×40) normally is expressed in the murine atrial myocardium and ventricular conduction system. In mice lacking C×40, several changes in the surface ECG have been described. In this study, we analyzed cardiac conduction in more detail. Methods and Results: In open chest mice under urethane anesthesia, epicardial electrodes were used to determine a number of atrial and ventricular pacing parameters. The corrected sinus node recovery time was significantly longer in C×40−/− mice than in C×40+/+ mice (44.4 ± 7.2 msec vs 35.5 ± 8.0 msec). In addition, the Wenckebach period was longer in C×40−/− mice compared with the wild type (84.6 ± 5.4 msec vs 78.8 ± 3.6 msec), with the AV node probably limiting AV conduction in both cases. Whereas arrhythmias could not be induced by ventricular burst pacing in any of the mice, atrial burst pacing induced atrial tachyarrhythmias in 5 of 10 C×40−/− mice, but not in any of 9 Cx40−/− mice. Conduction velocities were measured in vivo using an array of unipolar recording electrodes. Ventricular conduction velocity did not differ between the groups, but atrial conduction velocity was reduced by 30% in C×40−/− mice compared with the wild type. Heterozygous C×40+/− mice did not differ significantly from the wild type in any respect. Conclusion: These findings indicate that in the atria and the AV conduction system, C×40 is an important determinant of conduction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8167.1999.tb00194.x
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  • 2
    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
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  • 3
    Electronic Resource
    Electronic Resource
    Functional expression of connexin57 in horizontal cells of the mouse retina (2004)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 19 (2004), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Horizontal cells are interneurons of the vertebrate retina that exhibit strong electrical and tracer coupling but the identity of the channel-forming connexins has remained elusive. Here we show that horizontal cells of the mouse retina express connexin57 (Cx57). We have generated Cx57-deficient mice by replacing the Cx57 coding region with a lacZ reporter gene, expressed under control of the endogenous Cx57 promoter. These mice were fertile and showed no obvious anatomical or behavioural abnormalities. Cx57 mRNA was expressed in the retina of wild-type littermates but was absent from the retina of Cx57-deficient mice. Previously reported results that the Cx57 gene was very weakly expressed in several other mouse tissues turned out to be unspecific. Cx57 mRNA is abundantly expressed in the retina and weakly in the thymus of adult mice but absent in all other adult tissues tested, including brain. Furthermore, Cx57 is expressed in embryonic kidney at E16.5 to E18.5 days post-conception, as indicated by the pattern of lacZ expression. Within the retina, lacZ signals were assigned exclusively to horizontal cells based on co-localization with cell-type-specific marker proteins. Microinjection of Neurobiotin into horizontal cells of isolated retinae revealed less than 1% of tracer coupling in Cx57-deficient retinae compared with wild-type controls. Cx57 is the first connexin identified in mammalian horizontal cells and the first connexin whose expression is apparently restricted to only one type of neuron.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0953-816X.2004.03360.x
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  • 4
    Electronic Resource
    Electronic Resource
    Connexin43 is not expressed in principal cells of mouse cortex and hippocampus (2003)
    Oxford, UK : Blackwell Science, Ltd
    European journal of neuroscience 18 (2003), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Previous immunofluorescence analyses in mice and rats showed a mainly astrocytic expression of the gap junction protein connexin43 (Cx43) in brain. However, in situ hybridization of murine brain sections suggested strong expression of Cx43 mRNA in hippocampal and cortical pyramidal neurons and Purkinje cells. These findings contrast with recent immunoelectron microscopic studies that excluded prominent Cx43 protein expression in neurons. Both contrasting results could be explained by post-transcriptional control mechanisms. Here we demonstrate by conditional replacement of the Cx43 coding region by a lacZ reporter gene, mimicking transcriptional activity of the Cx43 gene, that Cx43 is not expressed in principal cells of murine brain. This histochemical approach used is not prone to cross-reactivity of mRNA probes or antibodies. Furthermore, we show that in situ hybridization signals, suggested to be specific for Cx43 in mouse neurons, are retained even when the Cx43 coding DNA in neurons is removed by cre-mediated deletion. Our results confirm the previous findings of a mainly astrocytic expression of Cx43 in adult mouse brain and underscore the importance of connexin-deficient mice as controls for in situ hybridization studies. We found no evidence for post-transcriptional control of the Cx43 gene in principal neurons. Thus, the synchronized activity of neuronal networks cannot depend on Cx43 containing gap junctions in these cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2003.02740.x
