Synergistic action of MLL, a TRX protein with template activating factor‐I, a histone chaperone

Shimoyama, Tae; Kato, Kohsuke; Miyaji-Yamaguchi, Mary; Nagata, Kyosuke

doi:10.1016/j.febslet.2004.12.064

Cited by 15 publications

(24 citation statements)

References 23 publications

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“…Thus, TAF-Ib may be recruited to specific genes through its interaction with specific DNA binding factors and may contribute to transcriptional regulation through its nucleosome assembly activity. TAF-Ib also has roles in phenomena such as gene translocation [127,145]; caspase-independent apoptosis, which depends on its digestion by the trypsinlike protease GzmA [146 -149]; cell-cycle regulation, which depends on its interaction with the CDK inhibitor [150,151]; and cancer regulation, which depends on binding to leukemia-related factor [152]. We propose that the basis of the multifunctional properties of TAF-Ib is its histone chaperone activity, which plays a role in nucleosome assembly and disassembly.…”

Section: Taf-ib/setmentioning

confidence: 99%

Histone chaperones: 30 years from isolation to elucidation of the mechanisms of nucleosome assembly and disassembly

Eitoku

Sato

Senda

et al. 2007

Cell. Mol. Life Sci.

182

197

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Some three decades have passed since the discovery of nucleosomes in 1974 and the first isolation of a histone chaperone in 1978. While various types of histone chaperones have been isolated and functionally analyzed, the elementary processes of nucleosome assembly and disassembly have been less well characterized. Recently, the tertiary structure of a hetero-trimeric complex composed of the histone chaperone CIA/ASF1 and the histone H3-H4 dimer was determined, and this complex was proposed to be an intermediate in nucleosome assembly and disassembly reactions. In addition, CIA alone was biochemically shown to dissociate the histone (H3-H4)2 tetramer into two histone H3-H4 dimers. This activity suggested that CIA regulates the semi-conservative replication of nucleosomes. Here, we provide an overview of prominent histone chaperones with the goal of elucidating the mechanisms that preserve and modify epigenetic information. We also discuss the reactions involved in nucleosome assembly and disassembly.

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Section: Taf-ib/setmentioning

confidence: 99%

Histone chaperones: 30 years from isolation to elucidation of the mechanisms of nucleosome assembly and disassembly

Eitoku

Sato

Senda

et al. 2007

Cell. Mol. Life Sci.

182

197

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“…The level off histone H3 acetylation of the HOXA locus remained unaltered within the time frame of the experiment ( Figure S2). As SET normally associates with the HOXA gene cluster 30 and has an inhibitory role on gene transcription as part of the INHAT complex, 31 we investigated whether SET-NUP214 may expression levels between the HOXA T-ALL subgroup (MLL, CALM-AF10, inv(7)(p15q34), and SET-NUP214; n ϭ 10) and other T-ALL subgroups (TAL1, LMO2, HOX11L2, or HOX11). The horizontal lines represent the medians.…”

