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Auteur : Grafiati
Publié le 11 mars 2023

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1

Hay, Duncan A., Catherine M. Rogers, Oleg Fedorov, Cynthia Tallant, Sarah Martin, Octovia P. Monteiro, Susanne Müller, Stefan Knapp, Christopher J. Schofield et Paul E. Brennan. « Design and synthesis of potent and selective inhibitors of BRD7 and BRD9 bromodomains ». MedChemComm 6, no 7 (2015) : 1381–86. http://dx.doi.org/10.1039/c5md00152h.

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Ali, Maria Mushtaq, Sajda Ashraf, Mohammad Nure-e-Alam, Urooj Qureshi, Khalid Mohammed Khan et Zaheer Ul-Haq. « Identification of Selective BRD9 Inhibitor via Integrated Computational Approach ». International Journal of Molecular Sciences 23, no 21 (4 novembre 2022) : 13513. http://dx.doi.org/10.3390/ijms232113513.

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Bromodomain-containing protein 9 (BRD9), a member of the bromodomain and extra terminal domain (BET) protein family, works as an epigenetic reader. BRD9 has been considered an essential drug target for cancer, inflammatory diseases, and metabolic disorders. Due to its high similarity among other isoforms, no effective treatment of BRD9-associated disorders is available. For the first time, we performed a detailed comparative analysis among BRD9, BRD7, and BRD4. The results indicate that residues His42, Gly43, Ala46, Ala54, Val105, and Leu109 can confer the BRD9 isoform selectivity. The predicted crucial residues were further studied. The pharmacophore model’s features were precisely mapped with some key residues including, Gly43, Phe44, Phe45, Asn100, and Tyr106, all of which play a crucial role in BRD9 inhibition. Docking-based virtual screening was utilized with the consideration of the conserved water network in the binding cavity to identify the potential inhibitors of BRD9. In this workflow, 714 compounds were shortlisted. To attain selectivity, 109 compounds were re-docked to BRD7 for negative selection. Finally, four compounds were selected for molecular dynamics studies. Our studies pave the way for the identification of new compounds and their role in causing noticeable, functional differences in isoforms and between orthologues.
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Shi, Mingsong, Jun He, Tiantian Weng, Na Shi, Wenyan Qi, Yong Guo, Tao Chen, Lijuan Chen et Dingguo Xu. « The binding mechanism of NHWD-870 to bromodomain-containing protein 4 based on molecular dynamics simulations and free energy calculation ». Physical Chemistry Chemical Physics 24, no 8 (2022) : 5125–37. http://dx.doi.org/10.1039/d1cp05490b.

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Lim, Ratana, Caitlyn Nguyen-Ngo et Martha Lappas. « Targeting bromodomain-containing proteins to prevent spontaneous preterm birth ». Clinical Science 133, no 23 (décembre 2019) : 2379–400. http://dx.doi.org/10.1042/cs20190919.

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Abstract Preterm birth is a global healthcare challenge. Spontaneous preterm birth (sPTB) is commonly caused by inflammation, yet there are currently no effective therapies available. The Bromodomain and Extra-Terminal motif (BET) proteins, Bromodomain-containing protein (Brd) 2 (Brd2), Brd3 and Brd4 regulate inflammation in non-gestational tissues. The roles of Brd2–4 in human pregnancy are unknown. Using human and mouse models, the present study has identified the Brd proteins part of the process by which inflammation induces parturition. Using human clinical samples, we demonstrate that labor and infection increase the expression of Brds in the uterus and fetal membranes. In primary human myometrial, amnion and decidual cells, we found that global Brd protein inhibition, as well as selective inhibition of Brds, suppressed inflammation-induced expression of mediators involved in myometrial contractions and rupture of fetal membranes. Importantly, studies in the mouse model demonstrate that the pan-Brd inhibitor JQ1 reduced intrauterine inflammation induced by bacterial endotoxin LPS as well as decreasing the effectiveness of LPS to induce parturition. These results implicate BET proteins as novel therapeutic targets for reducing inflammation associated with spontaneous preterm labor.
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Kapoor, Sabeeta, et Roderick H. Dashwood. « Abstract 5712 : Dietary polyphenols as BRD7 and 9 inhibitors for cancer interception ». Cancer Research 82, no 12_Supplement (15 juin 2022) : 5712. http://dx.doi.org/10.1158/1538-7445.am2022-5712.

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Abstract Introduction Epigenetic mechanisms play an important role in the initiation and advancement of colorectal cancer (CRC) and other malignancies due, in part, to deregulated bromodomain (BRD) functions1,2. We examined compounds from natural sources as BRD7/9 inhibitors, seeking lead candidates outside of the widely studied bromodomain and extraterminal (BET) family3. Methods As reported4,5, docking in silico involved STRAP and AutoDock Vina, ligand-protein interactions employed PDBePISA and LPC/CSU, and BROMOscan®-Bromodomain arrays were used to screen for BRD7/9 interacting compounds. BRD7/9 inhibitors also were assessed by isothermal titration calorimetry (ITC) and by anticancer activities in human colon cancer cells. Results Docking in silico identified several dietary polyphenols as potential BRD7/9 inhibitors, with binding energies ≤ -8.0 kcal/mol. BROMOscan® and ITC experiments prioritized aspalathin, orientin, epigallocatechin-3-gallate, quercetin and equol for further investigation. Treatment with selected polyphenols mimicked BRD7/9 siRNA-mediated knockdown in reducing colon cancer cell viability and inhibiting colony formation, leading to DNA damage and apoptosis induction. Normal colonic epithelial cells were unaffected by the treatments, signifying cancer-specific targeting. These findings suggest that dietary polyphenols can recognize and target BRD7/9 proteins for potential cancer interception. Acknowledgements Research supported in part by NCI grant CA122959, the John S. Dunn Foundation, and a Chancellor's Research Initiative.1)Jung G et al., Nat Rev Gastroenterol Hepatol 2020;17:111-130. 2)Fujisawa T, Filippakopoulos P. Nat Rev Mol Cell Biol 2017;18:246-262.3)Damiani E et al., J Cancer Prev 2020;25:189-203. 4)Rajendran P et al., Cancer Res 2019;79:918-927. 5)Kapoor S et al., Cancers (Basel) 2021;13:1438. Citation Format: Sabeeta Kapoor, Roderick H. Dashwood. Dietary polyphenols as BRD7 and 9 inhibitors for cancer interception [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5712.
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Lee, Junsik M., Renyan Liu et Sang Won Park. « The regulatory subunits of PI3K, p85α and p85β, differentially affect BRD7-mediated regulation of insulin signaling ». Journal of Molecular Cell Biology 13, no 12 (9 novembre 2021) : 889–901. http://dx.doi.org/10.1093/jmcb/mjab073.

