Interferon γ (IFNγ) gene transfer of an EMT6 tumor that is poorly responsive to IFNγ stimulation: increase in tumor immunogenicity is accompanied by induction of a mouse class II transactivator and class II MHC

1996 ◽  
Vol 42 (2) ◽  
pp. 99-107 ◽  
Author(s):  
Monica C. Panelli ◽  
E. Wang ◽  
Shanxiang Shen ◽  
Samuel F. Schluter ◽  
Ralph M. Bernstein ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Class Ii ◽  
Interferon Γ ◽  
Class Ii Transactivator ◽  
Class Ii Mhc ◽  
Tumor Immunogenicity ◽  
Emt6 Tumor ◽  
Mouse Class

scholarly journals 17β-Estradiol Inhibits Class II Major Histocompatibility Complex (MHC) Expression: Influence on Histone Modifications and CBP Recruitment to the Class II MHC Promoter

2004 ◽  
Vol 18 (8) ◽  
pp. 1963-1974 ◽  
Author(s):  
Jill Adamski ◽  
Zhendong Ma ◽  
Susan Nozell ◽  
Etty N. Benveniste
Keyword(s):  
Major Histocompatibility Complex ◽  
Histone Acetylation ◽  
Binding Protein ◽  
Class Ii ◽  
Interferon Γ ◽  
Class Ii Transactivator ◽  
Protein Levels ◽  
Histocompatibility Complex ◽  
Class Ii Mhc ◽  
17Β Estradiol

Abstract Major histocompatibility complex (MHC) class II proteins are important for the initiation of immune responses and are essential for specific recognition of foreign antigens by the immune system. Regulation of class II MHC expression primarily occurs at the transcriptional level. The class II transactivator protein is the master regulator that is essential for both constitutive and interferon-γ-inducible class II MHC expression. Estrogen [17β-estradiol (17β-E2)] has been shown to have immunomodulatory effects. In this study, we show that 17β-E2 down-regulates interferon-γ inducible class II MHC protein levels on brain endothelial cells, as well as other cell types (astrocytes, fibrosacroma cells, macrophages). The inhibitory effects of 17β-E2 on class II MHC expression are not due to changes in class II transactivator mRNA or protein levels, rather, 17β-E2 mediates inhibition at the level of class II MHC gene expression. We demonstrate that 17β-E2 attenuates H3 and H4 histone acetylation and cAMP response element binding protein-binding protein association with the class II MHC promoter, suggesting that 17β-E2 inhibits class II MHC expression by a novel mechanism involving modification of the histone acetylation status of the class II MHC promoter.

scholarly journals Pulling a Ligase out of a “HAT”: pCAF Mediates Ubiquitination of the Class II Transactivator

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Julie E. Morgan ◽  
Susanna F. Greer
Keyword(s):  
Posttranslational Modifications ◽  
Histone Acetyltransferase ◽  
E3 Ligase ◽  
Class Ii ◽  
Nuclear Region ◽  
Class Ii Transactivator ◽  
Mhc Ii ◽  
Major Histocompatibility Class Ii ◽  
Class Ii Mhc ◽  
Cellular Movement

The Class II Transactivator (CIITA) is essential to the regulation of Major Histocompatibility Class II (MHC II) genes transcription. As the “master regulator” of MHC II transcription, CIITA regulation is imperative and requires various posttranslational modifications (PTMs) in order to facilitate its role. Previously we identified various ubiquitination events on CIITA. Monoubiquitination is important for CIITA transactivity, while K63 linked ubiquitination is involved in crosstalk with ERK1/2 phosphorylation, where together they mediate cellular movement from the cytoplasm to nuclear region. Further, CIITA is also modified by degradative K48 polyubiquitination. However, the E3 ligase responsible for these modifications was unknown. We show CIITA ubiquitination and transactivity are enhanced with the histone acetyltransferase (HAT), p300/CBP associated factor (pCAF), and the E3 ligase region within pCAF is necessary for both. Additionally, pCAF mediated ubiquitination is independent of pCAF’s HAT domain, and acetylation deficient CIITA is K48 polyubiquitinated and degraded in the presence of pCAF. Lastly, we identify the histone acetyltransferase, pCAF, as the E3 ligase responsible for CIITA’s ubiquitination.

Interferon-γ response region in the promoter of the class II MHC gene, DPA

1992 ◽  
Vol 35 (3) ◽  
pp. 157-164 ◽  
Author(s):  
Minoru Sugawara ◽  
Paul D. Ponath ◽  
Zhi Yang ◽  
Jack L. Strominger
Keyword(s):  
Class Ii ◽  
Interferon Γ ◽  
Class Ii Mhc ◽  
Response Region

The Use of Mouse Class II MHC Peptides to Produce Site-Specific Monoclonal Antibodies

1989 ◽  
pp. 181-185
Author(s):  
Christopher J. Krco ◽  
Thomas G. Beito ◽  
Roger G. Little ◽  
Jay Zeller ◽  
Daniel M. McCormick ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Class Ii ◽  
Site Specific ◽  
Class Ii Mhc ◽  
Mouse Class
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