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Class II, major histocompatibility complex, transactivator

CIITA, class II transactivator, MHC class II transactivator
This gene encodes a protein with an acidic transcriptional activation domain, 4 LRRs (leucine-rich repeats) and a GTP binding domain. The protein is located in the nucleus and acts as a positive regulator of class II major histocompatibility complex gene transcription, and is referred to as the "master control factor" for the expression of these genes. The protein also binds GTP and uses GTP binding to facilitate its own transport into the nucleus. Once in the nucleus it does not bind DNA but rather uses an intrinsic acetyltransferase (AT) activity to act in a coactivator-like fashion. Mutations in this gene have been associated with bare lymphocyte syndrome type II (also known as hereditary MHC class II deficiency or HLA class II-deficient combined immunodeficiency), increased susceptibility to rheumatoid arthritis, multiple sclerosis, and possibly myocardial infarction. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: MHC, IFN-gamma, CAN, CD4, Histone
Papers using CIITA antibodies
Interferons, immunity and cancer immunoediting
Marx Alexander et al., In ISRN Oncology, 2005
... To detect CIITA we used a goat anti-human antibody from Santa Cruz Biotechnology (Santa Cruz, CA, USA), ...
Papers on CIITA
A phase II study of belinostat (PXD101) in relapsed and refractory aggressive B-cell lymphomas: SWOG S0520.
Persky et al., Tucson, United States. In Leuk Lymphoma, Feb 2016
Transcription of MHCII is controlled by CIITA which in turn is regulated by histone acetylation.
Repression of CIITA by the Epstein-Barr virus transcription factor Zta is independent of its dimerization and DNA binding.
Sinclair et al., Burgess Hill, United Kingdom. In J Gen Virol, Jan 2016
UNASSIGNED: Repression of the cellular CIITA gene is part of the immune evasion strategy of the γherpes virus Epstein-Barr virus (EBV) during its lytic replication cycle in B-cells.
Absence of nonhematopoietic MHC class II expression protects mice from experimental autoimmune myocarditis.
Acha-Orbea et al., Lausanne, Switzerland. In Eur J Immunol, Jan 2016
EAM was induced in susceptible mice lacking inducible expression of MHCII molecules on all nonhematopoietic cells (pIV-/- K14 CIITA Tg mice) by immunization with α-myosin heavy chain peptide (α-MyHC) in CFA.
HDAC4 mediates IFN-γ induced disruption of energy expenditure-related gene expression by repressing SIRT1 transcription in skeletal muscle cells.
Xu et al., Nanjing, China. In Biochim Biophys Acta, Dec 2015
Previously we have shown that the pro-inflammatory cytokine interferon gamma (IFN-γ) disrupts energy expenditure in skeletal muscle cells via hypermethylated in cancer 1 (HIC1)-class II transactivator (CIITA) dependent repression of SIRT1 transcription.
Comparing spatial expression dynamics of bovine blastocyst under three different procedures: in-vivo, in-vitro derived, and somatic cell nuclear transfer embryos.
Kawahara et al., In Jpn J Vet Res, Nov 2015
Comparing spatial expression dynamics of bovine blastocyst under three different procedures revealed that CIITA was expressed in ICM-side samples of all the embryo types.
Genomic alterations underlying immune privilege in malignant lymphomas.
Steidl et al., Vancouver, Canada. In Curr Opin Hematol, Jul 2015
These prominently include structural genomic changes of the CIITA and programmed death ligand (CD274/PDCD1LG2) loci, alterations affecting antigen presentation and mutations in JAK-STAT and NFκB signaling pathways.
Discovery of six new susceptibility loci and analysis of pleiotropic effects in leprosy.
Zhang et al., Jinan, China. In Nat Genet, Mar 2015
Besides confirming all previously published loci, we discovered six new susceptibility loci, and further gene prioritization analysis of these loci implicated BATF3, CCDC88B and CIITA-SOCS1 as new susceptibility genes for leprosy.
Structural genomic alterations in primary mediastinal large B-cell lymphoma.
Steidl et al., Vancouver, Canada. In Leuk Lymphoma, 2014
These structural alterations prominently include transcript and protein altering rearrangements and copy number variations of the programmed death ligands 1 (CD274) and 2 (PDCD1LG2), CIITA, JAK2 and REL.
MHC class I and II deficiencies.
