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Human T-cell leukemia virus type-1-encoded protein HBZ represses p53 function by inhibiting the acetyltransferase activity of p300/CBP and HBO1

Wright, Diana G., Marchal, Claire, Hoang, Kimson, Ankney, John A., Nguyen, Stephanie T., Rushing, Amanda W., Polakowski, Nicholas, Miotto, Benoit, Lemasson, Isabelle·2016·Oncotarget
DOI 10.18632/oncotarget.6424PMC PMC4811490
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Figure 1 HBZ inhibits p53-mediated activation of p21/CDKN1A and GADD45A HCT116 p53+/+ cells were transiently transfected with an HBZ or empty expression vector and treated with etoposide (ETO) or the DMSO vehicle control (control) for 8 hours. A. Expression of HAT proteins. Nuclear extracts were analyzed by Western blot using the antibodies indicated. B. mRNA levels of p53-responsive genes. The graph shows real-time PCR data averaged from three or more independent experiments ± S.D. C. mRNA levels of p21/CDKN1A and GADD45A genes. HeLa cells stably transfected with an HBZ or empty expression vector and treated with etoposide (ETO) or the DMSO vehicle control (control) for 6 hours. The graph shows real-time PCR data averaged from four independent experiments ± S.D. *P < 0.05; **P < 0.005 (two-tailed Student t test). D. p21/CDKN1A and GADD45A mRNA levels from MOLT-4 cells transduced with pBABE-GFP-HBZ or pBABE-GFP. The graph shows real-time PCR data averaged from two independent experiments ± S.D.
Figure 1 HBZ inhibits p53-mediated activation of p21/CDKN1A and GADD45A HCT116 p53+/+ cells were transiently transfected with an HBZ or empty expression vector and treated with etoposide (ETO) or the DMSO vehicle control (control) for 8 hours. A. Expression of HAT proteins. Nuclear extracts were analyzed by Western blot using the antibodies indicated. B. mRNA levels of p53-responsive genes. The graph shows real-time PCR data averaged from three or more independent experiments ± S.D. C. mRNA levels of p21/CDKN1A and GADD45A genes. HeLa cells stably transfected with an HBZ or empty expression vector and treated with etoposide (ETO) or the DMSO vehicle control (control) for 6 hours. The graph shows real-time PCR data averaged from four independent experiments ± S.D. *P < 0.05; **P < 0.005 (two-tailed Student t test). D. p21/CDKN1A and GADD45A mRNA levels from MOLT-4 cells transduced with pBABE-GFP-HBZ or pBABE-GFP. The graph shows real-time PCR data averaged from two independent experiments ± S.D.CC BY · PubMed Central
Figure 2 HBZ represses transcription from the p21/CDKN1A promoter through inhibition of p300 and HBO1 A. p300 and HBO1 produce an additive increase in transcription from the p21/CDKN1A promoter. HCT116 p53+/+ cells were cotransfected with p21-luc (200 ng), and expression vectors for Flag-p300 (400 ng), Flag-p/CAF (50 ng), Flag-MOZ (400 ng), HA-HBO1 (400 ng), or HA-Tip60 (50 ng) as indicated. The graph shows average luminescence values ± S.D. from one experiment performed in triplicate and is representative of three independent experiments. Cellular lysates used for the luciferase assay were also analyzed by Western blot using the antibodies indicated. # denotes a crossreactive protein or truncated product; Δ denotes a crossreactive protein. B. HBZ inhibits p300- and HBO1-mediated activation of transcription from the p21/CDKN1A promoter. HCT116 p53+/+ cells were cotransfected with p21-luc (200 ng) and expression vectors for Flag-p300 (400 ng), HA-HBO1 (400 ng), HBZ-Myc-His and/or HBZ-ΔbZIP-Myc-His as indicated. The graph shows average luminescence values ± S.D. from one experiment performed in triplicate and is representative of three independent experiments. Cellular lysates used for the luciferase assay were also analyzed by Western blot using the antibodies indicated. *P < 0.05; **P < 0.005 (two-tailed Student t test). C. HBZ inhibits etoposide-mediated activation of transcription from p21/CDKN1A promoter in T-cells. Jurkat T-cells were cotransfected with p21-luc (200 ng) and expression vectors for p53 (25 ng), HBZ-Myc-His and/or HBZ-Δb ZIP-Myc-His (800 ng) as indicated. Cells were treated with etoposide for 5 hours prior to harvesting. The graph shows average luminescence values ± S.D. from one experiment performed in triplicate and is representative of two independent experiments. *P < 0.05 (two-tailed Student t test).