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Abstract Bromodomain-containing protein 7 (BRD7) has been shown to interact with the regulatory subunit of phosphatidylinositol 3-kinase (PI3K), p85, in the insulin signaling pathway. Here, we show that upregulation of hepatic BRD7 improves glucose homeostasis even in the absence of either p85 isoform, p85α or p85β. However, BRD7 leads to differential activation of downstream effector proteins in the insulin signaling pathway depending on which isoform of p85 is present. In the presence of only p85α, BRD7 overexpression increases phosphorylation of insulin receptor (IR) upon insulin stimulation, without increasing the recruitment of p85 to IR substrate. Overexpression of BRD7 also increases activation of Akt in response to insulin, but does not affect basal phosphorylation levels of Akt. Meanwhile, the phosphorylation of glycogen synthase kinase 3β (GSK3β) is increased by overexpression of BRD7. On the other hand, in the presence of only p85β, BRD7 overexpression does not affect phosphorylation levels of IR, and Akt phosphorylation is not affected by insulin stimulation following BRD7 upregulation. However, BRD7 overexpression leads to increased basal phosphorylation levels of Akt and GSK3β. These data demonstrate that BRD7’s action on glucose homeostasis does not require the presence of both p85 isoforms, and p85α and p85β have unique roles in insulin signaling in the liver.
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Clark, Peter G. K., Darren J. Dixon et Paul E. Brennan. « Development of chemical probes for the bromodomains of BRD7 and BRD9 ». Drug Discovery Today : Technologies 19 (mars 2016) : 73–80. http://dx.doi.org/10.1016/j.ddtec.2016.05.002.

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Park, Sang Won, et Junsik M. Lee. « Emerging Roles of BRD7 in Pathophysiology ». International Journal of Molecular Sciences 21, no 19 (27 septembre 2020) : 7127. http://dx.doi.org/10.3390/ijms21197127.

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Bromodomain is a conserved structural module found in many chromatin-associated proteins. Bromodomain-containing protein 7 (BRD7) is a member of the bromodomain-containing protein family, and was discovered two decades ago as a protein that is downregulated in nasopharyngeal carcinoma. Since then, BRD7 has been implicated in a variety of cellular processes, including chromatin remodeling, transcriptional regulation, and cell cycle progression. Decreased BRD7 activity underlies the pathophysiological properties of various diseases in different organs. BRD7 plays an important role in the pathogenesis of many cancers and, more recently, its roles in the regulation of metabolism and obesity have also been highlighted. Here, we review the involvement of BRD7 in a variety of pathophysiological conditions, with a focus on glucose homeostasis, obesity, and cancer.
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Crodian, Jennifer S., Bethany M. Weldon, Yu-Chun Tseng, Birgit Cabot et Ryan Cabot. « Nuclear trafficking dynamics of Bromodomain-containing protein 7 (BRD7), a switch/sucrose non-fermentable (SWI/SNF) chromatin remodelling complex subunit, in porcine oocytes and cleavage-stage embryos ». Reproduction, Fertility and Development 31, no 9 (2019) : 1497. http://dx.doi.org/10.1071/rd19030.

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In the work presented here, we investigated how bromodomain-containing protein 7 (BRD7), a subunit associated with switch/sucrose non-fermentable (SWI/SNF) chromatin remodelling complexes, is trafficked between cellular compartments during embryo development. SWI/SNF complexes are multi-subunit complexes that contain a core catalytic subunit (SWI/SNF related, Matrix associated, Actin dependent Regulator of Chromatin, subfamily A, member 4, or member 2; SMARCA4 or SMARCA2) and a collection of additional subunits that guide the complexes to their appropriate loci; BRD7 is one of these additional subunits. We hypothesised that BRD7 is exported from the nuclei of porcine oocytes and embryos in a Chromosome Region Maintenance 1 (CRM1)-dependent manner and imported into the nuclei using the karyopherin α/β1 heterodimer. Porcine oocytes and embryos were treated with inhibitors of CRM1-mediated nuclear export and karyopherin α/β1-mediated nuclear import to test this hypothesis. An RNA interference assay and a dominant negative overexpression assay were also performed to determine if karyopherin α7 serves a specific role in BRD7 trafficking. Our findings indicate that BRD7 shuttles between nuclear and cytoplasmic compartments during cleavage development. The shuttling of BRD7 indicates that it serves a unique role in remodelling chromatin during this developmental window.
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KZHYSHKOWSKA, Julia, Andre RUSCH, Hans WOLF et Thomas DOBNER. « Regulation of transcription by the heterogeneous nuclear ribonucleoprotein E1B-AP5 is mediated by complex formation with the novel bromodomain-containing protein BRD7 ». Biochemical Journal 371, no 2 (15 avril 2003) : 385–93. http://dx.doi.org/10.1042/bj20021281.

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E1B-AP5 was initially identified as a target of the early adenovirus E1B-55kDa protein during the course of lytic infection. E1B-AP5 belongs to the heterogeneous nuclear ribonucleoprotein family and was demonstrated to be involved in mRNA processing and transport [Gabler, Schutt, Groitl, Wolf, Shenk and Dobner (1998) J. Virol. 72, 7960–7971]. In the present paper, we demonstrate that E1B-AP5 differentially regulates basic and ligand-dependent transcription. We found that E1B-AP5 represses basic transcription driven by several virus and cellular promoters, and mapped the repression activity to the N-terminal part of the protein. In contrast with basic repression, E1B-AP5 activated the glucocorticoid-dependent promoter in the absence of dexamethasone, but did not contribute to the dexamethasone-induced activation. Mutant analysis indicated the presence of an additional cellular factor that modulates E1B-AP5 transcriptional activity. Using yeast two-hybrid screening, we identified a novel chromatin-associated bromodomain-containing protein, BRD7, as an E1B-AP5 interaction partner. We confirmed E1B-AP5–BRD7 complex formation in vivo and in vitro. We found that, although BRD7 binds to histones H2A, H2B, H3 and H4 through its bromodomain, this domain was not necessary for the interaction with E1B-AP5. Indeed, the triple complex formation of E1B-AP5, BRD7 and histones was demonstrated. Disruption of the E1B-AP5–BRD7 complex increased E1B-AP5 repression activity for basic transcription and converted it from being an activator of the hormone-dependent promoter into being a strong repressor. We conclude that complex formation between BRD7 and E1B-AP5 links chromatin events with mRNA processing at the level of transcriptional regulation.
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Sample, Reilly A., et Rachel Paolini. « 77232 The role of the bromodomain and extra-terminal motif (BET) family of proteins in head and neck cancer tumorigenic phenotype ». Journal of Clinical and Translational Science 5, s1 (mars 2021) : 5. http://dx.doi.org/10.1017/cts.2021.415.