Etzioni et al., Haifa, Israel. In J Allergy Clin Immunol, 2014
These transacting factors are the class II transactivator and 3 subunits of regulatory factor X (RFX): RFX containing ankyrin repeats (RFXANK), the fifth member of the RFX family (RFX5), and RFX-associated protein (RFXAP).
New concepts of immune modulation in xenotransplantation.
Cooper et al., Pittsburgh, United States. In Transplantation, 2014
The exogenous immunosuppressive regimen may be significantly reduced by the presence of a graft from a pig transgenic for a mutant (human) class II transactivator gene, resulting in down-regulation of swine leukocyte antigen class II expression, or from a pig with "local" vascular endothelial cell expression of an immunosuppressive gene (e.g., CTLA4-Ig).
NLRC5: a key regulator of MHC class I-dependent immune responses.
van den Elsen et al., College Station, United States. In Nat Rev Immunol, 2012
NLRC5 and the master regulator for MHC class II genes, class II transactivator (CIITA), interact with similar MHC promoter-bound factors.
Unsolved Mysteries in NLR Biology.
Kanneganti et al., Memphis, United States. In Front Immunol, 2012
Although most NLRs play some role in immunity, their functions range from regulating antigen presentation (NLRC5, CIITA) to pathogen/damage sensing (NLRP1, NLRP3, NLRC1/2, NLRC4) to suppression or modulation of inflammation (NLRC3, NLRP6, NLRP12, NLRX1).
CIITA gene variants are associated with rheumatoid arthritis in Scandinavian populations.
Lie et al., Oslo, Norway. In Genes Immun, 2012
Our results support involvement of CIITA in RA, but imply that this is population dependent and that the aetiological variant is yet to be discovered.
Kaposi's sarcoma-associated herpesvirus inhibits expression and function of endothelial cell major histocompatibility complex class II via suppressor of cytokine signaling 3.
Blackbourn et al., Birmingham, United Kingdom. In J Virol, 2012
IFN-gamma-induced phosphorylation of STAT-1 and transcription of CIITA were suppressed in Kaposi's sarcoma-associated herpesvirus-inoculated endothelial cells via a mechanism involving SOCS3 (suppressor of cytokine signaling 3).
Mutated major histocompatibility complex class II transactivator up-regulates interleukin-33-dependent differentiation of Th2 subset through Nod2 binding for NLR (NOD-like receptor) signaling initiation.
Chou et al., Shanghai, China. In J Biol Chem, 2012
Mutated major histocompatibility complex class II transactivator up-regulates interleukin-33-dependent differentiation of Th2 subset through Nod2 binding for NLR (NOD-like receptor) signaling initiation.
Interaction analysis between HLA-DRB1 shared epitope alleles and MHC class II transactivator CIITA gene with regard to risk of rheumatoid arthritis.
Padyukov et al., Stockholm, Sweden. In Plos One, 2011
Data suggest that risk from the MHC class II transactivator (CIITA) locus is independent of the major risk for rheumatoid arthritis from HLA-DRB1 SE alleles, given that no significant interaction between rs3087456 and shared epitope alleles was observed.
Dysregulated recruitment of the histone methyltransferase EZH2 to the class II transactivator (CIITA) promoter IV in breast cancer cells.
Greer et al., Atlanta, United States. In Plos One, 2011
The silencing of MHC II molecules in highly metastatic breast cancer cells is associated with distinct epigenetic modifications targeted specifically to the chromatin of CIITApIV.
MHC class II transactivator CIITA is a recurrent gene fusion partner in lymphoid cancers.
Gascoyne et al., Vancouver, Canada. In Nature, 2011
findings suggest that recurrent rearrangements of CIITA may represent a novel genetic mechanism underlying tumour-microenvironment interactions across a spectrum of lymphoid cancers
Autonomous role of medullary thymic epithelial cells in central CD4(+) T cell tolerance.
Klein et al., München, Germany. In Nat Immunol, 2010
Here we diminished major histocompatibility complex (MHC) class II on mTECs through transgenic expression of a 'designer' microRNA specific for the MHC class II transactivator CIITA (called 'C2TA' here).
Regulation of antigen presentation by Mycobacterium tuberculosis: a role for Toll-like receptors.
Boom et al., Cleveland, United States. In Nat Rev Microbiol, 2010
Immune evasion allows M. tuberculosis to establish persistent or latent infection in macrophages and results in Toll-like receptor 2 (TLR2)-dependent inhibition of MHC class II transactivator expression, MHC class II molecule expression and antigen presentation.
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