Cyclin D3 interacts with human activating transcription factor 5 and potentiates its transcription activity

Liu, Wenjin; Sun, Maoyun; Jiang, Jianhai; Shen, Xıaoyun; Sun, Qing; Liu, Weicheng; Shen, Hongxing; Gu, Jianxin

doi:10.1016/j.bbrc.2004.07.053

Cited by 30 publications

(19 citation statements)

References 32 publications

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“…Generally, these functions are independent of CDKs, as shown by use of a cyclin D1 K114E mutant (analogous to the v-cyclin K104E mutation), kinase-defective CDKs, or cellular CDK inhibitors. Cyclin D3 is implicated in the modulation of hATF5 in a CDK-independent manner (40) and the vitamin D receptor in a CDKcompetitive manner (31). With respect to viral cyclin functions, the KSHV v-cyclin directly represses STAT3 transcriptional activity to overcome growth inhibition caused by oncostatin-M in transiently and stably transfected cells (16,41).…”

Section: Cdk-dependent V-cyclin Function During Acute Virus Replicationmentioning

confidence: 99%

Evidence for CDK-Dependent and CDK-Independent Functions of the Murine Gammaherpesvirus 68 v-Cyclin

Upton

Speck

2006

J Virol

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Gamma-2 herpesviruses encode homologues of mammalian D-type cyclins (v-cyclins), which likely function to manipulate the cell cycle, thereby providing a cellular environment conducive to virus replication and/or reactivation from latency. We have previously shown that the v-cyclin of murine gammaherpesvirus 68 is an oncogene that binds and activates cellular cyclin-dependent kinases (CDKs) and is required for efficient reactivation from latency. To determine the contribution of v-cyclin-mediated cell cycle regulation to the viral life cycle, recombinant viruses in which specific point mutations (E133V or K104E) were introduced into the v-cyclin open reading frame were generated, resulting in the disruption of CDK binding and activation. While in vitro growth of these mutant viruses was unaffected, lytic replication in the lungs following low-dose intranasal inoculation was attenuated for both mutants deficient in CDK binding as well as virus in which the entire v-cyclin open reading frame was disrupted by the insertion of a translation termination codon. This replication defect was not apparent in spleens of mice following intraperitoneal inoculation, suggesting a cell type-and/or route-specific dependence on v-cyclin-CDK interactions during the acute phase of virus infection. Notably, although a v-cyclin-null virus was highly attenuated for reactivation from latency, the E133V v-cyclin CDK-binding mutant exhibited only a modest defect in virus reactivation from splenocytes, and neither the E133V nor K104E v-cyclin mutants were compromised in reactivation from peritoneal exudate cells. Taken together, these data suggest that lytic replication and reactivation in vivo are differentially regulated by CDK-dependent and CDK-independent functions of v-cyclin, respectively.The eukaryotic cell cycle comprises a series of coordinated events leading to cellular DNA and the segregation of the replicated DNA to daughter cells. The transitions through this cycle are controlled by the temporal and spatial activation of highly conserved holoenzymes consisting of a short-lived regulatory cyclin subunit and a cyclin-dependent kinase (CDK) (5,54,55,71). Quiescent (G 0 ) cells stimulated by mitogens upregulate the highly redundant D-type cyclins (cyclins D1, D2, and/or D3), which bind and activate CDK4 and/or CDK6 to mediate progression of the cell cycle into and through the G 1 phase. Cyclin D/CDK activity allows for the expression of Etype cyclins, which bind and activate CDK2 to drive progression through the restriction point from the G 1 phase into the S phase. Cyclin A expression allows for the continued activation of CDK2 and subsequently binds and activates CDK1 as S phase progresses and the G 2 /M boundary is reached, at which stage cyclin B levels are maximal for the regulation of mitosis in conjunction with CDK1. The activities, localization, and stability of these holoenzymes are further affected by proteinprotein interactions and posttranslational modifications that act to positively or negatively modulate cyclin-CDK ...