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ABSTRACT IMPACT: Understanding the biology underpinning head and neck cancer invasion and metastasis could lead to novel targeted therapies that are both effective and tolerable for patients with this debilitating disease. OBJECTIVES/GOALS: The bromodomain and extra-terminal (BET) family of epigenetic regulators has been implicated in the tumorigenesis of various cancers. In head and neck squamous cell carcinoma (HNSCC), the majority of morbidity is due to invasion and metastasis, so there is special interest in understanding the development of these phenotypes in HNSCC cells. METHODS/STUDY POPULATION: Stable SCC9 knockdown cell lines were generated by infecting cells with a lentivirus encoding Cas9-KRAB and a lentivirus encoding gRNA targeting each of the candidate BET proteins: BRD2, BRD3, BRD4, and BRDT. Knockdown was confirmed by qRT-PCR. Next, standard assays for proliferation (CellTiter-glo), invasion (Matrigel), and migration (scratch-wound healing assay) were performed for all candidate knockdowns and compared to a non-target control. RESULTS/ANTICIPATED RESULTS: Proliferation assay results revealed that BRD4 knockdown had a significant negative effect on the proliferative capacity of SCC9 cells in vitro. Similarly, BRD4 knockdown SCC9 cell lines were less invasive and less migratory. Interestingly, knockdown of BRD2, BRD3, and BRDT had no effect on proliferation, invasiveness, or migration. DISCUSSION/SIGNIFICANCE OF FINDINGS: We have identified BRD4 as a key driver of the HNSCC tumorigenic phenotype. In the future, we plan to investigate the role of JQ1, a pan-BET inhibitor, on HNSCC cell phenotypes. Additionally, we will identify the downstream targets of BRD4, which may serve as potential therapeutic targets for both HNSCC as well as other cancers more broadly.
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Riching, Kristin M., James D. Vasta, Scott J. Hughes, Vittoria Zoppi, Chiara Maniaci, Andrea Testa, Marjeta Urh, Alessio Ciulli et Danette L. Daniels. « Translating PROTAC chemical series optimization into functional outcomes underlying BRD7 and BRD9 protein degradation ». Current Research in Chemical Biology 1 (2021) : 100009. http://dx.doi.org/10.1016/j.crchbi.2021.100009.

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Zhou, Ming, Xiao-Jie Xu, Hou-De Zhou, Hua-Ying Liu, Jia-Jin He, Xiao-Ling Li, Cong Peng et al. « BRD2 is one of BRD7-interacting proteins and its over-expression could initiate apoptosis ». Molecular and Cellular Biochemistry 292, no 1-2 (20 juin 2006) : 205–12. http://dx.doi.org/10.1007/s11010-006-9233-4.

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Kim, A. L., G. C. Jin, Y. Zhu et D. R. Bickers. « 227 Bromodomain-containing proteins BRD7 and BRD9 are novel interacting regulators of BCC resistance ». Journal of Investigative Dermatology 138, no 5 (mai 2018) : S38. http://dx.doi.org/10.1016/j.jid.2018.03.232.

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Yu, Zhifeng, Angela F. Ku, Justin L. Anglin, Rajesh Sharma, Melek Nihan Ucisik, John C. Faver, Feng Li et al. « Discovery and characterization of bromodomain 2–specific inhibitors of BRDT ». Proceedings of the National Academy of Sciences 118, no 9 (26 février 2021) : e2021102118. http://dx.doi.org/10.1073/pnas.2021102118.

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Bromodomain testis (BRDT), a member of the bromodomain and extraterminal (BET) subfamily that includes the cancer targets BRD2, BRD3, and BRD4, is a validated contraceptive target. All BET subfamily members have two tandem bromodomains (BD1 and BD2). Knockout mice lacking BRDT-BD1 or both bromodomains are infertile. Treatment of mice with JQ1, a BET BD1/BD2 nonselective inhibitor with the highest affinity for BRD4, disrupts spermatogenesis and reduces sperm number and motility. To assess the contribution of each BRDT bromodomain, we screened our collection of DNA-encoded chemical libraries for BRDT-BD1 and BRDT-BD2 binders. High-enrichment hits were identified and resynthesized off-DNA and examined for their ability to compete with JQ1 in BRDT and BRD4 bromodomain AlphaScreen assays. These studies identified CDD-1102 as a selective BRDT-BD2 inhibitor with low nanomolar potency and >1,000-fold selectivity over BRDT-BD1. Structure–activity relationship studies of CDD-1102 produced a series of additional BRDT-BD2/BRD4-BD2 selective inhibitors, including CDD-1302, a truncated analog of CDD-1102 with similar activity, and CDD-1349, an analog with sixfold selectivity for BRDT-BD2 versus BRD4-BD2. BROMOscan bromodomain profiling confirmed the great affinity and selectivity of CDD-1102 and CDD-1302 on all BET BD2 versus BD1 with the highest affinity for BRDT-BD2. Cocrystals of BRDT-BD2 with CDD-1102 and CDD-1302 were determined at 2.27 and 1.90 Å resolution, respectively, and revealed BRDT-BD2 specific contacts that explain the high affinity and selectivity of these compounds. These BD2-specific compounds and their binding to BRDT-BD2 are unique compared with recent reports and enable further evaluation of their nonhormonal contraceptive potential in vitro and in vivo.
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Tseng, Yu-Chun, Jennifer S. Crodian et Ryan Cabot. « Depletion of SMARCB1 and BRD7, two SWI/SNF chromatin remodelling complex subunits, differentially impact porcine embryo development ». Reproduction, Fertility and Development 34, no 7 (17 mars 2022) : 549–59. http://dx.doi.org/10.1071/rd21251.

