Regulation of MHC class I and II gene transcription: differences and similarities

Elsen, Peter J. van den; Gobin, Sam J. P.; Eggermond, Marja C.J.A. van; Peijnenburg, Ad

doi:10.1007/s002510050425

Cited by 120 publications

(87 citation statements)

References 122 publications

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“…2 Also, individual binding of CREB/ATF to the X2 box or NFY binding to the Y box of HLA-G was not observed in contrast to the binding of CREB/ATF and NFY to the X and Y boxes of HLA-B (19). 2 This explains the lack of induction of HLA-G by CIITA (14,18).…”

Section: Discussionmentioning

confidence: 87%

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HLA-G Transactivation by cAMP-response Element-binding Protein (CREB)

Gobin

Biesta

Steenwinkel

et al. 2002

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 87%

“…These regulatory elements include enhancer A, the ISRE, and the SXY module (14). Enhancer A and the ISRE mediate the constitutive and cytokine-induced expression of MHC class I (15,16).…”

mentioning

confidence: 99%

HLA-G Transactivation by cAMP-response Element-binding Protein (CREB)

Gobin

Biesta

Steenwinkel

et al. 2002

Journal of Biological Chemistry

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“…Because the class I and II promoters show significant sequence homologies (6), and both utilize CIITA as a coactivator (4,5), DAIs may be functioning by similar mechanisms in both class I and II. Tissue specific expression of class I is determined, in significant part, by transcriptional mechanisms that depend on upstream negative regulatory elements in the class I promoter (45) and factors binding to these elements may recruit HDACs and repress transcription.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, coactivators, such as class II transactivator (CIITA), 3 Bob1, and CBP/p300, play important roles in the transcriptional regulation of class II (1)(2)(3). Recently, CIITA has been reported to facilitate IFN-␥ induction of MHC class I in addition to class II Ags (4,5), and this, together with the similarities in the structure of the class I and II promoters (6), suggests a commonality in the regulation of MHC genes.…”

mentioning

confidence: 99%

Activation of MHC Class I, II, and CD40 Gene Expression by Histone Deacetylase Inhibitors

Magner¹,

Kazim

Stewart

et al. 2000

The Journal of Immunology

268

224

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Epigenetic mechanisms are involved in regulating chromatin structure and gene expression through repression. In this study, we show that histone deacetylase inhibitors (DAIs) that alter the acetylation of histones in chromatin enhance the expression of several genes on tumor cells including: MHC class I, II, and the costimulatory molecule CD40. Enhanced transcription results in a significant increase in protein expression on the tumor cell surface, and expression can be elicited on some tumors that are unresponsive to IFN-γ. The magnitude of induction of these genes cannot be explained by the effect of DAIs on the cell cycle or enhanced apoptosis. Induction of class II genes by DAIs was accompanied by activation of a repressed class II transactivator gene in a plasma cell tumor but, in several other tumor cell lines, class II was induced in the apparent absence of class II transactivator transcripts. These findings also suggest that the abnormalities observed in some tumors in the expression of genes critical to tumor immunity may result from epigenetic alterations in chromatin and gene regulation in addition to well-established mutational mechanisms.

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“…The major transcription initiation site represented by 8 out of 14 5'-RACE clones was the adenine residue located 26 bp upstream from the translation initiation codon. The promoter region of class Ia genes contains a series of conserved upstream DNA sequences [16]. None of these elements was found in the promoter region of rat or mouse Mill genes.…”

Section: Mill1 and Mill2 Have Multiple Transcription Initiation Sitesmentioning

confidence: 99%

Comparative genomics of the Mill family: a rapidly evolving MHC class I gene family

Watanabe¹,

Maruoka²,

Walter³

et al. 2004

Eur J Immunol

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Mill (MHC class I-like located near the leukocyte receptor complex) is a novel family of class I genes identified in mice that is most closely related to the human MICA/B family. In the present study, we isolated Mill cDNA from rats and carried out a comparative genomic analysis. Rats have two Mill genes orthologous to mouse Mill1 and Mill2 near the leukocyte receptor complex, with expression patterns similar to those of their mouse counterparts. Interspecies sequence comparison indicates that Mill is one of the most rapidly evolving class I gene families and that non-synonymous substitutions occur more frequently than synonymous substitutions in its § 1 domain, implicating the involvement of Mill in immune defenses. Interestingly, the § 2 domain of rat Mill2 contains a premature stop codon in many inbred strains, indicating that Mill2 is not essential for survival. A computer search of the database identified a horse Mill-like expressed sequence tag, indicating that Mill emerged before the radiation of mammals. Hence, the failure to find Mill in human indicates strongly that it was lost from the human lineage. Our present work provides convincing evidence that Mill is akin to the MICA/B family, yet constitutes a distinct gene family.

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Regulation of MHC class I and II gene transcription: differences and similarities

Cited by 120 publications

References 122 publications

HLA-G Transactivation by cAMP-response Element-binding Protein (CREB)

HLA-G Transactivation by cAMP-response Element-binding Protein (CREB)

Activation of MHC Class I, II, and CD40 Gene Expression by Histone Deacetylase Inhibitors

Comparative genomics of the Mill family: a rapidly evolving MHC class I gene family

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