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  • 1
    Electronic Resource
    Electronic Resource
    Connexin family of gap junction proteins (1990)
    Springer
    The journal of membrane biology 116 (1990), S. 187-194 
    Details
    ISSN: 1432-1424
    Keywords: gap junctions ; connexin ; intercellular communication ; molecular cloning
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01868459
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  • 2
    Electronic Resource
    Electronic Resource
    GENETIC DISEASES AND GENE KNOCKOUTS REVEAL DIVERSE CONNEXIN FUNCTIONS (1999)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Physiology 61 (1999), S. 283-310 
    Details
    ISSN: 0066-4278
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine , Biology
    Notes: Abstract Intercellular channels present in gap junctions allow cells to share small molecules and thus coordinate a wide range of behaviors. Remarkably, although junctions provide similar functions in all multicellular organisms, vertebrates and invertebrates use unrelated gene families to encode these channels. The recent identification of the invertebrate innexin family opens up powerful genetic systems to studies of intercellular communication. At the same time, new information on the physiological roles of vertebrate connexins has emerged from genetic studies. Mutations in connexin genes underlie a variety of human diseases, including deafness, demyelinating neuropathies, and lens cataracts. In addition, gene targeting of connexins in mice has provided new insights into connexin function and the significance of connexin diversity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.physiol.61.1.283
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  • 3
    Electronic Resource
    Electronic Resource
    Voltage gating of connexins (1994)
    [s.l.] : Nature Publishing Group
    Nature 371 (1994), S. 208-209 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] SIR - Connexins (Cx) oligomerize into channels (called connexons) that span a single plasma membrane. Connexons in adjacent cells align to form complete intercellular channels that are sensitive to the voltage difference between the cytoplasms of the coupled cells. Because the intercellular channel ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/371208a0
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  • 4
    Electronic Resource
    Electronic Resource
    Female infertility in mice lacking connexin 37 (1997)
    [s.l.] : Nature Publishing Group
    Nature 385 (1997), S. 525-529 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Immunocytochemistry was performed on frozen sections of mouse ovaries to investigate the composition of oocyte-granulosa cell gap junctions. Antibodies specific for connexins (Cx) 37,40 and 43 were used because their messenger RNAs had been previously detected in ovary6"8. Anti-Cx37 antibodies9 ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/385525a0
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  • 5
    Electronic Resource
    Electronic Resource
    Connexin mutations in deafness (1998)
    [s.l.] : Macmillan Magazines Ltd.
    Nature 394 (1998), S. 630-631 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Genetic deafness is one of the most prevalent inherited sensory disorders, affecting about 1 in 2,000 children. Mutations in the connexin 26 gene have been associated with autosomal recessive non-syndromic deafness (DFNB1). The connexin 26 gene is a member of the connexin family of genes, which ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/29202
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  • 6
    Electronic Resource
    Electronic Resource
    Functional defects of Cx26 resulting from a heterozygous missense mutation in a family with dominant deaf-mutism and palmoplantar keratoderma (1998)
    Springer
    Human genetics 〈Berlin〉 103 (1998), S. 393-399 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Mutations in GJB2 encoding the gap junction protein connexin-26 (Cx26) have been established as the basis of autosomal recessive non-syndromic hearing loss. The involvement of GJB2 in autosomal dominant deafness has also been proposed, although the putative mutation identified in one family with both deafness and palmoplantar keratoderma has recently been suggested to be merely a non-disease associated polymorphism. We have observed a similar phenotype in an Egyptian family that segregated with a heterozygous missense mutation of GJB2, leading to a non-conservative amino acid substitution (R75W). The deleterious dominant-negative effect of R75W on gap channel function was subsequently demonstrated in the paired oocyte expression system. Not only was R75W alone incapable of inducing electrical conductance between adjacent cells, but it almost completely suppressed the activity of co-expressed wildtype protein. The Cx26 mutant W77R, which has been implicated in autosomal recessive deafness, also failed to form functional gap channels by itself but did not significantly interfere with the function of wildtype Cx26. These data provide compelling evidence for the serious functional consequences of Cx26 mutations in dominant and recessive deafness.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004390050839
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  • 7
    Electronic Resource
    Electronic Resource
    Computationally modeling organizational learning and adaptability as resource allocation: An artificial adaptive systems approach (1996)
    Springer
    Computational & mathematical organization theory 2 (1996), S. 301-324 
    Details
    ISSN: 1572-9346
    Keywords: complex adaptive system ; organizational learning ; genetic algorithm ; resource allocation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mathematics