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<b>Context:</b>SWI/SNF chromatin remodelling complexes are composed of multiple protein subunits and can be categorised into three sub-families, including the BAF, PBAF, and GBAF complexes. We hypothesised that depletion of SMARCB1 and BRD7, two subunits unique to different SWI/SNF sub-families, would differentially impact porcine embryo development. <b>Aim:</b>The aim of these experiments was to determine the developmental requirements of two SWI/SNF subunits, SMARCB1 and BRD7. <b>Methods:</b>RNA interference assays were used to determine the developmental requirements of SMARCB1 and BRD7 in porcine embryos. <b>Key results:</b>Our findings indicate that knockdown of SMARCB1 dramatically reduces embryo developmental potential, with few embryos developing beyond the pronuclear stage. The knockdown of BRD7 had a less severe impact on developmental potential. <b>Conclusions:</b>Our findings also demonstrate that knockdown of SMARCB1 alters the expression of <i>NANOG</i> and <i>POU5F1</i> (also referred to as <i>OCT4</i>). <b>Implications:</b>These findings highlight the unique developmental requirements for sub-families of SWI/SNF chromatin remodelling complexes. This new knowledge will enable us to determine how discrete genomic loci are differentially remodelled during key points in embryo development.
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Wu, Wen-Jing, Kai-Shun Hu, Dong-Liang Chen, Zhao-Lei Zeng, Hui-Yan Luo, Feng Wang, De-Shen Wang, Zhi-Qiang Wang, Fan He et Rui-Hua Xu. « Prognostic relevance of BRD7 expression in colorectal carcinoma ». European Journal of Clinical Investigation 43, no 2 (7 décembre 2012) : 131–40. http://dx.doi.org/10.1111/eci.12024.

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Liu, Huaying, Cong Peng, Ming Zhou, Jie Zhou, Shourong Shen, Houde Zhou, Wei Xiong et al. « Cloning and Characterization of the BRD7 Gene Promoter ». DNA and Cell Biology 25, no 6 (juin 2006) : 346–58. http://dx.doi.org/10.1089/dna.2006.25.346.

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Coudé, Marie-Magdelaine, Thorsten Braun, Jeannig Berrou, Mélanie Dupont, Raphael Itzykson, Aline Masse, Emmanuel Raffoux et al. « Bromodomain Inhibition By OTX015 Regulates c-MYC and HEXIM1 in a Panel of Human Acute Leukemia Cell Lines ». Blood 124, no 21 (6 décembre 2014) : 5957. http://dx.doi.org/10.1182/blood.v124.21.5957.5957.

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Abstract Background: The bromodomain-containing protein 4 (BRD4) activates the transcription elongation factor b (P-TEFb) which regulates RNA polymerase II. Conversely, hexamethylene bisacetamide (HMBA) inducible protein 1 (HEXIM1) inactivates P-TEFb. BRD4/HEXIM1 interplay influences cell cycle progression and tumorigenesis. It has been widely demonstrated that BRD4 knockdown or inhibition by JQ1 is associated with c-MYC downregulation and antileukemic activity. We recently reported that the small molecule BRD2/3/4 inhibitor OTX015 (Oncoethix, Lausanne, Switzerland), currently in clinical development, mimics the effects of JQ1 (Braun et al, ASH 2013). We evaluated the effect of OTX015 on c-MYC, BRD2/3/4, and HEXIM1 in human in vitro leukemic models. Methods: c-MYC, BRD2/3/4 and HEXIM1 expression was assessed in six acute myeloid leukemia (AML; K562, HL-60, NB4, NOMO-1, KG1, OCI-AML3) and two acute lymphoid leukemia (ALL; JURKAT and RS4-11) cell lines after exposure to 500 nM OTX015. Quantitative RT-PCR and Western blotting were performed at different time points (24-72h). A heatmap was computed with R-software. Results: c-MYC RNA levels were ubiquitously downregulated in all AML and ALL cell lines after 24h exposure to OTX015 (Figure 1). c-MYC protein levels decreased to a variable extent at 24-72h in all cell lines evaluated other than KG1. BRD2, BRD3 and BRD4 mRNA expression was significantly decreased in K562 cells (known to be OTX015-resistant) after 48h exposure to OTX015 but was increased in HL60 and NOMO-1 cells, while minimal to no increases were observed in other cell lines. OTX015 induced a decrease in BRD2 protein expression in most cell lines, but not in K562 cells. In contrast, decreased BRD4 protein expression was only seen in the OCI-AML3, NB4 and K562 cell lines. BRD3 protein levels were not modified after OTX015 exposure in all cell lines evaluated other than KG1. HEXIM1 mRNA expression increased after 24h exposure to 500 nM OTX015 in all cell lines except OTX015-resistant K562 cells in which the increase was considered insignificant (less than two-fold). Increases in HEXIM1 protein levels were observed in OCI-AML3, JURKAT and RS4-11 cell lines at 24-72h but not in K562 cells. Conclusion: Taken together, these results show that BRD inhibition by OTX015 modulates HEXIM1 gene and protein expression, in addition to c-MYC decrease and BRD variations. HEXIM1 upregulation seems to be restricted to OTX015-sensitive cell lines and was not significantly affected in OTX015-resistant K562 cells. Further studies are needed to clarify the role of HEXIM1 in antileukemic activity of BRD inhibitors. Figure 1: Heatmap of gene expression after exposure to 500 nM OTX015 for 24 or 48h in AML and ALL cell lines. Repression in blue. Overexpression in red. Figure 1:. Heatmap of gene expression after exposure to 500 nM OTX015 for 24 or 48h in AML and ALL cell lines. Repression in blue. Overexpression in red. Disclosures Riveiro: OTD: Employment. Herait:OncoEthix: Employment. Dombret:OncoEthix: Research Funding.
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Kempen, Herman J., Daniel Bellus, Oleg Fedorov, Silke Nicklisch, Panagis Filippakopoulos, Sarah Picaud et Stefan Knapp. « Stimulation of Hepatic Apolipoprotein A-I Production by Novel Thieno-Triazolodiazepines : Roles of the Classical Benzodiazepine Receptor, PAF Receptor, and Bromodomain Binding ». Lipid Insights 6 (janvier 2013) : LPI.S13258. http://dx.doi.org/10.4137/lpi.s13258.

