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Article ; Online: Co-inhibition of BET and NAE enhances BIM-dependent apoptosis with augmented cancer therapeutic efficacy.

Zhang, Qian / Wu, Qian / Huan, Xia-Juan / Song, Shan-Shan / Bao, Xu-Bin / Miao, Ze-Hong / Wang, Ying-Qing

2024 Volume 223, Page(s) 116198

Abstract: Agents that inhibit bromodomain and extra-terminal domain (BET) proteins have been actively tested in the clinic as potential anticancer drugs. NEDD8-activating enzyme (NAE) inhibitors, represented by MLN4924, target the only activation enzyme in the ... ...

Abstract	Agents that inhibit bromodomain and extra-terminal domain (BET) proteins have been actively tested in the clinic as potential anticancer drugs. NEDD8-activating enzyme (NAE) inhibitors, represented by MLN4924, target the only activation enzyme in the neddylation pathway that has been identified as an attractive target for cancer therapy. In this study, we focus on the combination of BET inhibitors (BETis) and NAE inhibitors (NAEis) as a cancer therapeutic strategy and investigate its underlying mechanisms to explore and expand the application scope of both types of drugs. The results showed that this combination synergistically inhibited the proliferative activity of tumor cells from different tissues. Compared to a single drug, combination therapy had a weak effect on cycle arrest but significantly enhanced cell apoptosis. Furthermore, the growth of NCI-H1975 xenografts in nude mice was significantly inhibited by the combination without obvious body weight loss. Research on the synergistic mechanism demonstrated that combination therapy significantly increased the mRNA and protein levels of the proapoptotic gene BIM. The inhibition and knockout of BIM significantly attenuated the apoptosis induced by the combination, whereas the re-expression of BIM restored the synergistic effects, indicating that BIM induction plays a critical role in mediating the enhanced apoptosis induced by the co-inhibition of BET and NAE. Together, the enhanced transcription mediated by miR-17-92 cluster inhibition and reduced degradation promoted the increase in BIM levels, resulting in a synergistic effect. Collectively, these findings highlight the need for further clinical investigation into the combination of BETi and NAEi as a promising strategy for cancer therapy.
MeSH term(s)	Animals ; Humans ; Mice ; Antineoplastic Agents/pharmacology ; Apoptosis ; Cell Line, Tumor ; Cyclopentanes/pharmacology ; Mice, Nude ; Neoplasms ; Bcl-2-Like Protein 11/metabolism
Chemical Substances	Antineoplastic Agents ; Cyclopentanes ; Bcl-2-Like Protein 11 ; DNER protein, human
Language	English
Publishing date	2024-04-06
Publishing country	England
Document type	Journal Article
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2024.116198
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Article ; Online: The combination of methionine adenosyltransferase 2A inhibitor and methyltransferase like 3 inhibitor promotes apoptosis of non-small cell lung cancer cells and produces synergistic anti-tumor activity.

Xuan, Yi-Fei / Lu, Shan / Ou, Ying-Jie / Bao, Xu-Bin / Huan, Xia-Juan / Song, Shan-Shan / Miao, Ze-Hong / Wang, Ying-Qing

Biochemical and biophysical research communications

2024 Volume 716, Page(s) 150011

Abstract: Methionine adenosyltransferase 2 A (MAT2A) mediates the synthesis of methyl donor S-Adenosylmethionine (SAM), providing raw materials for methylation reactions in cells. MAT2A inhibitors are currently used for the treatment of tumors with ... ...

Abstract	Methionine adenosyltransferase 2 A (MAT2A) mediates the synthesis of methyl donor S-Adenosylmethionine (SAM), providing raw materials for methylation reactions in cells. MAT2A inhibitors are currently used for the treatment of tumors with methylthioadenosine phosphorylase (MTAP) deficiency in clinical research. Methyltransferase like 3 (METTL3) catalyzes N6-methyladenosine (m
Language	English
Publishing date	2024-04-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2024.150011
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Article ; Online: Loss of VOPP1 Contributes to BET Inhibitor Acquired Resistance in Non-Small Cell Lung Cancer Cells.

Sun, Lin / Wu, Qian / Huan, Xia-Juan / Tian, Chang-Qing / Wang, Ying-Qing / Miao, Ze-Hong

Molecular cancer research : MCR

2022 Volume 20, Issue 12, Page(s) 1785–1798

Abstract: Inhibitors targeting bromodomain and extraterminal (BET) proteins are promising anticancer drugs. The emergence of drug resistance during treatments will impair their therapeutic effectiveness. To investigate the mechanisms of acquired resistance to BET ... ...