Figure 2 HBZ represses transcription from the p21/CDKN1A promoter through inhibition of p300 and HBO1 A. p300 and HBO1 produce an additive increase in transcription from the p21/CDKN1A promoter. HCT116 p53+/+ cells were cotransfected with p21-luc (200 ng), and expression vectors for Flag-p300 (400 ng), Flag-p/CAF (50 ng), Flag-MOZ (400 ng), HA-HBO1 (400 ng), or HA-Tip60 (50 ng) as indicated. The graph shows average luminescence values ± S.D. from one experiment performed in triplicate and is representative of three independent experiments. Cellular lysates used for the luciferase assay were also analyzed by Western blot using the antibodies indicated. # denotes a crossreactive protein or truncated product; Δ denotes a crossreactive protein. B. HBZ inhibits p300- and HBO1-mediated activation of transcription from the p21/CDKN1A promoter. HCT116 p53+/+ cells were cotransfected with p21-luc (200 ng) and expression vectors for Flag-p300 (400 ng), HA-HBO1 (400 ng), HBZ-Myc-His and/or HBZ-ΔbZIP-Myc-His as indicated. The graph shows average luminescence values ± S.D. from one experiment performed in triplicate and is representative of three independent experiments. Cellular lysates used for the luciferase assay were also analyzed by Western blot using the antibodies indicated. *P < 0.05; **P < 0.005 (two-tailed Student t test). C. HBZ inhibits etoposide-mediated activation of transcription from p21/CDKN1A promoter in T-cells. Jurkat T-cells were cotransfected with p21-luc (200 ng) and expression vectors for p53 (25 ng), HBZ-Myc-His and/or HBZ-Δb ZIP-Myc-His (800 ng) as indicated. Cells were treated with etoposide for 5 hours prior to harvesting. The graph shows average luminescence values ± S.D. from one experiment performed in triplicate and is representative of two independent experiments. *P < 0.05 (two-tailed Student t test).CC BY · PubMed Central
Figure 3 HBZ inhibits acetylation of p53 K382 A. and B. HCT116 p53+/+ cells were transiently transfected with an HBZ, Tax or an empty expression vector and, 48 h post-transfection, were treated with etoposide (ETO), actinomycin D (ACT.D), doxorubicin (DOX) or the DMSO vehicle control (−) for 8 hours as indicated. Nuclear extracts were prepared and analyzed by Western blot using the antibodies indicated. C. Acetylation of histone H4 by p300 and MOZ. In vitro HAT assays were performed using recombinant histones (2 μM), p300 (2 nM) and MOZ-HAT (0.15 μM) and analyzed by Western blot using antibodies against histone H4 and acetylated histone H4 as indicated. D. Acetylation of p53 by p300 and MOZ. In vitro HAT assays were performed using the same concentrations of recombinant proteins as above, but with p53 (0.1 μM) replacing histones as the substrate. Reactions were analyzed by western blot using antibodies against acetylated lysine, p53 acetyl-K382 and p53. E. HBZ inhibits acetylation of p53 by p300. In vitro HAT assays were performed using recombinant p300 (2 nM), p53 (25 nM) and supplemented with GST (0.3 μM), GST-HBZ (0.3 μM), HBZ-AD (0.3 μM) or HBZ-bZIP (0.3 μM) where indicated. Reactions were analyzed by Western blot using antibodies against acetylated lysine, p53 acetyl-K382 and p53. Identical quantities from the same batch of proteins used in the HAT assay were resolved by SDS-PAGE and stained with Coomassie (lower panel).