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Expression and secretion of apolipoprotein A-I (apoA-I) by cultured liver cells can be markedly stimulated by triazolodiazepines (TZDs). It has been shown previously that the thieno-TZD Ro 11-1464 increases plasma levels of apoA-I and in vivomacrophage reverse cholesterol transport in mice. However, these effects were only seen at high doses, at which the compound could act on central benzodiazepine (BZD) receptors or platelet activating factor (PAF) receptors, interfering with its potential utility. In this work, we describe 2 new thieno-TZDs MDCO-3770 and MDCO-3783, both derived from Ro 11-1464. These compounds display the same high efficacy on apoA-I production, metabolic stability, and lack of cytotoxicity in cultured hepatocytes as Ro 11-1464, but they do not bind to the central BZD receptor and PAF receptor. The quinazoline RVX-208 was less efficacious in stimulating apoA-I production and displayed signs of cytotoxicity. Certain TZDs stimulating apoA-I production are now known to be inhibitors of bromodomain (BRD) extra-terminal (BET) proteins BRDT, BRD2, BRD3, and BRD4, and this inhibition was inferred as a main molecular mechanism for their effect on apoA-I expression. We show here that the thieno-TZD (+)-JQ1, a potent BET inhibitor, strongly stimulated apoA-I production in Hep-G2 cells, but that its enantiomer (-)-JQ1, which has no BET inhibitor activity, also showed considerable effect on apoA-I production. MDCO-3770 and MDCO-3783 also inhibited BRD3 and BRD4 in vitro, with potency somewhat below that of (+)-JQ1. We conclude that the effect of thieno-TZDs on apoA-I expression is not due to inhibition of the BZD or PAF receptors and is not completely explained by transcriptional repression by BET proteins.
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Stonestrom, Aaron J., Sarah C. Hsu, Kristen S. Jahn, Peng Huang, Cheryl A. Keller, Belinda M. Giardine, Stephan Kadauke et al. « Functions of BET proteins in erythroid gene expression ». Blood 125, no 18 (30 avril 2015) : 2825–34. http://dx.doi.org/10.1182/blood-2014-10-607309.

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Key Points BETs promote GATA1 chromatin occupancy and subsequently activate transcription; they are generally not required for repression. BRD2 and BRD4 are essential for full GATA1 activity whereas BRD3 function overlaps with BRD2.
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Ottinger, Matthias, Thomas Christalla, Kavita Nathan, Melanie M. Brinkmann, Abel Viejo-Borbolla et Thomas F. Schulz. « Kaposi's Sarcoma-Associated Herpesvirus LANA-1 Interacts with the Short Variant of BRD4 and Releases Cells from a BRD4- and BRD2/RING3-Induced G1 Cell CycleArrest ». Journal of Virology 80, no 21 (23 août 2006) : 10772–86. http://dx.doi.org/10.1128/jvi.00804-06.

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ABSTRACT The Kaposi's sarcoma-associated herpesvirus (KSHV) latency-associated nuclear antigen 1 (LANA-1) is required for the replication of episomal viral genomes. Regions in its N-terminal and C-terminal domains mediate the interaction with host cell chromatin. Several cellular nuclear proteins, e.g., BRD2/RING3, histones H2A and H2B, MeCP2, DEK, and HP1α, have been suggested to mediate this interaction. In this work, we identify the double-bromodomain proteins BRD4 and BRD3/ORFX as additional LANA-1 interaction partners. The carboxy-terminal region of the short variant of BRD4 (BRD4S) containing the highly conserved extraterminal domain directly interacts with an element in the LANA-1 carboxy-terminal domain. We show that ectopically expressed BRD4S and BRD2/RING3 delay progression into the S phase of the cell cycle in epithelial and B-cell lines and increase cyclin E promoter activity. LANA-1 partly releases epithelial and B cells from a BRD4S- and BRD2/RING3-induced G1 cell cycle arrest and also promotes S-phase entry in the presence of BRD4S and BRD2/RING3. This is accompanied by a reduction in BRD4S-mediated cyclin E promoter activity. Our data are in keeping with the notion that the direct interaction of KSHV LANA-1 with BRD4 and other BRD proteins could play a role in the G1/S phase-promoting functions of KSHV LANA-1. Further, our data support a model in which the LANA-1 C terminus contributes to a functional attachment to acetylated histones H3 and H4 via BRD4 and BRD2, in addition to the recently demonstrated direct interaction (A. J. Barbera, J. V. Chodaparambil, B. Kelley-Clarke, V. Joukov, J. C. Walter, K. Luger, and K. M. Kaye, Science 311:856-861, 2006) of the LANA-1 N terminus with histones H2A and H2B.
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Long, Mengping, Wei Hou, Yiqiang Liu et Taobo Hu. « A Histone Acetylation Modulator Gene Signature for Classification and Prognosis of Breast Cancer ». Current Oncology 28, no 1 (17 février 2021) : 928–39. http://dx.doi.org/10.3390/curroncol28010091.

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Regulators of histone acetylation are promising epigenetic targets for therapy in breast cancer. In this study, we comprehensively analyzed the expression of histone acetylation modulator genes in breast cancer using TCGA data sources. A gene signature composed of eight histone acetylation modulators (HAMs) was found to be effective for the classification and prognosis of breast cancers, especially in the HER2-enriched and basal-like molecular subtypes. The eight genes consist of two histone acetylation writers (GTF3C4 and CLOCK), two erasers (HDAC2 and SIRT7) and four readers (BRD4, BRD7, SP100, and BRWD3). Both histone acetylation writer genes and eraser genes were found to be differentially expressed between the two groups indicating a close relationship exists between overall histone acetylation level and prognosis of breast cancer in HER2-enriched and basal-like breast cancer.
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PARK, SANG, YOUNGAH HAN et MARIO A. SALAZAR HERNANDEZ. « The Regulation of BRD7 in the Insulin Signaling Pathway ». Diabetes 67, Supplement 1 (mai 2018) : 1983—P. http://dx.doi.org/10.2337/db18-1983-p.

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Wang, Lifei, Yan Wang, Juan Zhao, Yingxia Yu, Nianqian Kang et Zhiyong Yang. « Theoretical exploration of the binding selectivity of inhibitors to BRD7 and BRD9 with multiple short molecular dynamics simulations ». RSC Advances 12, no 26 (2022) : 16663–76. http://dx.doi.org/10.1039/d2ra02637f.

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Bromodomains (BRDs) are structurally conserved epigenetic reader modules observed in numerous chromatin- and transcription-associated proteins that have a capability to identify acetylated lysine residues.
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Wang, Lifei, Yan Wang, Juan Zhao, Yingxia Yu, Nianqian Kang et Zhiyong Yang. « Theoretical exploration of the binding selectivity of inhibitors to BRD7 and BRD9 with multiple short molecular dynamics simulations ». RSC Advances 12, no 26 (2022) : 16663–76. http://dx.doi.org/10.1039/d2ra02637f.