Abstract	Inhibitors targeting bromodomain and extraterminal (BET) proteins are promising anticancer drugs. The emergence of drug resistance during treatments will impair their therapeutic effectiveness. To investigate the mechanisms of acquired resistance to BET inhibitors (BETi), we generated a series of drug-resistant sublines by exposing non-small cell lung cancer (NSCLC) NCI-H1975 cells to the BETi ABBV-075. These sublines displayed cross-resistance to other tested BETis, increased migration abilities, reduced growth rates accompanied by an increased proportion of cells in G1 phase and decreased apoptotic responses to BETis. Changes in RNA expression and gene mutation profiles in the resistant variants indicate that emergence of BETi resistance is multifactorial. Importantly, all the tested ABBV-075-resistant variants showed loss of vesicular overexpressed in cancer prosurvival protein 1 (VOPP1) and an increase in the antiapoptotic BCL-2 protein. By knockdown, knockout, and reconstitution of VOPP1 in resistant cells, their parental cells, and other NSCLC cells, we confirmed that the loss of VOPP1 contributed to BETi resistance. Moreover, knockout of VOPP1 in the parental cells caused the increased expression of BCL-2, and the latter directly mediated BETi resistance. Through combined treatments with BETis and BCL-2 inhibitors (BCL-2i), we demonstrated that BCL-2is synergistically sensitized resistant cells to BETis. Implications: Based on these results, for the first time, we establish a causal link from VOPP1 loss to BCL-2 gain and then to BETi resistance, which provides new insights into BETi resistance and paves the way for further testing to circumvent BETi resistance.
MeSH term(s)	Humans ; Antineoplastic Agents/pharmacology ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Cell Line, Tumor ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Proto-Oncogene Proteins c-bcl-2/genetics ; Transcription Factors/genetics
Chemical Substances	Antineoplastic Agents ; mivebresib (VR86R11J7J) ; Proto-Oncogene Proteins c-bcl-2 ; Transcription Factors ; VOPP1 protein, human ; DNER protein, human
Language	English
Publishing date	2022-08-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-21-1000
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Zs.A 5744: Show issues

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Article ; Online: Proteasome inhibitors reduce CD73 expression partly via decreasing p-ERK in NSCLC cells.

Su, Ai-Ling / Tian, Chang-Qing / Ou, Ying-Jie / Bao, Xu-Bin / Huan, Xia-Juan / Miao, Ze-Hong / Wang, Ying-Qing

Life sciences

2023 Volume 332, Page(s) 122129

Abstract: Ecto-5'-nucleotidase (CD73), encoded by the NT5E gene, mediates tumor immunosuppression and has been targeted for the development of new anticancer drugs. Proteasome inhibitors impair protein degradation by inhibiting proteasome and have been used in the ...

Abstract	Ecto-5'-nucleotidase (CD73), encoded by the NT5E gene, mediates tumor immunosuppression and has been targeted for the development of new anticancer drugs. Proteasome inhibitors impair protein degradation by inhibiting proteasome and have been used in the clinic for cancer therapy. Here we report that proteasome inhibitors reduce the protein and mRNA levels of CD73. Among 127 tested small-molecule drugs, proteasome inhibitors were found to consistently decrease the protein and mRNA levels of CD73 in NSCLC NCI-H1299 cells. This effect was further confirmed in different NSCLC cells exposed to different proteasome inhibitors. In those treated cells, the protein levels of ERK and its active form p-ERK, the vital components in the MAPK pathway, were reduced. Consistently, inhibitors of MEK and ERK, another two members of the MAPK pathway, also lowered the protein and mRNA levels of CD73. Correspondingly, treatments with fibroblast growth factor 2 (FGF2), an activator of the MAPK pathway, enhanced the levels of p-ERK and partly rescued the proteasome inhibitor-driven reduction of CD73 mRNA and protein in NSCLC cells. However, exogenous CD73 overexpression in murine Lewis lung carcinoma (LLC) cells was not lowered either in vitro or in vivo, by the treatments with proteasome inhibitors and basically, did not affect their in vitro proliferative inhibition either. In contrast, CD73 overexpression dramatically reduced the in vivo anticancer activity of Bortezomib in immunocompetent mice, with tumor growth inhibition rates from 52.18 % for LLC/vector down to 8.75 % for LLC/NT5E homografts. These findings give new insights into the anticancer mechanisms of proteasome inhibitors.
Language	English
Publishing date	2023-09-26
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2023.122129
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Article: TNKS inhibitors potentiate proliferative inhibition of BET inhibitors via reducing β-Catenin in colorectal cancer cells.

