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Validated All-in-One™ qPCR Primer for CIITA(NM_000246.3) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
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.
Gene References into function
- CIITA is a novel GTP-binding protein
- Phosphorylation of CIITA by PKA inhibits activation of HLA-DR in monocytic cells
- Cooperation between CIITA, CBP, and pCAF doesn't require coactivator histone acetyltransferase activity
- The AIR-1 encoded class II transactivator (CIITA): the master coordinator of MHC class II gene expression and implications in the physiopathology of the immune system.
- In both in vivo and in vitro activated CD4+ T cells, CIITA expression is driven by CIITA promoter III only.
- carboxy terminal leucine-rich repeat region controls Nuclear localisation of CIITA
- Single nucleotide polymorphisms in MHC2TA
- we investigated the molecular basis of the defect in three patients in these families, all presenting a severe immunodeficiency; CIITA transcripts were detected in all three patients
- Interferon-gamma-induced chromatin remodeling at the CIITA locus is BRG1 dependent
- tumor cell lines with a defective expression of CIITA transcripts lack MHC class II expression
- Phagocytosis of bacteria can down-modulate HLA class II expression in normal human macrophages by acting at the level of expression of CIITA.
- Kinetics of a gamma interferon response: expression and assembly of CIITA promoter IV and inhibition by methylation.
- Leucine-rich repeats of the class II transactivator control its rate of nuclear accumulation
- CIITA requires the ATPase subunit of an hSWI/SNF complex, brahma-related gene 1 (BRG-1), to activate transcription.
- The promoter III isoform of MHC2TA is induced in activated T lymphocytes via the induction of binding of activation response element ARE-2.
- CIITA inhibits HIV-1 replication by blocking Tat protein.
- Phosphorylation of CIITA directs its oligomerization, accumulation and increased activity on MHCII promoters.
- The 5'-untranslated region of CIITA promoter III functions as an important regulatory region in B lymphocytes.
- DNA microarray analysis of the CIITA-expressing B cell line Raji identified a wide variety of CIITA-modulated genes with diverse functions which could impact antigen processing, signaling, proliferation, and differentiation.
- A novel model is proposed for the dynamic regulation of CIITA cellular localization mediated by its GTP-binding domain.
- Silencing of CIITA transcription is recessive in trophoblasts and involves an epigenetic mechanism other than promoter methylation. Trophoblasts may be missing a factor that regulates chromatin structure at the CIITA promoter.
- TncRNA suppressed interferon-gamma-induced human leukocyte antigen-DR and CIITA expression in HeLa cells and the mechanism involves inhibition of CIITA pIV through a defined inhibitory domain on the promoter
- identified two regions mediating degradation within the N-terminal domain of CIITA
- CIITA strongly inhibits HTLV-2 viral replication, but not virus entry, in B- and T-cell susceptible targets
- important role of DNA hyper-methylation in the control of CIITA expression in leukemic T cells.
- evidenced a highly residual CIITA protein expression in a B lymphoma cell line resulting from a transcriptional defect affecting MHC2TA expression.
- Overexpression of CIITA in a human gastric carcinoma cell line, AGS, results in decreased cathepsin E mRNA and protein. AGS cells expressing CIITA also exhibit decreased processing of ovalbumin antigen.
- MHC2TA is the single most important transcription factor for the regulation of genes required for MHCII-restricted antigen presentation.
- a model for CIITA function in which phosphorylation of these specific sites in CIITA in the nucleus serves to down-regulate CIITA activity.
- characterized the various regulatory elements and interacting factors of CIITA-PIII that account for specific activation in B lymphocytes
- There are coordinate decreases in the occupancy of RNA polymerase II on the collagen transcription start site with increasing CIITA occupancy during IFN-gamma treatment
- CIITA inhibits MMP-9 expression by binding to and sequestering CREB-binding protein
- Inability of uveal melanocytes and ocular melanoma cells to express class II MHC molecules after treatment with IFN-gamma maps to two distinct points in class II MHC biosynthetic pathway.
- CIITA methylation is a key mechanism that enables some gastrointestinal cancer cells to escape immune surveillance
- Six novel S'-Y' regulatory modules have been identified that are controlled by the human major histocompatibility class II-specific regulatory factor CIITA.
