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1 f interferon regulatory factor 1 and the MHC class II transactivator.
2 hal reporter construct and subsequently, the class II transactivator.
3 his in turn was caused by lack of functional class II transactivator.
4 nvestigated in cells stably transfected with class II transactivator.
5 used CRISPR/Cas9 to disrupt the gene for the class II transactivator.
6 is associated with up-regulation of the MHC class II transactivator, a key transcription factor with
7 t ovariectomy up-regulates IFN-gamma-induced class II transactivator, a multitarget immune modulator,
8 prevented transcription of the gene encoding class II transactivator, a transactivator protein requir
9 also induced by HPIV3 in cells defective in class II transactivator, an important intermediate of th
11 nsfection of small interfering RNA targeting class II transactivator attenuates major histocompatibil
12 ecules by small interfering RNA targeting of class II transactivator can reduce the capacity of human
20 The major histocompatibility complex (MHC) class II transactivator (CIITA) acts as a master switch
22 une evasion strategies such as inhibition of class II transactivator (CIITA) and MHC-II expression, t
23 ractions of chromatin-modifying enzymes with class II transactivator (CIITA) and relevant DNA-binding
24 ty complex (MHC)-II and its master regulator class II transactivator (CIITA) are downregulated in CML
25 a signal transduction (Jak/Stat pathway) and class II transactivator (CIITA) are required components
26 igation has defined major histocompatibility class II transactivator (CIITA) as a key factor in media
27 lines were used to demonstrate that the MHC class II transactivator (CIITA) can induce surface expre
29 ells and in a cell line that is defective in class II transactivator (CIITA) demonstrates that NK cel
30 feron-gamma treatment or transduction of the class II transactivator (CIITA) gene induces class II ex
32 anges in cancer immunity mediated by the MHC class II transactivator (CIITA) have not been extensivel
34 scriptional regulation, which is governed by class II transactivator (CIITA) in all cells, microbial
35 P-deficient cells, transfection of exogenous class II transactivator (CIITA) into these RFX-B-deficie
49 complex along with major histocompatibility class II transactivator (CIITA) is induced by interferon
53 The major histocompatibility complex (MHC) class II transactivator (CIITA) is the 'master coactivat
59 The major histocompatibility complex (MHC) class II transactivator (CIITA) is the master regulatory
61 amma-inducible transcription at multiple MHC class II transactivator (CIITA) promoters and suppressed
62 s II MHC genes requires the induction of the class II transactivator (CIITA) protein, a master regula
63 ctivation of class II MHC genes requires the class II transactivator (CIITA) protein, a regulator tha
64 The major histocompatibility complex (MHC) class II transactivator (CIITA) regulates the expression
65 s strictly dependent upon the binding of the class II transactivator (CIITA) to the highly conserved
69 Depending on whether MHC-II genes and the class II transactivator (CIITA) were being expressed, tw
71 have now transduced tumor cells with the MHC class II transactivator (CIITA), a regulatory gene that
73 tion analysis demonstrated that induction of class II transactivator (CIITA), and consequently, HLA-D
75 ter regulator of MHC class II transcription, class II transactivator (CIITA), identified HLA-DOA and
76 re, inhibition of promoter activities of MHC class II transactivator (CIITA), IFN-gamma-activated sit
77 ated inhibition of MNV replication in vitro, class II transactivator (CIITA), interferon regulatory f
78 mary and immortalized astrocytes up-regulate class II transactivator (CIITA), invariant chain (Ii) (p
81 anism involved interactions between CTCF and class II transactivator (CIITA), the master regulator of
82 uires recruitment of a master regulator, the class II transactivator (CIITA), to the MHC class II pro
83 orrelating to a decrease in the mRNA for the class II transactivator (CIITA), whereas CIITA expressio
84 nodeficiency have mutations in a gene termed class II transactivator (CIITA), which coordinately cont
85 non-DNA-binding master regulator of MHC-II, class II transactivator (CIITA), which is crucial for en
86 t the major histocompatibility complex (MHC) class II transactivator (CIITA), which is required for e
87 of several immune function genes, including class II transactivator (CIITA), which regulates class I
89 in line with the role of CREBBP in promoting class II transactivator (CIITA)-dependent transcriptiona
104 of the key mechanisms includes repression of class-II transactivator (CIITA) and MHC-II expression in
105 y the major histocompatibility complex (MHC) class II transactivator, CIITA, which binds to myogenin
108 3 that inhibits promoter function of the HLA class II transactivator, decreasing expression of genes
110 tion and targeted IFN response factor 1- and class II transactivator-dependent and independent promot
111 pathways including Stat-3, beta-catenin, and class II transactivator-dependent antigen presentation.
118 was accompanied by activation of a repressed class II transactivator gene in a plasma cell tumor but,
119 t from a pig transgenic for a mutant (human) class II transactivator gene, resulting in down-regulati
120 in reaction analysis for gene transcripts of class II transactivator, HLA-DRagr;, and HLA-DRbeta1 sho
121 nducible genes-MHC class II gene E beta; MHC class II transactivator; IFN regulatory factor-1; and Mg
124 demonstrate that NOD mice lacking the CIITA (class II transactivator) molecule, and hence deficient i
125 tion of the IFN gamma-responsive chromosomal class II transactivator promoter revealed that MCMV infe
127 by either IFN-alpha/beta (Mx1) or IFN-gamma (class II transactivator protein [CIITA] and inducible ni
128 gen-activated protein kinase, NF-kappaB, the class II transactivator, RFX5, and the IFN regulatory fa
129 ion arises from biallelic gene disruption in class II transactivator that leaves other essential prop
131 ested that NLRC5 acts in a manner similar to class II transactivator to drive MHC expression and reve
133 e selective: while transcription of CD64 and class II transactivator were decreased, certain other IF
135 d proteins form a platform that attracts the class II transactivator, which initiates and elongates M
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