Wu, Qian / Xuan, Yi-Fei / Su, Ai-Ling / Bao, Xu-Bin / Miao, Ze-Hong / Wang, Ying-Qing

American journal of cancer research

2022 Volume 12, Issue 3, Page(s) 1069–1087

Abstract: Colorectal cancer (CRC) is an aggressive malignancy with limited options for treatment. Targeting the bromodomain and extra terminal domain (BET) proteins by using BET inhibitors (BETis) could effectively interrupt the interaction with acetylated ... ...

Abstract	Colorectal cancer (CRC) is an aggressive malignancy with limited options for treatment. Targeting the bromodomain and extra terminal domain (BET) proteins by using BET inhibitors (BETis) could effectively interrupt the interaction with acetylated histones, inhibit genes transcription and have shown a certain effect on CRC inhibition. To improve the efficacy, the inhibitors of Tankyrases, which cause accumulation of AXIN through dePARsylation, in turn facilitate the degradation of β-Catenin and suppress the growth of adenomatous polyposis coli (APC)-mutated CRCs, were tested together with BETi as a combination treatment. We examined the effects of BETi and Tankyrases inhibitor (TNKSi) together on the proliferation, cell cycle and apoptosis of human CRCs cell lines with
Language	English
Publishing date	2022-03-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2589522-9
ISSN	2156-6976
ISSN	2156-6976
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Article ; Online: Polymerase independent repression of FoxO1 transcription by sequence-specific PARP1 binding to FoxO1 promoter.

Tian, Yu-Nan / Chen, Hua-Dong / Tian, Chang-Qing / Wang, Ying-Qing / Miao, Ze-Hong

Cell death & disease

2020 Volume 11, Issue 1, Page(s) 71

Abstract: Poly(ADP-ribose) polymerase 1 (PARP1) regulates gene transcription in addition to functioning as a DNA repair factor. Forkhead box O1 (FoxO1) is a transcription factor involved in extensive biological processes. Here, we report that PARP1 binds to two ... ...

Abstract	Poly(ADP-ribose) polymerase 1 (PARP1) regulates gene transcription in addition to functioning as a DNA repair factor. Forkhead box O1 (FoxO1) is a transcription factor involved in extensive biological processes. Here, we report that PARP1 binds to two separate motifs on the FoxO1 promoter and represses its transcription in a polymerase-independent manner. Using PARP1-knock out (KO) cells, wild-type-PARP1-complemented cells and catalytic mutant PARP1
MeSH term(s)	Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Proliferation/genetics ; DNA Damage/drug effects ; Forkhead Box Protein O1/genetics ; Forkhead Box Protein O1/metabolism ; Gene Expression Regulation/genetics ; Gene Knockout Techniques ; Humans ; Mutation ; Poly (ADP-Ribose) Polymerase-1/antagonists & inhibitors ; Poly (ADP-Ribose) Polymerase-1/genetics ; Poly (ADP-Ribose) Polymerase-1/metabolism ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; Promoter Regions, Genetic ; Protein Binding ; Sarcoma, Ewing/genetics ; Sarcoma, Ewing/metabolism ; Up-Regulation
Chemical Substances	FOXO1 protein, human ; Forkhead Box Protein O1 ; Poly(ADP-ribose) Polymerase Inhibitors ; PARP1 protein, human (EC 2.4.2.30) ; Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30)
Language	English
Publishing date	2020-01-28
Publishing country	England
Document type	Journal Article
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-020-2265-y
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Article ; Online: Marine-derived angiogenesis inhibitors for cancer therapy.

Wang, Ying-Qing / Miao, Ze-Hong

Marine drugs

2013 Volume 11, Issue 3, Page(s) 903–933

Abstract: Angiogenesis inhibitors have been successfully used for cancer therapy in the clinic. Many marine-derived natural products and their analogues have been reported to show antiangiogenic activities. Compared with the drugs in the clinic, these agents ... ...