- No polymorphism in promoters I, III and IV of CIITA gene exists in chronic hepatitis B patients and controls suggesting that the promoter of CIITA gene might be a conserved domain.
- CIITA induction is required for interferon gamma-mediated repression of COL1A1 and COL1A2
- Constitutive expression of human CIITA in transgenic mice pre-disposes CD4 T cells to produce Th2 type cytokines, indicating that CIITA expression is important for proper CD4 T-cell differentiation.
- type IV promoter is active in B lymphocytes and potentially contributes to the expression of CIITA and MHC II in these cells; in vivo genomic footprint analysis demonstrated proteins binding at the GAS, IRF-E and E box sites of CIITA pIV
- ANKRA, RFXANK, and CIITA are novel targets of class IIa HDACs which may deacetylases play a role in regulating MHCII expression
- arginine methylation of CBP is required for IFN-gamma induction of MHC-II. A kinetic analysis shows that CIITA, CARM1, and H3-R17 methylation all precede CBP loading on the MHC-II promoter during IFN-gamma treatment.
- Promoter polymorphism rs3087456 in the MHC class II transactivator gene is not associated with susceptibility for selected autoimmune diseases in German patient groups.
- In this cohort of Austrian patients, no association between the MHC2TA polymorphism and rheumatoid arthritis was found.
- The MHC2TA -168*G/A SNP was not associated with increased susceptibility to rheumatoid arthritis
- findings do not provide support for the notion that this gene plays a major role in the etiology of rheumatoid arthritis
- IFN-gamma upregulates the activity of CIITA in multiple myeloma
- PPARgamma is within the RFX5.CIITA complex as judged by co-immunoprecipitation and DNA affinity precipitation studies
- that recruitment of CIITA to the human leukocyte antigen (HLA)-DR promoter and activation of HLA-DR transcription is also GTP-dependent.
- -168A/G and +1614G/C polymorphisms do not predispose to multiple sclerosis or rheumatoid arthritis. The latter may be protective against juvenile idiopathic arthritis.
- Our data suggest that a strong gene-environment interaction occurs between HHV-6A (human herpes viru 6)active replication and MHC2TA rs4,774C or another polymorphism in tight linkage disequilibrium with it.
- data support neither allelic nor genotype association between the MHC2TA SNP and systemic lupus erythematosus.
- A meta-analysis of 6,861 patients and 9,270 controls reveals no evidence for association between the MHC2TA -168A/G polymorphism and risk for rheumatoid arthritis.
- MHC2TA -168A/G polymorphism (rs3087456) is not associated with RA yet underscore the importance of including shared epitope allele carrier status, secondary phenotypes and more complete characterisation of MHC2TA variation in future studies.
- The polymorphisms of CIITA promoter IV are associated with persistent HBV infection. The CC haplotype with the lowest activity of promoter and CC/CC genotype are responsible for persistent HBV infection.
- Polymorphisms of the MHC2TA gene do not play a role in the susceptibility to systemic lupus erythematosus in a Spanish population.
- Reporter gene assays with PIII and PIV CIITA promoters indicate constitutive expression of PIII in MSCs and a switch to PIV by IFN-gamma, indicating the presence of factors for effect promoter responses.
- ERK1/2-mediated phosphorylation of CIITA down-regulates CIITA activity by priming it for nuclear export, thus providing a means for cells to tightly regulate the extent of antigen presentation.
- CIITA expression was downregulated by DCR3 in tumor-associated macrophages
- CIITA is uniquely dedicated for genes implicated in antigen presentation.
- Two alleles at 16p13 are independently associated with the risk of Addison's disease in the Norwegian population, suggesting this chromosomal region to harbor common autoimmunity gene(s), CLEC16A and CIITA being possible independent candidates.
- 168A-->G polymorphism of the MHC2TA gene is not associated with susceptibility to colorectal cancer.
- downregulation of MHC-II expression occurs by multiple distinct mechanisms in DLBCL. However, decreases in CIITA expression appear to be the most prevalent mechanism.
- Zta may suppress CIITA transcription
