Class II transactivator protein (CIITA) protein contains an acidic region in its N-terminal with transactivation activity, that binds to proteins in the basal transcription machinery and to cAMP response element-binding protein (CREB)-binding protein (CBP). The protein contains motifs for nuclear translocation, GTP binding motif and C-terminal leucine-rich repeats. CIITA is expressed constitutively in B lymphocytes and in immature dendritic cells, while in other cells its expression is induced by IFN-γ .
Monoclonal Anti-CIITA (mouse IgG1 isotype) is derived from the hybridoma 7-1H produced by the fusion of mouse myeloma cells (Sp20 cells) and splenocytes from BALB/c mice immunized with purified N-terminal recombinant CIITA, amino acids 1-350. CIITA is expressed constitutively in B lymphocytes and in immature dendritic cells, while in other cells its expression is induced by IFN-γ.
Monoclonal Anti-CIITA recognizes human1 and mouse † CIITA.
Application
The antibody may be used in immunoblotting (∼130 kDa) and immunocytochemistry.
Biochem/physiol Actions
Class II transactivator protein (CIITA) interacts with specific transcription factors and creates the appropriate transcriptional scaffold required for HLA-D gene expression.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
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International immunology, 14(8), 839-848 (2002-07-31)
The class II transactivator (CIITA) controls both the constitutive and IFN-gamma inducible expression of HLA-D genes. In addition, through the squelching of another transactivator CREB-binding protein, CIITA was more recently shown to have a wider cellular function, including cell cycle
Journal of immunology (Baltimore, Md. : 1950), 158(10), 4741-4749 (1997-05-15)
The MHC class II transactivator gene (CIITA) coordinately controls the expression of the three major human class II genes, HLA-DR, HLA-DQ, and HLA-DP. Indeed, patients with one form of MHC class II immunodeficiency disease, due to defective CIITA genes, lack
International immunology, 14(5), 481-491 (2002-04-30)
MHC class II expression defects have been evidenced in several human tumor cell lines originating from lung cancers or retinoblastoma. Accordingly, the mouse adenocarcinoma and fibrosarcoma cell lines, RAG and L(tk-), do not express I-A and I-E molecules even when
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