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. 1981 Sep;78(9):5754-8.
doi: 10.1073/pnas.78.9.5754.

Control of expression of histocompatibility antigens (H-2) and beta 2-microglobulin in F9 teratocarcinoma stem cells

C M Croce, A Linnenbach, K Huebner, J R Parnes, D H Margulies, E Appella, J G Seidman

Control of expression of histocompatibility antigens (H-2) and beta 2-microglobulin in F9 teratocarcinoma stem cells

C M Croce et al. Proc Natl Acad Sci U S A. 1981 Sep.

Abstract

Murine teratocarcinoma stem cells, unlike most other cell types, do not express major histocompatibility antigens. The steady-state levels of beta 2-microglobulin and H-2 mRNA from F9-derived teratocarcinoma stem and differentiated cells were examined by blot hybridization using cloned DNA probes specific for these mRNAs. No H-2- or beta 2-microglobulin-specific RNA was detected in F9 teratocarcinoma stem cells (clone 12-1); thus, F9 teratocarcinoma stem cells (clone 12-1) contain no more than 1/10 the H-2 and beta 2-microglobulin mRNAs of the differentiated daughter cells (clone 12-1a). We suggest that this regulation of major histocompatibility antigen expression is due to transcriptional control of the major histocompatibility antigen genes, H-2 and beta 2-microglobulin. The transcriptional regulation of these genes is accompanied by a change in their DNase I sensitivity. Normally, transcriptionally inactive genes are DNase I resistant, while active genes are DNase I sensitive. In contrast, the silent major histocompatibility antigen genes of teratocarcinoma stem cells are more DNase I sensitive than the active genes of the differentiated cells.

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References

    1. Nature. 1969 May 24;222(5195):783-4 - PubMed
    1. Proc Natl Acad Sci U S A. 1981 Aug;78(8):5071-5 - PubMed
    1. Proc Natl Acad Sci U S A. 1972 Jun;69(6):1408-12 - PubMed
    1. Transplantation. 1973 Feb;15(2):211-4 - PubMed
    1. Transplantation. 1973 Dec;16(6):675-8 - PubMed

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