Reciprocal Modulation of Transcriptional Activities between HIV-1 Tat and MHC Class II Transactivator CIITA

Okamoto, Hiroshi; Asamitsu, Kaori; Nishimura, Hiroyuki; Kamatani, Naoyuki; Okamoto, Takashi

doi:10.1006/bbrc.2000.3972

Cited by 24 publications

(20 citation statements)

References 39 publications

(35 reference statements)

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“…CIITA is a transcription factor known to initiate the expression of MHC II and exerts its function primarily by binding general transcription factors (17,46), histone acetyltransferases (18,42), and the positive transcription elongation factor b complex. Previous studies have shown that CIITA and Tat compete for P-TEFb binding (35,53). Competition between CIITA and clade-specific Tat proteins revealed that Tat E competed to a higher extent with CIITA to bind P-TEFb than did Tat B.…”

Section: Discussionmentioning

confidence: 85%

Regulation of Human Immunodeficiency Virus Type 1 Gene Expression by Clade-Specific Tat Proteins

Desfosses

Solis

Sun

et al. 2005

J Virol

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The major group of human immunodeficiency virus type 1 (HIV-1) strains that comprise the current global pandemic have diversified during their worldwide spread into at least 10 distinct subtypes, or clades. Subtype C predominates in sub-Saharan Africa and is responsible for the majority of worldwide HIV-1 infections, subtype B predominates in North America and Europe, and subtype E is prevalent in Southeast Asia. Significant amino acid variations have been observed among the clade-specific Tat proteins. For the present study, we examined clade-specific interactions between Tat, transactivation-responsive (TAR) element, and P-TEFb proteins and how these interactions may modulate the efficiency of HIV-1 transcription. Clade-specific Tat proteins significantly modified viral gene expression. Tat proteins derived from HIV-1 clades C and E were strong transactivators of long terminal repeat (LTR) activity; Tat E also had a longer half-life than the other Tat proteins and interacted more efficiently with the stem-loop TAR element. Chimeric Tat proteins harboring the Tat E activation domain were strong transactivators of LTR expression. While Tat B, C, and E were able to rescue a Tat-defective HIV-1 proviral clone, Tat E was significantly more efficient at rescue than Tat C, possibly due to the relative stability of the Tat protein. Swapping the activation domains of Tat B, C, and E identified the cyclin T1 association domain as a critical determinant of the transactivation efficiency and of Tat-defective HIV-1 provirus rescue.

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Section: Discussionmentioning

confidence: 85%

Regulation of Human Immunodeficiency Virus Type 1 Gene Expression by Clade-Specific Tat Proteins

Desfosses

Solis

Sun

et al. 2005

J Virol

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“…Finally, as mentioned earlier, the HIV Tat protein can inhibit MHCII expression by interfering with the function of CIITA in HIV-infected or Tat-transfected fibroblasts and T cell lines [34,114]. Tat does this by competing with CIITA for binding to cyclin T1, a component of the transcriptional elongation complex P-TEFb [34,114].…”

Section: Repression Of Ciita Expression By Pathogensmentioning

confidence: 83%

“…However, although TGF-g is well known to inhibit the expression of CIITA, it instead stimulates HIV replication [32]. Furthermore, in other studies HIV infection and LTR activity were found to be reduced in CIITA + cell lines [33,34]. Considering these conflicting findings it is presently not clear exactly how CIITA affects transcription driven by the HIV promoter in vivo under physiological conditions.…”

Section: The Specificity Of Ciitamentioning

confidence: 97%

Mini‐review: Specificity and expression of CIITA, the master regulator of MHC class II genes

et al. 2004

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The class II transactivator (CIITA) has been referred to as the "master control factor" for the expression of MHC class II (MHCII) genes. As our knowledge on the specificity and function of CIITA grows, it is becoming increasingly evident that this sobriquet is entirely justified. First, despite extensive investigations, the major target genes of CIITA remain those implicated in the presentation of antigenic peptides by MHCII molecules. Although other putative target genes have been reported, the contribution of CIITA to their expression remains indirect, controversial or comparatively minor relative to its decisive role as a regulator of MHCII and related genes. Second, the most important parameter dictating MHCII expression is by far the expression pattern of the gene encoding CIITA (MHC2TA). The vast majority of signals that activate or repress MHCII expression under physiological and pathological situations converge on one or more of the three alternative promoters that drive transcription of the MHC2TA gene. In short, with respect to its specificity and its exquisitely controlled pattern of expression, CIITA is by a long stretch the single most important transcription factor for the regulation of genes required for MHCII-restricted antigen-presentation.

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“…Similarly, CIITA has been shown to interact with cyclin T1 and to require the activity of its associated kinase, cyclin-dependent kinase 9 (cdk9), to activate transcription (25). Presumably, CIITA promotes efficient transcriptional elongation through this interaction, a hypothesis supported by inhibition of MHC class II gene transcription by dominant-negative cdk9 (39).…”

mentioning

confidence: 99%

The Class II Transactivator Requires brahma-Related Gene 1 To Activate Transcription of Major Histocompatibility Complex Class II Genes

Mudhasani

Fontes

2002

Molecular and Cellular Biology

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The class II transactivator (CIITA) is the key regulator of major histocompatibility complex (MHC) class II gene transcription. We demonstrate here that CIITA requires the ATPase subunit of an hSWI/SNF complex, brahma-related gene 1 (BRG-1), to activate transcription. When introduced into a cell line lacking BRG-1, CIITA was unable to activate cellular MHC class II genes. Reexpression of the wild-type but not an ATPbinding-deficient BRG-1 protein in this cell line restored the ability of CIITA to transactivate transcription of MHC class II genes. Interestingly, when the activity of CIITA was assayed in the BRG-1-deficient cell line by using a plasmid-based reporter assay, BRG-1 was not required for transcriptional activation, suggesting that the chromatin structure on the plasmid is such that BRG-1 is not necessary. Coimmunoprecipitation experiments were performed to determine if BRG-1 and CIITA proteins associate with each other in cells. We found that the two proteins coimmunoprecipitate and that amino acids 1 to 140 of CIITA are sufficient for binding. Taken together, these data suggest that BRG-1 and, very likely, an hSWI/SNF complex are required for transcription of MHC class II genes. The complex is likely recruited to MHC class II promoters, at least in part, by interaction with CIITA.

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Reciprocal Modulation of Transcriptional Activities between HIV-1 Tat and MHC Class II Transactivator CIITA

Cited by 24 publications

References 39 publications

Regulation of Human Immunodeficiency Virus Type 1 Gene Expression by Clade-Specific Tat Proteins

Regulation of Human Immunodeficiency Virus Type 1 Gene Expression by Clade-Specific Tat Proteins

Mini‐review: Specificity and expression of CIITA, the master regulator of MHC class II genes

The Class II Transactivator Requires brahma-Related Gene 1 To Activate Transcription of Major Histocompatibility Complex Class II Genes

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