Section: Set-nup214 Directly Activated Hoxa Expression Possibly By Rmentioning

confidence: 99%

mentioning

confidence: 99%

The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia

Vlierberghe

Grotel

Tchinda

et al. 2008

Blood

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201

178

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T-cell acute lymphoblastic leukemia (T-ALL) is mostly characterized by specific chromosomal abnormalities, some occurring in a mutually exclusive manner that possibly delineate specific T-ALL subgroups. One subgroup, including MLLrearranged, CALM-AF10 or inv (7)(p15q34) patients, is characterized by elevated expression of HOXA genes. Using a gene expression-based clustering analysis of 67 T-ALL cases with recurrent molecular genetic abnormalities and 25 samples lacking apparent aberrations, we identified 5 new patients with elevated HOXA levels. Using microarray-based comparative genomic hybridization (array-CGH), a cryptic and recurrent deletion, del (9)(q34.11q34.13), was exclusively identified in 3 of these 5 patients. This deletion results in a conserved SET-NUP214 fusion product, which was also identified in the T-ALL cell line LOUCY. SET-NUP214 binds in the promoter regions of specific HOXA genes, where it interacts with CRM1 and DOT1L, which may transcriptionally activate specific members of the HOXA cluster. Targeted inhibition of SET-NUP214 by siRNA abolished expression of HOXA genes, inhibited proliferation, and induced differentiation in LOUCY but not in other T-ALL lines. We conclude that SET-NUP214 may contribute to the pathogenesis of T-ALL by enforcing T-cell differentiation arrest. IntroductionT-cell acute lymphoblastic leukemia (T-ALL) is a thymocyte malignancy, and represents about 15% of pediatric patients with ALL. T-ALL often presents with a high tumor mass, accompanied by a rapid progression of disease. Still, about 30% of patients with T-ALL relapse during therapy or within the first 2 years following treatment and eventually die. 1 Over the last few years, great progress has been made in unravelling the genetics of T-ALL, including recurrent chromosomal translocations (TAL1, LYL1, LMO1, LMO2, HOX11/TLX1, HOX11L2/TLX3, MYB, and Cyclin D2), deletions (SIL-TAL1, del(6q), del(9)(p21), and del(11)(p12p13)), amplifications (NUP214-ABL1), duplications (MYB), and mutations (RAS and NOTCH1). [2][3][4][5][6][7][8][9][10][11][12][13] Some of these abnormalities are mutually exclusive and may delineate distinct T-ALL subgroups (ie, TAL1, LMO1, LMO2, HOX11, HOX11L2, MLL, and Inv(7)). Others are shared by some of these subgroups and may lead to the deregulation of cell cycle (ie, del(9)(p21) that includes the CDKN2A/p15 and CDKN2B/p16 loci). 3,4 Some may be acquired during leukemic growth, like the episomal NUP214-ABL1 amplification. 6 NOTCH1 activation mutations are present in more than half of all patients with T-ALL regardless of the presence of other rearrangements. 7 It has been hypothesized that activation of NOTCH1 represents one of the most advanced abnormalities in T-ALL that may enable for uncontrolled proliferation and/or inhibition of apoptosis, possibly through up-regulation of the target genes cMYC and DELTEX1. [14][15][16] In contrast to the wide variety of genetic abnormalities in T-ALL, initial microarray studies have revealed only 5 different expression clusters: immature/LYL1, TAL...

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“…In addition, TAF-I promotes vitamin D 3 receptor-and Gal4-VP16-dependent transcription from the chroma-tin template in vitro (14) and stimulates the transcription of a subset of genes in HeLa cells in a histone acetylation-independent manner (27). TAF-I also plays an important role in transcription regulated by transcription factors such as MLL (mixed lineage leukemia), Sp1, and KLF5 (39,53,56).…”

mentioning

confidence: 99%

Transcription Regulation of the rRNA Gene by a Multifunctional Nucleolar Protein, B23/Nucleophosmin, through Its Histone Chaperone Activity

Murano

Okuwaki

Hisaoka

et al. 2008

Molecular and Cellular Biology

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148

129

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It is well established that the transcription rate of the rRNA gene is closely associated with profound alterations in the cell growth rate. Regulation of rRNA gene transcription is likely to be dependent on the dynamic conversion of the chromatin structure. Previously, we identified B23/nucleophosmin, a multifunctional nucleolar phosphoprotein, as a component of template activating factor III that remodels the chromatinlike structure of the adenovirus genome complexed with viral basic proteins. It has also been shown that B23 has histone chaperone activity. Here, we examined the effect of B23 on rRNA gene transcription. B23 was found to be associated with the rRNA gene chromatin. Small-interfering-RNA-mediated down-regulation of the B23 expression level resulted in reduction of the transcription rate of the rRNA gene. We constructed a B23 mutant termed B23⌬C, which lacks the domain essential for the histone chaperone activity and inhibited the histone binding activity of B23 in a dominant-negative manner. Expression of B23⌬C decreased rRNA gene transcription and the rate of cell proliferation. These results suggest that B23 is involved in the transcription regulation of the rRNA gene as a nucleolar histone chaperone.

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Synergistic action of MLL, a TRX protein with template activating factor‐I, a histone chaperone

Cited by 15 publications

References 23 publications

Histone chaperones: 30 years from isolation to elucidation of the mechanisms of nucleosome assembly and disassembly

Histone chaperones: 30 years from isolation to elucidation of the mechanisms of nucleosome assembly and disassembly

The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia

Transcription Regulation of the rRNA Gene by a Multifunctional Nucleolar Protein, B23/Nucleophosmin, through Its Histone Chaperone Activity

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