    Notes: Abstract A framework for and a computational model of organizational behavior based on an artificial adaptive system (AAS) is presented. An AAS, a modeling approach based on genetic algorithms, enables the modeling of organizational learning and adaptability. This learning can be represented as decisions to allocate resources to the higher performing organizational agents (i.e., individuals, groups, departments, or processes, depending on the level of analysis) critical to the organization's survival in different environments. Adaptability results from the learning function enabling the organizations to change as the environment changes. An AAS models organizational behavior from a micro-unit perspective, where organizational behavior is a function of the aggregate actions and interactions of each of the individual agents of which the organization is composed. An AAS enables organizational decision making in a dynamic environment to be modeled as a satisficing process and not as a maximization process. To demonstrate the feasibility and usefulness of such an approach, a financial trading adaptive system (FTAS) organization is computationally modeled based on the AAS framework. An FTAS is an example of how the learning mechanism in an AAS can be used to allocate resources to critical individuals, processes, functions, or departments within an organization.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00132314
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  • 8
    Electronic Resource
    Electronic Resource
    Connexin32, a gap junction protein, is a persistent oogenetic product through preimplantation development of the mouse (1989)
    Chichester [u.a.] : Wiley-Blackwell
    Developmental Genetics 10 (1989), S. 318-323 
    Details
    ISSN: 0192-253X
    Keywords: Mouse embryos ; Gap junctions ; Connexin43 ; mRNA ; Life and Medical Sciences ; Genetics
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: Gap junctions appear de novo during compaction in the eight-cell stage of mouse development. This is a critical event in the life of the embryo, because gap junctional intercellular communication is an essential requirement for maintaining compaction and, hence, for development of the blastocyst. Recently, a family of genes encoding gap junction proteins (connexins) has been identified and cloned, and we have taken advantage of the availability of antibodies and cDNA probes to investigate the expression of these genes in early development. We found that a protein with antigenic and size similarity to the “liver” gap junction protein, connexin32, is present throughout preimplantation development from the zygote through the late morula. Connexin32 mRNA, however, could not be detected in any preimplantation stage. This, and the presence of connexin32 in zygotes before activation of embryonic transcription, leads us to conclude that this protein is inherited as an oogenetic product that persists well beyond the transition from the oogenetic to embryonic program of gene expression. Furthermore, we found that mRNA for another gap junction protein, connexin43, is fairly abundant in preimplantation embryos. We conclude that it is more likely connexin43, and not connexin32, that is used to assemble new connexons as the level of intercellular coupling increases after compaction.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/dvg.1020100407
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  • 9
    Electronic Resource
    Electronic Resource
    Zygotic expression of the connexin43 gene supplies subunits for gap junction assembly during mouse preimplantation development (1991)
    New York, NY [u.a.] : Wiley-Blackwell
    Molecular Reproduction and Development 30 (1991), S. 18-26 
    Details
    ISSN: 1040-452X
    Keywords: Gap junction protein ; Gene expression ; Compaction ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: De novo assembly of gap junctions begins during compaction in the eight-cell stage of mouse development, and intercellular coupling mediated by gap junctions appears to be required for maintenance of the compacted state. We have begun to explore the expression of the family of genes encoding the connexins, the proteins that form the gap junction channels. We recently reported that a protein with antigenic and size similarity with connexin32, the rat liver gap junction protein, is inherited as an oogenetic product by the mouse zygote, but its gene appears not to be transcribed prior to implantation (Barron et al., Dev Genet 10:318-323, 1989). Here we report that another member of this gene family, connexin43, is transcribed by the embryonic genome from shortly after the time of genomic activation. As revealed by Northern blotting, connexin43 mRNA is absent from ovulated oocytes, becomes detectable in the 4-cell stage, and accumulates steadily thereafter to reach a maximum in blastocysts. In contrast, no transcripts of connexin26 could be detected in any preimplantation stage. A protein with antigenic and size similarity with connexin43 from rat heart was found by Western blotting to accumulate from the four-cell stage onward. Immunofluorescence analysis with embryo whole mounts was used to demonstrate that this protein is incorporated into punctate interblastomeric foci during compaction, consistent with its assembly into gap junction plaques. We conclude that connexin43 is one member of the connexin gene family whose zygotic expression is critical for preimplantation morphogenesis.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/mrd.1080300103
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  • 10
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    Gap Junctions Contribute to Differential Light Adaptation across Direction-Selective Retinal Ganglion Cells (2018)
    Cell Press
    Details
    Publication Date: 2018-10-01
    Print ISSN: 0896-6273
    Electronic ISSN: 1097-4199
    Topics: Biology , Medicine
    Published by Cell Press
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