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  • 5
    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
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  • 6
    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
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  • 7
    Electronic Resource
    Electronic Resource
    Electrophysiological properties of gap junction channels in hepatocytes isolated from connexin32-deficient and wild-type mice (1999)
    Springer
    Pflügers Archiv 437 (1999), S. 846-856 
    Details
    ISSN: 1432-2013
    Keywords: Key words Connexin26 ; Connexin32 ; Electrophysiology ; Gap junction ; Gap junction channel ; Hepatocyte
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Hepatocytes were isolated from wild-type and connexin32-deficient (Cx32-deficient) mice. Pairs of cells were chosen to study the electrical properties of gap junction channels using the dual voltage-clamp method. The total gap junction currents revealed that Cx32-deficient hepatocytes express one type of connexin (Cx26) and wild-type hepatocytes express two types of connexins (Cx26 and Cx32). The unitary gap junction currents suggest that Cx32-deficient cells have homotypic channels (Cx26–Cx26) while wild-type cells form homotypic (Cx26–Cx26, Cx32–Cx32) and heterotypic channels (Cx26–Cx32). Homotypic channels exhibited a main conductance and a residual conductance, both virtually insensitive to gap junction voltage (V j) (Cx32–Cx32: γj,main=31 pS, γj,residual=9 pS; Cx26–Cx26: γj,main=102 pS, γj,residual=17 pS). Residual states were regularly seen in Cx32–Cx32 channels, but rarely in Cx26–Cx26 channels. Heterotypic channels showed a main conductance and a residual conductance. The former was sensitive to V j (average γj,main=52 pS). The electrophysiological data suggest that Cx32 hemichannels are more abundant than Cx26 hemichannels in prenatal (ratio 4:1) and adult wild-type hepatocytes (ratio 23:1) and that the total number of gap junction channels is larger in prenatal cells than in adult cells. The diversity of the relationship g j,ss/g j,inst=f(V j) (g j,ss: gap junction conductance at steady state; g j,inst: instantaneous gap junction conductance; V j: transjunctional voltage) seen in wild-type cells suggests that the ratio Cx26/Cx32 hemichannels is variable among hepatocytes. A comparison of total and unitary conductances implies that Cx26 hemichannels are down-regulated in Cx32-deficient cells and that docking between Cx26 and Cx32 hemichannels occurs randomly. While the gap junction currents are compatible with homotypic and heterotypic channels, the presence of heteromeric channels cannot be excluded.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050854
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  • 8
    Electronic Resource
    Electronic Resource
    Heterotypic gap junction channels (connexin26 – connexin32) violate the paradigm of unitary conductance (1995)
    Springer
    Pflügers Archiv 429 (1995), S. 870-872 
    Details
    ISSN: 1432-2013
    Keywords: HeLa cells ; connexin26 ; connexin32 ; gap junction channels ; heterotypic channels ; single channel conductance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Human HeLa cells transfected with mouse DNA coding for connexin26 (Cx26) or connexin32 (Cx32) were used to examine the properties of heterotypic Cx26 – Cx32 gap junction channels. Intercellular current flow was examined in induced cell pairs by means of the dual voltage-clamp method. We found that Cx26 – Cx32 channels exhibit voltage-dependent conductances, γ j: γj (main state) increases with increasing positivity at the cytoplasmic aspect of the Cx26 connexon and decreases with increasing negativity (slope: 32 pS/100 mV; γ j γj(main state) reaches 48 pS as V j approaches 0 mV); γ j(residual state) with a similar V j-dependence is present when the cytoplasmic end of Cx26 connexon is positive, but absent when it is negative. The single channel data provide an explanation for the asymmetric relationships between the gap junction conductance, g j, and V j. The results are consistent with the notion that docking of two connexons co-determines the biophysical properties of a gap junction channel.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374812
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  • 9
    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
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  • 10
    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
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