Abstract	Angiogenesis inhibitors have been successfully used for cancer therapy in the clinic. Many marine-derived natural products and their analogues have been reported to show antiangiogenic activities. Compared with the drugs in the clinic, these agents display interesting characteristics, including diverse sources, unique chemical structures, special modes of action, and distinct activity and toxicity profiles. This review will first provide an overview of the current marine-derived angiogenesis inhibitors based on their primary targets and/or mechanisms of action. Then, the marine-derived antiangiogenic protein kinase inhibitors will be focused on. And finally, the clinical trials of the marine-derived antiangiogenic agents will be discussed, with special emphasis on their application potentials, problems and possible coping strategies in their future development as anticancer drugs.
MeSH term(s)	Angiogenesis Inhibitors/isolation & purification ; Angiogenesis Inhibitors/pharmacology ; Animals ; Antineoplastic Agents/isolation & purification ; Antineoplastic Agents/pharmacology ; Aquatic Organisms ; Drug Design ; Humans ; Neoplasms/blood supply ; Neoplasms/drug therapy ; Neoplasms/pathology ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/pathology ; Protein Kinase Inhibitors/isolation & purification ; Protein Kinase Inhibitors/pharmacology
Chemical Substances	Angiogenesis Inhibitors ; Antineoplastic Agents ; Protein Kinase Inhibitors
Language	English
Publishing date	2013-03-15
Publishing country	Switzerland
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2175190-0
ISSN	1660-3397 ; 1660-3397
ISSN (online)	1660-3397
ISSN	1660-3397
DOI	10.3390/md11030903
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Article ; Online: Tanshinone I inhibits tumor angiogenesis by reducing Stat3 phosphorylation at Tyr705 and hypoxia-induced HIF-1α accumulation in both endothelial and tumor cells.

Wang, Yan / Li, Jia-Xin / Wang, Ying-Qing / Miao, Ze-Hong

Oncotarget

2015 Volume 6, Issue 18, Page(s) 16031–16042

Abstract: Tanshinone I (Tanshinone-1), a major active principle of Salvia miltiorrhiza (Danshen), has been shown to overcome tumor drug resistance and metastasis. Here we report that tanshinone-1 inhibits angiogenesis. Tanshinone-1 inhibited proliferation, ... ...

Abstract	Tanshinone I (Tanshinone-1), a major active principle of Salvia miltiorrhiza (Danshen), has been shown to overcome tumor drug resistance and metastasis. Here we report that tanshinone-1 inhibits angiogenesis. Tanshinone-1 inhibited proliferation, migration and tube formation of vascular endothelial cells, rat aortic ring sprouting and the neovascularization of the chick chorioallantoic membrane in a concentration-dependent manner. In endothelial cells, tanshinone-1 almost completely inhibited phosphorylation of Stat3 at Tyr705 regardless of hypoxia or normoxia but only slightly decreased the hypoxia-induced HIF-1α accumulation. In tumor cells, contrastively, tanshinone-1 could not only make phosphorylation of Stat3 at Tyr705 disappear but also reduce the hypoxia-induced accumulation of HIF-1α to its baseline levels at normoxia. Consequently, VEGF secretion from tumor cells was reduced, which could potentiate the direct inhibition of tanshinone-1 on endothelial cells. Together with its overcoming tumor drug resistance and metastasis, our results reveal unique characteristics of tanshinone-1 and its improved derivatives as promising angiogenesis inhibitors.
MeSH term(s)	Animals ; Antineoplastic Agents, Phytogenic/pharmacology ; Aorta/metabolism ; Aorta/pathology ; Apoptosis ; Blotting, Western ; Cell Movement ; Cell Proliferation ; Chickens ; Chorioallantoic Membrane/metabolism ; Diterpenes, Abietane/pharmacology ; Endothelium, Vascular/cytology ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/metabolism ; Enzyme-Linked Immunosorbent Assay ; Humans ; Hypoxia/physiopathology ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Neoplasms/blood supply ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/prevention & control ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/pathology ; Neovascularization, Pathologic/prevention & control ; Phosphorylation/drug effects ; RNA, Messenger/genetics ; RNA, Small Interfering/genetics ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; STAT3 Transcription Factor/antagonists & inhibitors ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; Tumor Cells, Cultured ; Tyrosine/metabolism
Chemical Substances	Antineoplastic Agents, Phytogenic ; Diterpenes, Abietane ; Hypoxia-Inducible Factor 1, alpha Subunit ; RNA, Messenger ; RNA, Small Interfering ; STAT3 Transcription Factor ; tanshinone (03UUH3J385) ; Tyrosine (42HK56048U)
Language	English
Publishing date	2015-06-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.3648
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Article ; Online: Generation of an induced pluripotent stem cell line, FJMUUHi001-A, from a hereditary Parkinson's disease patient with homozygous mutation of c.189dupA in PARK7.

Chen, Zhi-Ting / Zhao, Zhen-Hua / Chen, Li-Na / Fan, Fei / Cai, Guo-En / Weng, Hui-Dan / Wang, Ying-Qing / Liao, Lian-Ming / Chen, Xiao-Chun / Huang, En / Ye, Qin-Yong

Stem cell research

2021 Volume 51, Page(s) 102175

Abstract: PARK7 mutations are accountable for the inherited Parkinson's disease. An induced pluripotent stem cell (iPSC) line FJMUUHi001-A was generated by expressing five reprogramming factors, OCT3/4, SOX2, c-MYC, KLF4 and BCL-XL, in peripheral blood mononuclear ...