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Bromodomains (BRDs) are structurally conserved epigenetic reader modules observed in numerous chromatin- and transcription-associated proteins that have a capability to identify acetylated lysine residues.
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Rashad, Maha M., Mona K. Galal, Adel M. EL-Behairy, Eman M. Gouda et Said Z. Moussa. « Maternal exposure to di-n-butyl phthalate induces alterations of c-Myc gene, some apoptotic and growth related genes in pups’ testes ». Toxicology and Industrial Health 34, no 11 (19 septembre 2018) : 744–52. http://dx.doi.org/10.1177/0748233718791623.

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The aim of this study was to investigate the effects of maternal exposure to di-( n-butyl) phthalate (DBP) on testicular development and function in pre-pubertal and post-pubertal male rat offspring. Fourteen pregnant female rats were equally divided into two groups: a control group and a DBP-treated group. During gestation day (GD) 12 to postnatal day (PND) 14, the control group was administered 1 ml/day corn oil, and the DBP-treated group was administered DBP 500 mg/kg/day by oral gavage. On PND 25 (pre-puberty) and PND 60 (post-puberty), blood for serum and the testes were collected from five male offspring of each group. To determine the relationship between the methylation state of the c-Myc promoter and the expression of the c-Myc gene, some apoptotic-related genes, such as p53 and Bax, the anti-apoptotic Bcl-2 gene, and some growth arrest-related genes, such as BRD7 and GAS1, were examined. Compared with the control ( p < 0.05), at pre-puberty, DBP induces c-Myc hyper-methylation with significant downregulation for c-Myc, p53, Bax genes, and significant upregulation for Bcl-2, BRD7, and GAS1, while at post puberty, the methylation state and expression of c-Myc and apoptosis-related genes returned to control levels in the same sequence with the fold change in the expression of BRD7 and GAS1 genes. These findings suggest that DBP induced a transient pre-pubertal increase in c-Myc promoter methylation that may be associated with disruption of both apoptotic and growth mechanisms in the testes.
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LEE, JUNSIK M., YOO KIM, MARIO A. SALAZAR HERNANDEZ et SANG PARK. « 305-LB : BRD7 Deficiency Leads to the Development of Obesity ». Diabetes 68, Supplement 1 (juin 2019) : 305—LB. http://dx.doi.org/10.2337/db19-305-lb.

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Gao, Yushun, Bing Wang et Shugeng Gao. « BRD7 Acts as a Tumor Suppressor Gene in Lung Adenocarcinoma ». PLOS ONE 11, no 8 (31 août 2016) : e0156701. http://dx.doi.org/10.1371/journal.pone.0156701.

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YU, Ying. « Screening of BRD7 interacting proteins by yeast two-hybrid system ». Science in China Series C 45, no 5 (2002) : 546. http://dx.doi.org/10.1360/02yc9060.

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Park, Young-Ae, Jeong-Won Lee, Jung-Joo Choi, Hye-Kyung Jeon, YoungJae Cho, ChelHun Choi, Tae-Joong Kim, Nak Woo Lee, Byoung-Gie Kim et Duk-Soo Bae. « The interactions between MicroRNA-200c and BRD7 in endometrial carcinoma ». Gynecologic Oncology 124, no 1 (janvier 2012) : 125–33. http://dx.doi.org/10.1016/j.ygyno.2011.09.026.

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Wang, Xiao-meng, Ying-cui Wang, Xiang-juan Liu, Qi Wang, Chun-mei Zhang, Li-ping Zhang, Hui Liu, Xin-yu Zhang, Yang Mao et Zhi-ming Ge. « BRD7 mediates hyperglycaemia-induced myocardial apoptosisviaendoplasmic reticulum stress signalling pathway ». Journal of Cellular and Molecular Medicine 21, no 6 (13 décembre 2016) : 1094–105. http://dx.doi.org/10.1111/jcmm.13041.

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Liu, Huaying, Ming Zhou, Xiaomin Luo, Liming Zhang, Zhaoxia Niu, Cong Peng, Jian Ma et al. « Transcriptional regulation of BRD7 expression by Sp1 and c-Myc ». BMC Molecular Biology 9, no 1 (2008) : 111. http://dx.doi.org/10.1186/1471-2199-9-111.

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Wang, Na, Fudong Li, Hongyu Bao, Jie Li, Jihui Wu et Ke Ruan. « NMR Fragment Screening Hit Induces Plasticity of BRD7/9 Bromodomains ». ChemBioChem 17, no 15 (27 juin 2016) : 1456–63. http://dx.doi.org/10.1002/cbic.201600184.

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Wang, Xin, Ana P. Kutschat, Moyuru Yamada, Evangelos Prokakis, Patricia Böttcher, Koji Tanaka, Yuichiro Doki, Feda H. Hamdan et Steven A. Johnsen. « Bromodomain protein BRDT directs ΔNp63 function and super-enhancer activity in a subset of esophageal squamous cell carcinomas ». Cell Death & ; Differentiation 28, no 7 (3 mars 2021) : 2207–20. http://dx.doi.org/10.1038/s41418-021-00751-w.

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AbstractEsophageal squamous cell carcinoma (ESCC) is the predominant subtype of esophageal cancer with a particularly high prevalence in certain geographical regions and a poor prognosis with a 5-year survival rate of 15–25%. Despite numerous studies characterizing the genetic and transcriptomic landscape of ESCC, there are currently no effective targeted therapies. In this study, we used an unbiased screening approach to uncover novel molecular precision oncology targets for ESCC and identified the bromodomain and extraterminal (BET) family member bromodomain testis-specific protein (BRDT) to be uniquely expressed in a subgroup of ESCC. Experimental studies revealed that BRDT expression promotes migration but is dispensable for cell proliferation. Further mechanistic insight was gained through transcriptome analyses, which revealed that BRDT controls the expression of a subset of ΔNp63 target genes. Epigenome and genome-wide occupancy studies, combined with genome-wide chromatin interaction studies, revealed that BRDT colocalizes and interacts with ΔNp63 to drive a unique transcriptional program and modulate cell phenotype. Our data demonstrate that these genomic regions are enriched for super-enhancers that loop to critical ΔNp63 target genes related to the squamous phenotype such as KRT14, FAT2, and PTHLH. Interestingly, BET proteolysis-targeting chimera, MZ1, reversed the activation of these genes. Importantly, we observed a preferential degradation of BRDT by MZ1 compared with BRD2, BRD3, and BRD4. Taken together, these findings reveal a previously unknown function of BRDT in ESCC and provide a proof-of-concept that BRDT may represent a novel therapeutic target in cancer.
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Ciulli, Alessio. « Targeted Protein Degradation with Small Molecules : How PROTACs Work ». Proceedings 22, no 1 (16 décembre 2019) : 115. http://dx.doi.org/10.3390/proceedings2019022115.

