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A transcription factor interacting with the class I gene enhancer is inactive in tumorigenic cell lines which suppress major histocompatibility complex class I genes.

Henseling U, Schmidt W, Schöler HR, Gruss P, Hatzopoulos AK
Mol Cell Biol. 1990 10 (8): 4100-9

PMID: 2196446 · PMCID: PMC360928 · DOI:10.1128/mcb.10.8.4100

AKR leukemias display different amounts of major histocompatibility complex class I antigens on the cell surface. The absence of H-2Kk molecules correlates with the ability of these cell lines to form tumors in vivo as well as to escape lysis by cytotoxic T lymphocytes in vitro. In this report it is shown that the 5' regulatory area of the H-2Kk gene failed to activate transcription in H-2Kk-negative cells. Examination of the proteins interacting with the H-2Kk enhancer in expressing and nonexpressing cells revealed clear differences. In particular, the level of a nuclear protein interacting at position -166 was greatly reduced in the negative cell lines. A transcription factor, known as H2TF1 or KBF1, has been shown previously to interact with this binding site and to be essential for the expression of certain class I genes as well as the expression of beta 2-microglobulin. These results demonstrate that the molecular mechanism of class I gene suppression in malignant tumor cells is at the level of transcription and is most probably modulated by H2TF1/KBFI. In addition, it is shown that the same transcription factor is only present in mouse tissues expressing class I antigens.

MeSH Terms (18)

Animals Base Sequence Cell Line Enhancer Elements, Genetic Flow Cytometry Fluorescent Antibody Technique Genes, MHC Class I H-2 Antigens Leukemia, Experimental Mice Molecular Sequence Data Oligonucleotide Probes Restriction Mapping RNA, Messenger Suppression, Genetic Transcription, Genetic Transcription Factors Tumor Cells, Cultured

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