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  • 1
    Electronic Resource
    Electronic Resource
    Disruption of c- mos causes parthenogenetic development of unfertilized mouse eggs (1994)
    [s.l.] : Nature Publishing Group
    Nature 370 (1994), S. 65-68 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The targeting vector, pMSl(neo)tk (Fig. \d] contains a neo-mycin-resistance (neor) gene inserted into the middle of the single c-mos coding exon. This insertion introduces an amber stop codon into the c-mos reading frame to terminate translation upstream of sequences essential for kinase ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/370065a0
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  • 2
    Electronic Resource
    Electronic Resource
    Ion-transporting activity in the murine colonic epithelium of normal animals and animals with cystic fibrosis (1994)
    Springer
    Pflügers Archiv 428 (1994), S. 508-515 
    Details
    ISSN: 1432-2013
    Keywords: Murine colonic epithelium ; Cystic fibrosis ; Electrogenic chloride secretion ; Electrogenic potassium secretion ; Electrogenic sodium absorption ; Ba2+ ; TEA+ ; 86Rb fluxes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Electrogenic ion transport in the isolated co-Ionic epithelium from normal and transgenic mice with cystic fibrosis (CF mice) has been investigated under short-circuit current (I sc) conditions. Normal tissues showed chloride secretion in response to carbachol or forskolin, which was sensitive to the Na-K-2Cl cotransport inhibitor, frusemide. Responses to both agents were maintained for at least 12 h in vitro, but the responses to carbachol changed in format throughout this period. By contrast CF colons failed to show the normal secretory responses to carbachol and forskolin, most preparations showing a decrease in I sc that was immediately reversed by frusemide. In CF colons addition of Ba2+ ions or tetraethylammonium (TEA+) to the apical bathing solution antagonised the reduction in I sc caused by the secretagogues. It is concluded that the reduction in I sc in CF colons is due to electrogenic K+ secretion and this was confirmed by flux studies using rubidium-86. In normal colons exposed to TEA+ the responses to for-skolin were greater, but not significantly so, presumably because the minor K+-secretory responses are dominated by major chloride-secretory responses. Again rubidium-86 fluxes showed an increase of K+ secretion in normal colons receiving forskolin. Since the amiloride-sensitive current was not different in CF and normal colons there was no evidence that the CF mice were stressed in a way that increased mineralocorticoid levels and hence K+ secretion. Knowledge of the phenotype of the colonic epithelium of the CF mouse sets the baseline from which attempts at gene therapy for the gut must be judged.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374572
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  • 3
    Electronic Resource
    Electronic Resource
    Inactivation of the murine cftr gene abolishes cAMP-mediated but not Ca2+-mediated secretagogue-induced volume decrease in small-intestinal crypts (1993)
    Springer
    Pflügers Archiv 425 (1993), S. 434-438 
    Details
    ISSN: 1432-2013
    Keywords: Small-intestinal crypts ; Intestinal secretion ; Cystic fibrosis ; Chloride conductance ; DIDS ; Glibenclamide ; Mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The cellular volume of crypts isolated from 2- to 3-week-old mouse small intestine has been measured to assess the capacity of the epithelial cells to respond to secretagogues. Vasoactive intestinal polypeptide (VIP) or carbachol, respectively cAMP- and calcium-mediated secretagogues, produced a reduction crypt volume attributed to KCl loss through channels activated by the agonists. Consistent with the participation of separate chloride channels, 4,4′-diisothiocyanatostilbene-2,2′-disulphonic acid (DIDS) blocked the carbacholbut not the VIP-induced volume decrease, whilst gl- ibenclamide abolished the VIP effect without affecting the carbachol-induced volume decrease. Animals homozygous for a disrupted cftr gene, introduced by gene targeting, were also used as the source for crypt isolation. In these CFTR(-/-) crypts, VIP failed to elicit any reduction in cellular volume, while the response to carbachol was indistinguishable from that seen in crypts from age-matched control animals. These results are consistent with murine CFTR being a cAMP-activated chloride channel inhibited by glibenclamide and resistant to DIDS. A separate chloride conductance activated by calcium mobilization in small-intestinal crypts appears to be independent of CFTR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374869
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  • 4
    Electronic Resource
    Electronic Resource
    Calcium-activated chloride conductance is not increased in pancreatic duct cells of CF mice (1995)
    Springer
    Pflügers Archiv 430 (1995), S. 26-33 
    Details
    ISSN: 1432-2013
    Keywords: Pancreas ; Pancreatic duct cell ; Calcium-activated chloride conductance ; CFTR ; Cystic fibrosis ; Transgenic mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Calcium-activated anion secretion is elevated in the pancreatic ductal epithelium of transgenic cf/cf mice which lack the cystic fibrosis transmembrane conductance regulator (CFTR). To elucidate whether this effect is due to increased activity of calcium-activated chloride channels, we have studied the relationship between CFTR and calcium-activated chloride currents in pancreatic duct cells isolated from Cambridge cf/cf mice. CFTR chloride currents activated by cAMP were detected in 59% (29/49) of wild-type cells and in 50% (20/40) of heterozygous cells. However, we could not detect any CFTR currents in the homozygous cf/cf cells (0/25). The maximum CFTR current density measured at a membrane potential of 60 mV was 23.5±2.8 pA/pF (n=29) in wild-type cells, and about half that value, i.e. 12.4±1.6 pA/pF (n=20) in heterozygotes (P=0.004). Calcium-activated chloride currents were detected in 73% (24/33) of wild-type, 75% (21/28) of heterozygous and in 58% (7/12) of homozygous cf/cf cells. There was no significant difference between the steady-state calcium-activated current densities in the three genotypic groups; the current measured at 60 mV being 527±162 pA/pF (n=24) from wild-type, 316±35 pA/pF (n=21) from heterozygote and 419±83 pA/pF (n=7) from homozygous cells. Our data suggest that lack of CFTR does not enhance the calcium-activated chloride conductance in murine pancreatic duct cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00373836