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Bivalent degrader molecules (also termed PROTACs) target proteins for degradation through recruitment to E3 ligases. PROTACs are a revolutionary new modality class with therapeutic potential. Formation of a ternary complex between the degrader, the ligase, and the target leads to tagging by ubiquitination and proteasomal degradation of the target protein. In 2015, we disclosed MZ1, a potent degrader made of a ligand we had previously discovered for the E3 ligase von Hippel–Lindau (VHL), and a pan-selective ligand for the BET proteins Brd2, Brd3, and Brd4. We made the unexpected but fascinating observation that MZ1 induces preferential degradation of Brd4 over Brd2 and Brd3—despite engaging BET proteins with the same binary affinity. This demonstrated a now well-established feature of PROTACs: They can achieve a narrower degradation profile in spite of broad target engagement. Our co-crystal structure of a PROTAC ternary complex (VHL:MZ1:Brd4) illuminated the role of cooperative molecular recognition inducing de novo contacts to form a stable ternary. Our work is revealing the structural basis and guiding principles of PROTAC degradation selectivity and mode of action.
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Mantovani, Fiamma, Jarno Drost, P. Mathijs Voorhoeve, Giannino Del Sal et Reuven Agami. « Gene regulation and tumor suppression by the bromodomain-containing protein BRD7 ». Cell Cycle 9, no 14 (15 juillet 2010) : 2849–53. http://dx.doi.org/10.4161/cc.9.14.12309.

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Zhang, Zili, Mei Guo, Min Shen, Desong Kong, Feng Zhang, Jiangjuan Shao, Shanzhong Tan et al. « The BRD7-P53-SLC25A28 axis regulates ferroptosis in hepatic stellate cells ». Redox Biology 36 (septembre 2020) : 101619. http://dx.doi.org/10.1016/j.redox.2020.101619.

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Chiu, Yu-Hsin, Jennifer Y. Lee et Lewis C. Cantley. « BRD7, a Tumor Suppressor, Interacts with p85α and Regulates PI3K Activity ». Molecular Cell 54, no 1 (avril 2014) : 193–202. http://dx.doi.org/10.1016/j.molcel.2014.02.016.

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Golick, Lena, Youngah Han, Yoo Kim et Sang Won Park. « BRD7 regulates the insulin-signaling pathway by increasing phosphorylation of GSK3β ». Cellular and Molecular Life Sciences 75, no 10 (10 novembre 2017) : 1857–69. http://dx.doi.org/10.1007/s00018-017-2711-x.

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Drost, Jarno, Fiamma Mantovani, Francesca Tocco, Ran Elkon, Anna Comel, Henne Holstege, Ron Kerkhoven et al. « BRD7 is a candidate tumour suppressor gene required for p53 function ». Nature Cell Biology 12, no 4 (14 mars 2010) : 380–89. http://dx.doi.org/10.1038/ncb2038.

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Xu, Liang, Ye Chen, Anand Mayakonda, Lynnette Koh, Yuk Kien Chong, Dennis L. Buckley, Edwin Sandanaraj et al. « Targetable BET proteins- and E2F1-dependent transcriptional program maintains the malignancy of glioblastoma ». Proceedings of the National Academy of Sciences 115, no 22 (15 mai 2018) : E5086—E5095. http://dx.doi.org/10.1073/pnas.1712363115.

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Competitive BET bromodomain inhibitors (BBIs) targeting BET proteins (BRD2, BRD3, BRD4, and BRDT) show promising preclinical activities against brain cancers. However, the BET protein-dependent glioblastoma (GBM)-promoting transcriptional network remains elusive. Here, with mechanistic exploration of a next-generation chemical degrader of BET proteins (dBET6), we reveal a profound and consistent impact of BET proteins on E2F1- dependent transcriptional program in both differentiated GBM cells and brain tumor-initiating cells. dBET6 treatment drastically reduces BET protein genomic occupancy, RNA-Pol2 activity, and permissive chromatin marks. Subsequently, dBET6 represses the proliferation, self-renewal, and tumorigenic ability of GBM cells. Moreover, dBET6-induced degradation of BET proteins exerts superior antiproliferation effects compared to conventional BBIs and overcomes both intrinsic and acquired resistance to BBIs in GBM cells. Our study reveals crucial functions of BET proteins and provides the rationale and therapeutic merits of targeted degradation of BET proteins in GBM.
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Xu, Chunmei, Miao Yu, Qingqing Zhang, Zhisheng Ma, Kang Du, Huiqin You, Jing Wei, Deshou Wang et Wenjing Tao. « Genome-Wide Identification and Characterization of the BRD Family in Nile Tilapia (Oreochromis niloticus) ». Animals 12, no 17 (1 septembre 2022) : 2266. http://dx.doi.org/10.3390/ani12172266.

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The bromodomain (BRD) proteins specifically recognize the N-acetyllysine motifs, which is a key event in the reading process of epigenetic marks. BRDs are evolutionarily highly conserved. Over recent years, BRDs attracted great interest because of their important roles in biological processes. However, the genome-wide identification of this family was not carried out in many animal groups, in particular, in teleosts. Moreover, the expression patterns were not reported for any of the members in this family, and the role of the BRD family was not extensively studied in fish reproduction. In this study, we identified 16 to 120 BRD genes in 24 representative species. BRDs expanded significantly in vertebrates. Phylogenetic analysis showed that the BRD family was divided into eight subfamilies (I–VIII). Transcriptome analysis showed that BRDs in Nile tilapia (Oreochromis niloticus) exhibited different expression patterns in different tissues, suggesting that these genes may play different roles in growth and development. Gonadal transcriptome analysis showed that most of the BRDs display sexually dimorphic expression in the gonads at 90 and 180 dah (days after hatching), including 21 testis-dominated genes (brdt, brd4a and brd2b, etc.), and nine ovary-dominated genes (brd3b, brd2a and kat2a, etc.). Consistent with transcriptomic data, the results of qRT-PCR and fluorescence in situ hybridization showed that brdt expression was higher in the testis than in the ovary, suggesting its critical role in the spermatogenesis of the tilapia. Male fish treated with JQ1 (BET subfamily inhibitor) displayed abnormal spermatogenesis. The numbers of germ cells were reduced, and the expression of steroidogenic enzyme genes was downregulated, while the expression of apoptosis-promoting genes was elevated in the testis tissue of treated fish. Our data provide insights into the evolution and expression of BRD genes, which is helpful for understanding their critical roles in sex differentiation and gonadal development in teleosts.
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Liu, Zhixiong, Minbiao Yan, Yaoji Liang, Min Liu, Kun Zhang, Dandan Shao, Rencai Jiang et al. « Nucleoporin Seh1 Interacts with Olig2/Brd7 to Promote Oligodendrocyte Differentiation and Myelination ». Neuron 102, no 3 (mai 2019) : 587–601. http://dx.doi.org/10.1016/j.neuron.2019.02.018.