Figure 3 HBZ inhibits acetylation of p53 K382 A. and B. HCT116 p53+/+ cells were transiently transfected with an HBZ, Tax or an empty expression vector and, 48 h post-transfection, were treated with etoposide (ETO), actinomycin D (ACT.D), doxorubicin (DOX) or the DMSO vehicle control (−) for 8 hours as indicated. Nuclear extracts were prepared and analyzed by Western blot using the antibodies indicated. C. Acetylation of histone H4 by p300 and MOZ. In vitro HAT assays were performed using recombinant histones (2 μM), p300 (2 nM) and MOZ-HAT (0.15 μM) and analyzed by Western blot using antibodies against histone H4 and acetylated histone H4 as indicated. D. Acetylation of p53 by p300 and MOZ. In vitro HAT assays were performed using the same concentrations of recombinant proteins as above, but with p53 (0.1 μM) replacing histones as the substrate. Reactions were analyzed by western blot using antibodies against acetylated lysine, p53 acetyl-K382 and p53. E. HBZ inhibits acetylation of p53 by p300. In vitro HAT assays were performed using recombinant p300 (2 nM), p53 (25 nM) and supplemented with GST (0.3 μM), GST-HBZ (0.3 μM), HBZ-AD (0.3 μM) or HBZ-bZIP (0.3 μM) where indicated. Reactions were analyzed by Western blot using antibodies against acetylated lysine, p53 acetyl-K382 and p53. Identical quantities from the same batch of proteins used in the HAT assay were resolved by SDS-PAGE and stained with Coomassie (lower panel).CC BY · PubMed Central
Figure 4 HBO1 contributes to p53-mediated activation of p21/CDKN1A A. HBO1 augments p53-dependent transcription. H1299 cells were cotransfected with pG13-luc (150 ng), and expression vectors for HA-p53 (200 ng), Flag-HBO1 (increasing concentration up to 1 μg), Flag-HBO1G485 (increasing concentration up to 1 μg), or a combination of those as indicated. The graph shows relative luminescence values ± S.D. from a triplicate experiment. Data are normalized to the control condition artificially set to 1 (lane 1 for the graph on the left and lane 6 for the graph on the right). B. Etoposide induces HBO1 recruitment to the p21/CDKN1A and GADD45A promoters. Chromatin immunoprecipitation (ChIP) analysis was performed on chromatin prepared from untreated HCT116 p53+/+ cells (grey bars) or cells treated with etoposide (black bars) using p53 and HBO1 antibodies or a preimmune serum (IgG). Precipitated DNA fragments were subjected to real-time PCR analysis with primers amplifying the BNDF promoter, the p53 binding region in the p21/CDKN1A promoter and the GADD45A promoter. Data are presented as fold enrichment over a control unrelated regions. C. HBO1 recruitment to the p21/CDKN1A and GADD45A promoters is dependent on p53. ChIP analysis in H1299 cells untreated (grey bars) or treated with etoposide (black bars) using an HBO1 antibody or a preimmune serum (IgG). Precipitated DNA fragments were subjected to real-time PCR analysis with primers amplifying the BNDF promoter, the p53 binding region in the p21/CDKN1A promoter, the GADD45A promoter and an HBO1 binding site in the HOXA9 promoter. D. Characterization of H1299 and HCT116 p53+/+ cells used in the study by Western blot. E. HBO1 depletion reduces transcription of p21/CDKN1A and GADD45A induced by etoposide. RT-PCR analyses of p21/CDKN1A and GADD45A expression were performed on mRNAs prepared from HCT116 cells transiently transfected with a specific siRNA against HBO1 or a control siRNA and further treated with ETO or not. Expression in each condition is normalized to the condition: -ETO, NT. F. The efficiency of the siRNA was estimated by Western blot.