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Section: Cdk-dependent V-cyclin Function During Acute Virus Replicationmentioning

confidence: 99%

Evidence for CDK-Dependent and CDK-Independent Functions of the Murine Gammaherpesvirus 68 v-Cyclin

Upton

Speck

2006

J Virol

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“…CDK11 p110 isoforms also interact with pre-mRNA splicing factors including cyclin L, RNPS1, 9G8, ELL2, TFIIF, TFIIS and FACT, and promotes pre-mRNA processing [12,[21][22][23]. We have reported that cyclin D3, the cyclin partner of CDK11 p58 , interacts directly with human Activating Transcription Factor 5 (hATF5), and enhances its transcription activity [24]. All these data suggest that members of CDK11 are associated with transcriptional regulation as well as cell cycle progression.…”

Section: Introductionmentioning

confidence: 99%

Cyclin‐dependent kinase 11^p58 interacts with HBO1 and enhances its histone acetyltransferase activity

Zong

Liu

et al. 2005

FEBS Letters

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CDK11p58 , a 58 kDa protein of the PITSLRE kinase family, plays an important role in cell cycle progression, and is closely related to cell apoptosis. To gain further insight into the function of CDK11 p58 , we screened a human fetal liver cDNA library for its interacting proteins using the yeast twohybrid system. Here we report that histone acetyltransferase (HAT) HBO1, a MYST family protein, interacts with CDK11 p58 in vitro and in vivo. CDK11 p58 and HBO1 colocalize in the cell nucleus. Recombinant CDK11 p58 enhances the HAT activity of HBO1 significantly in vitro. Meanwhile, overexpression of CDK11 p58 in mammalian cells leads to the enhanced HAT activity of HBO1 towards free histones. Thus, we conclude that CDK11 p58 is a new interacting protein and a novel regulator of HBO1. Both of the proteins may be involved in the regulation of eukaryotic transcription.

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“…Although less well explored, a CDK-independent role for cyclin D3 has also been reported, including inhibition of granulocyte differentiation (19). More recent studies have attributed cyclin D3 with the ability to bind and activate certain transcription factors, such as human activating transcription factor 5 (25). In the case of cyclin D3 mutant mice it has been found that they fail to undergo development of immature T lymphocytes (39).…”

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confidence: 99%

Cyclin D3 Promotes Adipogenesis through Activation of Peroxisome Proliferator-Activated Receptor γ

Sarruf

Iankova

Abella

et al. 2005

Molecular and Cellular Biology

122

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In addition to their role in cell cycle progression, new data reveal an emerging role of D-type cyclins in transcriptional regulation and cellular differentiation processes. Using 3T3-L1 cell lines to study adipogenesis, we observed an up-regulation of cyclin D3 expression throughout the differentiation process. Surprisingly, cyclin D3 was only minimally expressed during the initial stages of adipogenesis, when mitotic division is prevalent. This seemingly paradoxical expression led us to investigate a potential cell cycle-independent role for cyclin D3 during adipogenesis. We show here a direct interaction between cyclin D3 and the nuclear receptor peroxisome proliferator-activated receptor ␥ (PPAR␥). Our experiments reveal cyclin D3 acts as a ligand-dependent PPAR␥ coactivator, which, together with its cyclin-dependent kinase partner, phosphorylates the A-B domain of the nuclear receptor. Overexpression and knockdown studies with cyclin D3 had marked effects on PPAR␥ activity and subsequently on adipogenesis. Chromatin immunoprecipitation assays confirm the participation of cyclin D3 in the regulation of PPAR␥ target genes. We show that cyclin D3 mutant mice are protected from diet-induced obesity, display smaller adipocytes, have reduced adipogenic gene expression, and are insulin sensitive. Our results indicate that cyclin D3 is an important factor governing adipogenesis and obesity.

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Cyclin D3 interacts with human activating transcription factor 5 and potentiates its transcription activity

Cited by 30 publications

References 32 publications

Evidence for CDK-Dependent and CDK-Independent Functions of the Murine Gammaherpesvirus 68 v-Cyclin

Evidence for CDK-Dependent and CDK-Independent Functions of the Murine Gammaherpesvirus 68 v-Cyclin

Cyclin‐dependent kinase 11^p58 interacts with HBO1 and enhances its histone acetyltransferase activity

Cyclin D3 Promotes Adipogenesis through Activation of Peroxisome Proliferator-Activated Receptor γ

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Cyclin D3 interacts with human activating transcription factor 5 and potentiates its transcription activity

Cited by 30 publications

References 32 publications

Evidence for CDK-Dependent and CDK-Independent Functions of the Murine Gammaherpesvirus 68 v-Cyclin

Evidence for CDK-Dependent and CDK-Independent Functions of the Murine Gammaherpesvirus 68 v-Cyclin

Cyclin‐dependent kinase 11p58 interacts with HBO1 and enhances its histone acetyltransferase activity

Cyclin D3 Promotes Adipogenesis through Activation of Peroxisome Proliferator-Activated Receptor γ

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Cyclin‐dependent kinase 11^p58 interacts with HBO1 and enhances its histone acetyltransferase activity