TY - JOUR
T1 - Differential transcriptional control of the h-2k and h-2d loci of the major histocompatibility complex in fibrosacoma cells
AU - Aboud, Mordlechai
AU - Amitai, Hagit
AU - Huleihel, Mahmoud
AU - Har-Vardi, Iris
AU - Gopas, Jacob
AU - Segal, Shraga
N1 - Funding Information:
This study was supported by grants from the Israeli Cancer Association and the Chief scientist Office of the Israeli Health Ministry to M. Aboud, and from the German-Israeli Foundation (GIF) for Scientific Research and Development to s. segal.
PY - 1991/1/1
Y1 - 1991/1/1
N2 - In this study we demonstrate a differential transcription of H-2K and H-2D class-I genes in two different tumor cell clones; one is highly metastatic (IE-7) and the other is not metastatic (IC-9), both derived from the same fibrosarcoma, T-10, induced in an (H-2b x H-2k)F1 mouse. The expression of the two parental H-2K alleles is transcriptionally suppressed in both of these clones. In addition the IC-9 clone does not transcribe also the H-2Dk allele. Our data rule out the possibility that this suppression results from enhanced RNA degradation, impaired polyadenylation, DNA rearrangement, or changes in DMA methylation within these genes. Interferons (IFN) are known to enhance MHC expression by acting on a consensus IFN responsive element present in the promoter region of MHC genes. However, IFN-aL, which is the most potent IFN in this respect, failed to activate the expression of the silent MHC genes in our cells. This finding may reflect a deffect within the promoter region of these genes or changes in their chromatin structure.
AB - In this study we demonstrate a differential transcription of H-2K and H-2D class-I genes in two different tumor cell clones; one is highly metastatic (IE-7) and the other is not metastatic (IC-9), both derived from the same fibrosarcoma, T-10, induced in an (H-2b x H-2k)F1 mouse. The expression of the two parental H-2K alleles is transcriptionally suppressed in both of these clones. In addition the IC-9 clone does not transcribe also the H-2Dk allele. Our data rule out the possibility that this suppression results from enhanced RNA degradation, impaired polyadenylation, DNA rearrangement, or changes in DMA methylation within these genes. Interferons (IFN) are known to enhance MHC expression by acting on a consensus IFN responsive element present in the promoter region of MHC genes. However, IFN-aL, which is the most potent IFN in this respect, failed to activate the expression of the silent MHC genes in our cells. This finding may reflect a deffect within the promoter region of these genes or changes in their chromatin structure.
UR - http://www.scopus.com/inward/record.url?scp=0025945306&partnerID=8YFLogxK
U2 - 10.3109/08820139109082628
DO - 10.3109/08820139109082628
M3 - Article
AN - SCOPUS:0025945306
SN - 0882-0139
VL - 20
SP - 475
EP - 485
JO - Immunological Investigations
JF - Immunological Investigations
IS - 5-6
ER -