Figure 4 HBO1 contributes to p53-mediated activation of p21/CDKN1A A. HBO1 augments p53-dependent transcription. H1299 cells were cotransfected with pG13-luc (150 ng), and expression vectors for HA-p53 (200 ng), Flag-HBO1 (increasing concentration up to 1 μg), Flag-HBO1G485 (increasing concentration up to 1 μg), or a combination of those as indicated. The graph shows relative luminescence values ± S.D. from a triplicate experiment. Data are normalized to the control condition artificially set to 1 (lane 1 for the graph on the left and lane 6 for the graph on the right). B. Etoposide induces HBO1 recruitment to the p21/CDKN1A and GADD45A promoters. Chromatin immunoprecipitation (ChIP) analysis was performed on chromatin prepared from untreated HCT116 p53+/+ cells (grey bars) or cells treated with etoposide (black bars) using p53 and HBO1 antibodies or a preimmune serum (IgG). Precipitated DNA fragments were subjected to real-time PCR analysis with primers amplifying the BNDF promoter, the p53 binding region in the p21/CDKN1A promoter and the GADD45A promoter. Data are presented as fold enrichment over a control unrelated regions. C. HBO1 recruitment to the p21/CDKN1A and GADD45A promoters is dependent on p53. ChIP analysis in H1299 cells untreated (grey bars) or treated with etoposide (black bars) using an HBO1 antibody or a preimmune serum (IgG). Precipitated DNA fragments were subjected to real-time PCR analysis with primers amplifying the BNDF promoter, the p53 binding region in the p21/CDKN1A promoter, the GADD45A promoter and an HBO1 binding site in the HOXA9 promoter. D. Characterization of H1299 and HCT116 p53+/+ cells used in the study by Western blot. E. HBO1 depletion reduces transcription of p21/CDKN1A and GADD45A induced by etoposide. RT-PCR analyses of p21/CDKN1A and GADD45A expression were performed on mRNAs prepared from HCT116 cells transiently transfected with a specific siRNA against HBO1 or a control siRNA and further treated with ETO or not. Expression in each condition is normalized to the condition: -ETO, NT. F. The efficiency of the siRNA was estimated by Western blot.CC BY · PubMed Central
Figure 5 HBZ inhibits HBO1 HAT activity A. HBZ and HBO1 interact in vivo. Whole cell extracts were prepared from HEK293T/17 cells transfected with expression vectors for HBZ-Myc-His and/or HBO1-HA (6 μg of each vector). Extracts were analyzed by immunoprecipitation (IP) and Western blotting using Myc and HA epitope antibodies as indicated. Whole cell extracts (10% of the IP inputs) are shown in lanes 1 to 3. B. HBZ interacts with endogenous HBO1. Nuclear extract was prepared from H1299 cells transfected with an expression vector for HBZ-Flag (3 μg) and analyzed by IP using preimmune serum (IgG) or a Flag epitope antibody as indicated. The Western blot was probed with Flag and HBO1 antibodies. The nuclear extract (20% of the IP input) is shown in lane 1. C. HBZ and HBO1 interact directly. Recombinant HBO1 (10 pmol) was incubated with 25 pmol of GST, GST-HBZ or GST-bZIP. Bound proteins were detected by Western blot using 6xHis and GST antibodies. A fraction of the HBO1 input (10%) is shown in lane 1. D. HBZ inhibits HBO1 HAT activity. In vitro HAT assays were performed using recombinant histones (2 μM), p300 (2 nM), HBO1 (18 nM), GST (0.2 μM), GST-HBZ (0.2 μM), HBZ-AD (0.2 μM) and HBZ-bZIP (0.2 μM) as indicated and analyzed by Western blot using antibodies against acetylated lysine, acetylated histone H4 and histone H4 as indicated. E. HBO1 does not acetylate p53. In vitro HAT assays were performed using the same concentrations of the indicated recombinant proteins as above, but with p53 (0.1 μM) replacing histones as the substrate. Reactions were analyzed by Western blot using antibodies against acetylated lysine and p53. Only a portion of the HAT assay was loaded in lane 2. F. HBZ inhibits HBO1-mediated activation of the p21/CDKN1A promoter. H1299 cells were cotransfected with pG13-luc (150 ng), and expression vectors for HA-p53 (200 ng), Flag-HBZ (150 ng), Flag-HBO1 (200 ng), Flag-HBO1G485 (200 ng), or combination of those as indicated. The graph shows relative luminescence values ± S.D. from a triplicate experiment. Data are normalized to the control condition (lane 1) artificially set to 1. *P < 0.05 (two-tailed Student t test).
