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  • 1
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    Online Resource
    Unraveling of the Polymorphic Cλ2-Cλ3 Amplification and the Ke+Oz− Polymorphism in the Human Igλ Locus
    The American Association of Immunologists ; 2002
    In:  The Journal of Immunology Vol. 169, No. 1 ( 2002-07-01), p. 271-276
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 169, No. 1 ( 2002-07-01), p. 271-276
    Abstract: Two polymorphisms of the human Igλ (IGL) locus have been described. The first polymorphism concerns a single, 2- or 3-fold amplification of 5.4 kb of DNA in the Cλ2-Cλ3 region. The second polymorphism is the Mcg−Ke+Oz− isotype, which has only been defined via serological analyses in Bence-Jones proteins of multiple myeloma patients and was assumed to be encoded by a polymorphic Cλ2 segment because of its high homology with the Mcg−Ke−Oz− Cλ2 isotype. It has been speculated that the Mcg−Ke+Oz− isotype might be encoded by a Cλ gene segment of the amplified Cλ2-Cλ3 region. We now unraveled both IGL gene polymorphisms. The amplification polymorphism appeared to result from a duplication, triplication, or quadruplication of a functional J-Cλ2 region and is likely to have originated from unequal crossing over of the J-Cλ2 and J-Cλ3 region via a 2.2-kb homologous repeat. The amplification polymorphism was found to result in the presence of one to five extra functional J-Cλ2 per genome regions, leading to decreased Igκ:Igλ ratios on normal peripheral blood B cells. Via sequence analysis, we demonstrated that the Mcg−Ke+Oz− isotype is encoded by a polymorphic Cλ2 segment that differs from the normal Cλ2 gene segment at a single nucleotide position. This polymorphism was identified in only 1.5% (2 of 134) of individuals without J-Cλ2 amplification polymorphism and was not found in the J-Cλ2 amplification polymorphism of 44 individuals, indicating that the two IGL gene polymorphisms are not linked.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.169.1.271
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2002
    detail.hit.zdb_id: 1475085-5
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  • 2
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    Basic helix-loop-helix proteins E2A and HEB induce immature T-cell receptor rearrangements in nonlymphoid cells
    American Society of Hematology ; 2001
    In:  Blood Vol. 98, No. 8 ( 2001-10-15), p. 2456-2465
    Details
    In: Blood, American Society of Hematology, Vol. 98, No. 8 ( 2001-10-15), p. 2456-2465
    Abstract: T-cell receptor (TCR) gene rearrangements are mediated via V(D)J recombination, which is strictly regulated during lymphoid differentiation, most probably through the action of specific transcription factors. Investigated was whether cotransfection ofRAG1 and RAG2 genes in combination with lymphoid transcription factors can induce TCR gene rearrangements in nonlymphoid human cells. Transfection experiments showed that basic helix-loop-helix transcription factors E2A and HEB induce rearrangements in the TCRD locus (Dδ2-Dδ3 and Vδ2-Dδ3) and TCRG locus (ψ Vγ7-Jγ2.3 and Vγ8-Jγ2.3). Analysis of these rearrangements and their circular excision products revealed some peculiar characteristics. The Vδ2-Dδ3 rearrangements were formed by direct coupling without intermediate Dδ2 gene segment usage, and most Dδ2-Dδ3 recombinations occurred via direct coupling of the respective upstream and downstream recombination signal sequences (RSSs) with deletion of the Dδ2 and Dδ3 coding sequences. Subsequently, the E2A/HEB–induced TCR gene recombination patterns were compared with those in early thymocytes and acute lymphoblastic leukemias of T- and B-lineage origin, and it was found that the TCR rearrangements in the transfectants were early (immature) and not necessarily T-lineage specific. Apparently, some parts of theTCRD (Vδ2-Dδ region) and TCRG genes are accessible for recombination not only in T cells, but also in early B-cells and even in nonlymphoid cells if the appropriate transcription factors are present. The transfection system described here appeared to be useful for studying the accessibility of immunoglobulin and TCR genes for V(D)J recombination, but might also be applied to study the induction of RSS-mediated chromosome aberrations.
    Type of Medium: Online Resource
    ISSN: 1528-0020 , 0006-4971
    URL: Article
    DOI: 10.1182/blood.V98.8.2456
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2001
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 3
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    Unraveling the Consecutive Recombination Events in the Human IGK Locus
    The American Association of Immunologists ; 2004
    In:  The Journal of Immunology Vol. 173, No. 6 ( 2004-09-15), p. 3878-3888
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 173, No. 6 ( 2004-09-15), p. 3878-3888
    Abstract: In addition to the classical Vκ-Jκ, Vκ-κ deleting element (Kde), and intron-Kde gene rearrangements, atypical recombinations involving Jκ recombination signal sequence (RSS) or intronRSS elements can occur in the Igκ (IGK) locus, as observed in human B cell malignancies. In-depth analysis revealed that atypical JκRSS-intronRSS, Vκ-intronRSS, and JκRSS-Kde recombinations not only occur in B cell malignancies, but rather reflect physiological gene rearrangements present in normal human B cells as well. Excision circle analysis and recombination substrate assays can discriminate between single-step vs multistep rearrangements. Using this combined approach, we unraveled that the atypical Vκ-intronRSS and JκRSS-Kde pseudohybrid joints most probably result from ongoing recombination following an initial aberrant JκRSS-intronRSS signal joint formation. Based on our observations in normal and malignant human B cells, a model is presented to describe the sequential (classical and atypical) recombination events in the human IGK locus and their estimated relative frequencies (0.2–1.0 vs & lt;0.03). The initial JκRSS-intronRSS signal joint formation (except for Jκ1RSS-intronRSS) might be a side event of an active V(D)J recombination mechanism, but the subsequent formation of Vκ-intronRSS and JκRSS-Kde pseudohybrid joints can represent an alternative pathway for IGK allele inactivation and allelic exclusion, in addition to classical Cκ deletions. Although usage of this alternative pathway is limited, it seems essential for inactivation of those IGK alleles that have undergone initial aberrant recombinations, which might otherwise hamper selection of functional Ig L chain proteins.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.173.6.3878
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2004
    detail.hit.zdb_id: 1475085-5
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