NDLI: Analysis of the defect in DNA end joining in the murine scid mutation.

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In vivo transcriptional analysis of the TATA-less promoter of the Drosophila melanogaster vermilion gene.

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Activation of c-Src in cells bearing v-Crk and its suppression by Csk.

Regulation of collagen I gene expression by ras.

Activated lck tyrosine protein kinase stimulates antigen-independent interleukin-2 production in T cells.

Localization of a DNA replication origin and termination zone on chromosome III of Saccharomyces cerevisiae.

Biphasic increase in c-jun mRNA is required for induction of AP-1-mediated gene transcription: differential effects of muscarinic and thrombin receptor activation.

Molecular involvement of the pvt-1 locus in a gamma/delta T-cell leukemia bearing a variant t(8;14)(q24;q11) translocation.

Analysis of the defect in DNA end joining in the murine scid mutation.

Maximal serum stimulation of the c-fos serum response element requires both the serum response factor and a novel binding factor, SRE-binding protein.

A proposed mechanism for promoter-associated DNA rearrangement events at a variant surface glycoprotein gene expression site.

cis-acting elements involved in the alternative translation initiation process of human basic fibroblast growth factor mRNA.

GAL11 protein, an auxiliary transcription activator for genes encoding galactose-metabolizing enzymes in Saccharomyces cerevisiae.

Construction of a Bifunctional mRNA in the Mouse by Using the Internal Ribosomal Entry Site of the Encephalomyocarditis Virus

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Analysis of the defect in DNA end joining in the murine scid mutation.

Content Provider	PubMed Central
Author	Harrington, J. Hsieh, C. L. Gerton, J. Bosma, G. Lieber, M. R.
Abstract	Murine severe combined immune deficiency (scid) is marked by a 5,000-fold reduction in coding joint formation in V(D)J recombination of antigen receptors. Others have demonstrated a sensitivity to double-strand breaks generated by ionizing radiation and bleomycin. We were interested in establishing the extent of the defect in intramolecular and intermolecular DNA end joining in lymphoid and nonlymphoid cells from scid mice. We conducted a series of studies probing the ability of these cells to resolve free ends of linear DNA molecules having various biochemical end configurations. We find that the stable integration of linear DNA into scid fibroblasts is reduced 11- to 75-fold compared with that in normal fibroblasts. In contrast, intramolecular and intermolecular end joining occur at normal frequencies in scid lymphocytes and fibroblasts. This normal level of end joining is observed regardless of the type of overhang and regardless of the requirement for nucleolytic activities prior to ligation. The fact that free ends having a wide variety of end configurations are recircularized normally in scid cells rules out certain models for the defect in scid. We discuss the types of DNA end joining reactions that are and are not affected in this double-strand break repair defect in the context of a hairpin model for V(D)J recombination.
Starting Page	4758
File Format	PDF
ISSN	10985549
e-ISSN	10985549
Journal	Molecular and Cellular Biology
Issue Number	10
Volume Number	12
Language	English
Publisher Date	1992-10-01
Access Restriction	Open
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Molecular Biology

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