Abstract	PARK7 mutations are accountable for the inherited Parkinson's disease. An induced pluripotent stem cell (iPSC) line FJMUUHi001-A was generated by expressing five reprogramming factors, OCT3/4, SOX2, c-MYC, KLF4 and BCL-XL, in peripheral blood mononuclear cells from a 32-year old patient carrying a homozygous mutation of c.189dupA in PARK7. The iPSCs with a normal karyotype had the abilities to differentiate into three germ layers and expressed pluripotency markers without detectable residual plasmids. The cell line FJMUUHi001-A carrying the truncating protein PARK7 could be a useful tool to help comprehend the function of PARK7 in the iPSCs and differentiated cells from them.
MeSH term(s)	Adult ; Cell Differentiation ; Cell Line ; Cellular Reprogramming ; Humans ; Induced Pluripotent Stem Cells ; Leukocytes, Mononuclear ; Mutation/genetics ; Parkinson Disease/genetics ; Protein Deglycase DJ-1
Chemical Substances	PARK7 protein, human (EC 3.1.2.-) ; Protein Deglycase DJ-1 (EC 3.1.2.-)
Language	English
Publishing date	2021-01-13
Publishing country	England
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1876-7753
ISSN (online)	1876-7753
DOI	10.1016/j.scr.2021.102175
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Article ; Online: Novel bivalent BET inhibitor N2817 exhibits potent anticancer activity and inhibits TAF1.

Wu, Qian / Chen, Dan-Qi / Sun, Lin / Huan, Xia-Juan / Bao, Xu-Bin / Tian, Chang-Qing / Hu, Jianping / Lv, Kai-Kai / Wang, Ying-Qing / Xiong, Bing / Miao, Ze-Hong

Biochemical pharmacology

2021 Volume 185, Page(s) 114435

Abstract: Bromodomain and extra-terminal domain (BET) family proteins are promising anticancer targets. Most BET inhibitors in clinical trials are monovalent. They competitively bind to one of the bromodomains (BD1 and BD2) in BET proteins and exhibit relatively ... ...

Abstract	Bromodomain and extra-terminal domain (BET) family proteins are promising anticancer targets. Most BET inhibitors in clinical trials are monovalent. They competitively bind to one of the bromodomains (BD1 and BD2) in BET proteins and exhibit relatively weak anticancer activity, poor pharmacokinetics, and low metabolic stability. Here, we evaluated the anticancer activity of a novel bivalent BET inhibitor, N2817, which consists of two molecules of the monovalent BET inhibitor 8124-053 connected by a common piperazine ring, rendering a long linker unnecessary. Compared with ABBV-075, one of the potent monovalent BET inhibitors reported to date, N2817 showed greater potency in inhibiting proliferation, arresting cell-cycle, inducing apoptosis, and suppressing the growth of tumor xenografts. Moreover, N2817 showed high metabolic stability, a relatively long half-life, and no brain penetration after oral administration. Additionally, N2817 directly bound and inhibited another BD-containing protein, TAF1 (BD2), as evidenced by a reduction in mRNA and protein levels. TAF1 inhibition contributed to the anticancer effect of N2817. Therefore, this study offers a new paradigm for designing bivalent BET inhibitors and introduces a novel potent bivalent BET inhibitor and a new anticancer mechanism.
MeSH term(s)	A549 Cells ; Animals ; Antineoplastic Agents/pharmacology ; Dose-Response Relationship, Drug ; Female ; HCT116 Cells ; Histone Acetyltransferases/antagonists & inhibitors ; Histone Acetyltransferases/metabolism ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Inbred ICR ; Mice, Nude ; Proteins/antagonists & inhibitors ; Proteins/metabolism ; TATA-Binding Protein Associated Factors/antagonists & inhibitors ; TATA-Binding Protein Associated Factors/metabolism ; Transcription Factor TFIID/antagonists & inhibitors ; Transcription Factor TFIID/metabolism ; Tumor Burden/drug effects ; Tumor Burden/physiology ; Xenograft Model Antitumor Assays/methods
Chemical Substances	Antineoplastic Agents ; Proteins ; TATA-Binding Protein Associated Factors ; Transcription Factor TFIID ; bromodomain and extra-terminal domain protein, human ; Histone Acetyltransferases (EC 2.3.1.48) ; TATA-binding protein associated factor 250 kDa (EC 2.7.11.1)
Language	English
Publishing date	2021-02-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2021.114435
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