Figure 5 HBZ inhibits HBO1 HAT activity A. HBZ and HBO1 interact in vivo. Whole cell extracts were prepared from HEK293T/17 cells transfected with expression vectors for HBZ-Myc-His and/or HBO1-HA (6 μg of each vector). Extracts were analyzed by immunoprecipitation (IP) and Western blotting using Myc and HA epitope antibodies as indicated. Whole cell extracts (10% of the IP inputs) are shown in lanes 1 to 3. B. HBZ interacts with endogenous HBO1. Nuclear extract was prepared from H1299 cells transfected with an expression vector for HBZ-Flag (3 μg) and analyzed by IP using preimmune serum (IgG) or a Flag epitope antibody as indicated. The Western blot was probed with Flag and HBO1 antibodies. The nuclear extract (20% of the IP input) is shown in lane 1. C. HBZ and HBO1 interact directly. Recombinant HBO1 (10 pmol) was incubated with 25 pmol of GST, GST-HBZ or GST-bZIP. Bound proteins were detected by Western blot using 6xHis and GST antibodies. A fraction of the HBO1 input (10%) is shown in lane 1. D. HBZ inhibits HBO1 HAT activity. In vitro HAT assays were performed using recombinant histones (2 μM), p300 (2 nM), HBO1 (18 nM), GST (0.2 μM), GST-HBZ (0.2 μM), HBZ-AD (0.2 μM) and HBZ-bZIP (0.2 μM) as indicated and analyzed by Western blot using antibodies against acetylated lysine, acetylated histone H4 and histone H4 as indicated. E. HBO1 does not acetylate p53. In vitro HAT assays were performed using the same concentrations of the indicated recombinant proteins as above, but with p53 (0.1 μM) replacing histones as the substrate. Reactions were analyzed by Western blot using antibodies against acetylated lysine and p53. Only a portion of the HAT assay was loaded in lane 2. F. HBZ inhibits HBO1-mediated activation of the p21/CDKN1A promoter. H1299 cells were cotransfected with pG13-luc (150 ng), and expression vectors for HA-p53 (200 ng), Flag-HBZ (150 ng), Flag-HBO1 (200 ng), Flag-HBO1G485 (200 ng), or combination of those as indicated. The graph shows relative luminescence values ± S.D. from a triplicate experiment. Data are normalized to the control condition (lane 1) artificially set to 1. *P < 0.05 (two-tailed Student t test).CC BY · PubMed Central
Figure 6 HBZ inhibits binding of HBO1 to the p21/CDKN1A promoter following etoposide treatment A. Graphic representation of the p21/CDKN1A promoter showing 5′ and 3′ p53 responsive elements (RE, white boxes) and the transcription start site (TSS). Bold horizontal lines denote real-time PCR amplicons. ChIP analyses were performed on chromatin prepared from untreated (grey bars) or etoposide-treated (black bars) cells using an HBO1 antibody or a preimmune serum (IgG). Precipitated DNA fragments were subjected to real-time PCR analysis. Data are presented as fold enrichment over a control unrelated regions. B. Analysis of a HeLa clonal cell line containing the empty pcDNA 3.1 vector. C. Analysis of a HeLa clonal cell line stably expressing HBZ.
Figure 6 HBZ inhibits binding of HBO1 to the p21/CDKN1A promoter following etoposide treatment A. Graphic representation of the p21/CDKN1A promoter showing 5′ and 3′ p53 responsive elements (RE, white boxes) and the transcription start site (TSS). Bold horizontal lines denote real-time PCR amplicons. ChIP analyses were performed on chromatin prepared from untreated (grey bars) or etoposide-treated (black bars) cells using an HBO1 antibody or a preimmune serum (IgG). Precipitated DNA fragments were subjected to real-time PCR analysis. Data are presented as fold enrichment over a control unrelated regions. B. Analysis of a HeLa clonal cell line containing the empty pcDNA 3.1 vector. C. Analysis of a HeLa clonal cell line stably expressing HBZ.CC BY · PubMed Central
Figure 7 HBZ delays cell cycle arrest in G2/M following treatment with etoposide A. HBZ does not alter the level of apoptosis induced by etoposide. HCT116 p53+/+ cells were transiently transfected with an HBZ or empty expression vector and, 48 h post-transfection, were treated with etoposide (ETO) or the DMSO vehicle (control) for 24 hours as indicated. Plots are from a representative experiment and the bar graph shows the average flow cytometry data of early apoptosis (grey bars) and late apoptosis (darker grey bars) from three independent experiments ± S.D. B. HBZ decreases G2/M arrest in an asynchronous cell population. HCT116 p53+/+ cells were transiently transfected with an HBZ or the empty expression vector and, 48 h post-transfection, were treated with etoposide (ETO), or the DMSO vehicle (control) for 24 hours as indicated. The graph shows the average flow cytometry data from three independent experiments ± S.D. *P < 0.05 (two-tailed Student t test). C. HBZ delays G2/M arrest in a synchronized cell population. Transfected HCT116 p53+/+ cells were arrested in G1 phase by serum starvation and treated with etoposide (ETO), or the DMSO vehicle (control) for the times indicated. The graph shows the average flow cytometry data from two independent experiments ± S.D.
