Identification and characterization of a new major histocompatibility complex class I gene in carp (Cyprinus carpio L .)

1996 ◽  
Vol 44 (1) ◽  
pp. 49-61 ◽  
Author(s):  
Saskia H. M. van Erp ◽  
Brian Dixon ◽  
Felipe Figueroa ◽  
Egbert Egberts ◽  
R. J. M. Stet
1987 ◽  
Vol 7 (11) ◽  
pp. 4003-4009
Author(s):  
C Bieberich ◽  
T Yoshioka ◽  
K Tanaka ◽  
G Jay ◽  
G Scangos

The regulated expression of major histocompatibility complex class I antigens is essential for assuring proper cellular immune responses. To study H-2 class I gene regulation, we have transferred a foreign class I gene to inbred mice and have previously shown that the heterologous class I gene was expressed in a tissue-dependent manner. In this report, we demonstrate that these mice expressed the transgenic class I molecule on the cell surface without any alteration in the level of endogenous H-2 class I antigens. Skin grafts from transgenic mice were rapidly rejected by mice of the background strain, indicating that the transgenic antigen was expressed in an immunologically functional form. As with endogenous H-2 class I genes, the class I transgene was inducible by interferon treatment and suppressible by human adenovirus 12 transformation. Linkage analysis indicated that the transgene was not closely linked to endogenous class I loci, suggesting that trans-regulation of class I genes can occur for class I genes located outside the major histocompatibility complex.


Genetica ◽  
2017 ◽  
Vol 145 (6) ◽  
pp. 541-558
Author(s):  
Drashti R. Parmar ◽  
Siuli Mitra ◽  
Snehalata Bhadouriya ◽  
Tirupathi Rao ◽  
Vaishnavi Kunteepuram ◽  
...  

1990 ◽  
Vol 10 (8) ◽  
pp. 4100-4109 ◽  
Author(s):  
U Henseling ◽  
W Schmidt ◽  
H R Schöler ◽  
P Gruss ◽  
A K Hatzopoulos

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.


1987 ◽  
Vol 7 (11) ◽  
pp. 4003-4009 ◽  
Author(s):  
C Bieberich ◽  
T Yoshioka ◽  
K Tanaka ◽  
G Jay ◽  
G Scangos

The regulated expression of major histocompatibility complex class I antigens is essential for assuring proper cellular immune responses. To study H-2 class I gene regulation, we have transferred a foreign class I gene to inbred mice and have previously shown that the heterologous class I gene was expressed in a tissue-dependent manner. In this report, we demonstrate that these mice expressed the transgenic class I molecule on the cell surface without any alteration in the level of endogenous H-2 class I antigens. Skin grafts from transgenic mice were rapidly rejected by mice of the background strain, indicating that the transgenic antigen was expressed in an immunologically functional form. As with endogenous H-2 class I genes, the class I transgene was inducible by interferon treatment and suppressible by human adenovirus 12 transformation. Linkage analysis indicated that the transgene was not closely linked to endogenous class I loci, suggesting that trans-regulation of class I genes can occur for class I genes located outside the major histocompatibility complex.


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