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  • 5
    Electronic Resource
    Electronic Resource
    The intrinsic Cl–conductance of mouse kidney cortex brush-border membrane vesicles is not related to CFTR (1997)
    Springer
    Pflügers Archiv 434 (1997), S. 575-580 
    Details
    ISSN: 1432-2013
    Keywords: Key words Brush-border ; Membrane vesicle ; Cystic fibrosis transmembrane regulator (cftr) ; Alternate Cl ; conductance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstracts  Brush-border membrane vesicles (BBMV) were prepared from whole Balb/c mice kidneys by a Mg2+ precipitation technique. The presence of an intrinsic Cl–conductance co-expressed with Na+/glucose cotransport was inferred by the anion dependence of [14C]glucose uptake and overshoot with inward Na+-anion gradients. In Na+-equilibrated conditions, an inside-negative membrane potential difference (p.d.) produced by an inward Cl–gradient alone was capable of driving intravesicular [14C]glucose accumulation. The apparent anion conductance had a selectivity of Br– = I– = Cl– 〉  F–〉〉 gluconate, was inhibited by 0.5 mM 5-nitro-2- (3-phenylpropylamino)-benzoic acid (NPPB) but was unaffected by 0.5 mM 4,4′-diisothiocyanatostilbene 2,2′-disulphonate (DIDS). BBMV were isolated from mice in which the CFTR gene had been disrupted by a termination mutation (–/–) and compared with normal litter mates (+/+) and heterozygotes (–/+)[18]. [14C]Glucose uptake in NaCl media was significantly greater than glucose uptake in Na gluconate media for all three genotypes measured at 20 s: for homozygous –/– animals [14C]glucose uptake was increased by 2.80 ± 0.53 fold in Cl–media compared to gluconate media, n = 6; for wild-type +/+, by 2.16 ± 0.53 fold, n = 8; and for heterozygous +/– animals, by 2.17 ± 0.45 fold, n = 8. The observation of a Cl–-dependent component in BBMV isolated from homozygous –/– mutant animals shows that the chloride conductance in these vesicles cannot be due to cftr expression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050438
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  • 6
    Electronic Resource
    Electronic Resource
    A comparison of topoisomerase I activity in normal and transformed cells (1986)
    Springer
    Bioscience reports 6 (1986), S. 301-307 
    Details
    ISSN: 1573-4935
    Keywords: topoisomerase I ; transformed cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract Many viral oncogenes encode protein~yrosine kinase activities. However, importantin vivo substrates of these enzymes have yet to be identified. Recently, type I topoisomerases were shown to bein vitro substrates for two tyrosine kinases. Following tyrosine phosphorylation, topoisomerase I activity was reduced 10-fold (Tse-Dinhet al. Nature 312:785–786, 1984). To determine whether topoisomerase I activity was modulated by tyrosine phosphorylationin vivo, we have measured topoisomerase I activity in nuclear lysates prepared from both normal fibroblasts and cells transformed by two different viral oncogenes (v-abl, v-src). Under a variety of experimental conditions, we have found no evidence to support the notion that type I topoisomerase activity is modulated by tyrosine phosphorylationin vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01115159
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  • 7
    Electronic Resource
    Electronic Resource
    Generation of a pseudogene during retroviral infection (1995)
    Springer
    Mammalian genome 6 (1995), S. 90-95 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract During evolution, up to 10% of the mammalian genome may have arisen by rare retroposition events. This process involves reverse transcription of RNA intermediates that originate from retroviral and retrovial-like sequences, highly and middle repetitive DNA elements, and processed pseudogenes. The mechanism, and contemporary nature, for retrotransposition of the viral family and long interspersed elements has been well studied; however, it has proven difficult to demonstrate that the process by which pseudogenes retropose is continuing. In this report a mutation in the murine hypoxanthine-guanosine phosphoribosyl transferase (hprt) gene, which was previously isolated following retroviral infection of ES cells, is shown to result from a de novo retroposition of an α-tubulin pseudogene. Repair of this insertion by homologous recombination restores the activity of the hprt locus, thus confirming the site of mutation. This retroposon bears all the hallmarks of a naturally processed pseudogene [intron loss, presence of a poly(A) tail, and target site duplication] while the retroposition event took place at a known time in well-defined conditions, during retroviral infection of ES cells. The study of this mutation demonstrates that under appropriate conditions pseudogenes of protein-coding genes can still retropose in the mammalian genome. The coincidence of this mutagenic event with retroviral infection suggests that in this situation the reverse transcriptase may have had a retroviral origin, which would implicate a retroviral role in facilitating pseudogene formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00303250
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