Figure 7 HBZ delays cell cycle arrest in G2/M following treatment with etoposide A. HBZ does not alter the level of apoptosis induced by etoposide. HCT116 p53+/+ cells were transiently transfected with an HBZ or empty expression vector and, 48 h post-transfection, were treated with etoposide (ETO) or the DMSO vehicle (control) for 24 hours as indicated. Plots are from a representative experiment and the bar graph shows the average flow cytometry data of early apoptosis (grey bars) and late apoptosis (darker grey bars) from three independent experiments ± S.D. B. HBZ decreases G2/M arrest in an asynchronous cell population. HCT116 p53+/+ cells were transiently transfected with an HBZ or the empty expression vector and, 48 h post-transfection, were treated with etoposide (ETO), or the DMSO vehicle (control) for 24 hours as indicated. The graph shows the average flow cytometry data from three independent experiments ± S.D. *P < 0.05 (two-tailed Student t test). C. HBZ delays G2/M arrest in a synchronized cell population. Transfected HCT116 p53+/+ cells were arrested in G1 phase by serum starvation and treated with etoposide (ETO), or the DMSO vehicle (control) for the times indicated. The graph shows the average flow cytometry data from two independent experiments ± S.D.CC BY · PubMed Central
Figure 8 Model summarizing the effects of HBZ on p53-regulated transcription of p21/CDKN1A Etoposide-induced DNA damage, stimulates p53-dependent recruitment of p300 and HBO1 to the promoter (dashed blue arrows). During this process p300 acetylates p53 at K382 (ac-labeled arrow) and other lysine residues to increase the DNA-binding activity of p53 (solid blue arrow). HBO1 recruitment may be facilitated by associated ING and JADE/BRPF proteins, which interact with methylated histone H3 through their PHD finger domains. These interactions may position HBO1 in proximity to the transcription start site, where it acetylates histones. By inhibiting the HAT domains of p300 and HBO1, HBZ represses acetylation of p53 and promoter-associated histones. HBZ also restricts the recruitment of HBO1, which may lead to further reduction in acetylation of histones at the promoter. The sum of the effects of HBZ is to dampen the level of activation of p21/CDKN1A (and GADD45A) transcription, leading to a delay in cell cycle arrest induced by etoposide.
Figure 8 Model summarizing the effects of HBZ on p53-regulated transcription of p21/CDKN1A Etoposide-induced DNA damage, stimulates p53-dependent recruitment of p300 and HBO1 to the promoter (dashed blue arrows). During this process p300 acetylates p53 at K382 (ac-labeled arrow) and other lysine residues to increase the DNA-binding activity of p53 (solid blue arrow). HBO1 recruitment may be facilitated by associated ING and JADE/BRPF proteins, which interact with methylated histone H3 through their PHD finger domains. These interactions may position HBO1 in proximity to the transcription start site, where it acetylates histones. By inhibiting the HAT domains of p300 and HBO1, HBZ represses acetylation of p53 and promoter-associated histones. HBZ also restricts the recruitment of HBO1, which may lead to further reduction in acetylation of histones at the promoter. The sum of the effects of HBZ is to dampen the level of activation of p21/CDKN1A (and GADD45A) transcription, leading to a delay in cell cycle arrest induced by etoposide.CC BY · PubMed Central

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Cited by

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Metadata

Authors
Wright, D. G., Marchal, C., Hoang, K., Ankney, J. A., Nguyen, S. T., Rushing, A. W., Polakowski, N., Miotto, B., & Lemasson, I.
Venue
Oncotarget
Publisher
Impact Journals, LLC
Published
2015-11-28
Volume
7
Issue
2
Pages
1687-1706
ISSN
1949-2553
DOI
10.18632/oncotarget.6424
PMC
PMC4811490
Cited by
44
References
16
Language
en

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CoChat. (2026). Citation check: Human T-cell leukemia virus type-1-encoded protein HBZ represses p53 function by inhibiting the acetyltransferase activity of p300/CBP and HBO1. https://app.cochat.ai/papers/10.18632/oncotarget.6424
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Wright, D. G., Marchal, C., Hoang, K., Ankney, J. A., Nguyen, S. T., Rushing, A. W., Polakowski, N., Miotto, B., & Lemasson, I. (2016). Human T-cell leukemia virus type-1-encoded protein HBZ represses p53 function by inhibiting the acetyltransferase activity of p300/CBP and HBO1. Oncotarget. https://doi.org/10.18632/oncotarget.6424

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