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Karim, Rezaul Md, Alice Chan, Jin-Yi Zhu et Ernst Schönbrunn. « Structural Basis of Inhibitor Selectivity in the BRD7/9 Subfamily of Bromodomains ». Journal of Medicinal Chemistry 63, no 6 (24 février 2020) : 3227–37. http://dx.doi.org/10.1021/acs.jmedchem.9b01980.

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Clark, Peter G. K., Lucas C. C. Vieira, Cynthia Tallant, Oleg Fedorov, Dean C. Singleton, Catherine M. Rogers, Octovia P. Monteiro et al. « LP99 : Discovery and Synthesis of the First Selective BRD7/9 Bromodomain Inhibitor ». Angewandte Chemie 127, no 21 (13 avril 2015) : 6315–19. http://dx.doi.org/10.1002/ange.201501394.

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Clark, Peter G. K., Lucas C. C. Vieira, Cynthia Tallant, Oleg Fedorov, Dean C. Singleton, Catherine M. Rogers, Octovia P. Monteiro et al. « LP99 : Discovery and Synthesis of the First Selective BRD7/9 Bromodomain Inhibitor ». Angewandte Chemie International Edition 54, no 21 (13 avril 2015) : 6217–21. http://dx.doi.org/10.1002/anie.201501394.

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Shang, Enyuan, Glicella Salazar, Thomas E. Crowley, Xiang Wang, Rocio A. Lopez, Xiangyuan Wang et Debra J. Wolgemuth. « Identification of unique, differentiation stage-specific patterns of expression of the bromodomain-containing genes Brd2, Brd3, Brd4, and Brdt in the mouse testis ». Gene Expression Patterns 4, no 5 (septembre 2004) : 513–19. http://dx.doi.org/10.1016/j.modgep.2004.03.002.

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Ottinger, Matthias, Daniel Pliquet, Thomas Christalla, Ronald Frank, James P. Stewart et Thomas F. Schulz. « The Interaction of the Gammaherpesvirus 68 orf73 Protein with Cellular BET Proteins Affects the Activation of Cell Cycle Promoters ». Journal of Virology 83, no 9 (25 février 2009) : 4423–34. http://dx.doi.org/10.1128/jvi.02274-08.

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ABSTRACT Infection of mice with murine gammaherpesvirus 68 (MHV-68) provides a valuable animal model for gamma-2 herpesvirus (rhadinovirus) infection and pathogenesis. The MHV-68 orf73 protein has been shown to be required for the establishment of viral latency in vivo. This study describes a novel transcriptional activation function of the MHV-68 orf73 protein and identifies the cellular bromodomain containing BET proteins Brd2/RING3, Brd3/ORFX, and BRD4 as interaction partners for the MHV-68 orf73 protein. BET protein members are known to interact with acetylated histones, and Brd2 and Brd4 have been implicated in fundamental cellular processes, including cell cycle regulation and transcriptional regulation. Using MHV-68 orf73 peptide array assays, we identified Brd2 and Brd4 interaction sites in the orf73 protein. Mutation of one binding site led to a loss of the interaction with Brd2/4 but not the retinoblastoma protein Rb, to impaired chromatin association, and to a decreased ability to activate the BET-responsive cyclin D1, D2, and E promoters. The results therefore pinpoint the binding site for Brd2/4 in a rhadinoviral orf73 protein and suggest that the recruitment of a member of the BET protein family allows the MHV-68 orf73 protein to activate the promoters of G1/S cyclins. These findings point to parallels between the transcriptional activator functions of rhadinoviral orf73 proteins and papillomavirus E2 proteins.
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Hagiwara, Masayuki, Atsushi Fushimi, Nami Yamashita, Atrayee Bhattacharya, Hasan Rajabi, Mark D. Long, Yota Yasumizu, Mototsugu Oya, Song Liu et Donald Kufe. « MUC1-C activates the PBAF chromatin remodeling complex in integrating redox balance with progression of human prostate cancer stem cells ». Oncogene 40, no 30 (23 juin 2021) : 4930–40. http://dx.doi.org/10.1038/s41388-021-01899-y.

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AbstractThe polybromo-associated PBAF (SWI/SNF) chromatin remodeling complex, which includes PBRM1, ARID2, and BRD7, regulates cell differentiation and genomic integrity. MUC1-C is an oncogenic protein that drives lineage plasticity in prostate cancer (PC) progression. The present work demonstrates that MUC1-C induces PBRM1, ARID2, and BRD7 expression by the previously unrecognized E2F1-mediated activation of their respective promoters. The functional significance of the MUC1-C→PBAF pathway is supported by demonstrating involvement of MUC1-C in associating with nuclear PBAF and driving the NRF2 antioxidant gene transcriptome in PC cells. Mechanistically, MUC1-C forms a complex with NRF2 and PBRM1 on the NRF2 target SLC7A11 gene that encodes the xCT cystine-glutamate antiporter, increases chromatin accessibility and induces SLC7A11/xCT expression. We also show that MUC1-C and PBRM1 are necessary for induction of other NRF2 target genes, including G6PD and PGD that regulate the pentose phosphate pathway. Our results further demonstrate that MUC1-C integrates activation of PBRM1 with the regulation of antioxidant genes, ROS levels, pluripotency factor expression and the cancer stem cell (CSC) state. These findings reveal a role for MUC1-C in regulating PBAF, redox balance and lineage plasticity of PC CSC progression. Our findings also uncover involvement of MUC1-C in integrating the PBAF and BAF pathways in cancer.
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