Mini-Review Article

BRD4 Protein as a Target for Lung Cancer and Hematological Cancer Therapy: A Review

Author(s): Mengmeng Zhang, Yingbo Li, Zilong Zhang, Xin Zhang, Wei Wang, Xiaomei Song and Dongdong Zhang*

Volume 24, Issue 14, 2023

Published on: 16 October, 2023

Page: [1079 - 1092] Pages: 14

DOI: 10.2174/0113894501269090231012090351

Price: $65

conference banner
Abstract

The BET protein family plays a crucial role in regulating the epigenetic landscape of the genome. Their role in regulating tumor-related gene expression and its impact on the survival of tumor cells is widely acknowledged. Among the BET family constituents, BRD4 is a significant protein. It is a bromodomain-containing protein located at the outer terminal that recognizes histones that have undergone acetylation. It is present in the promoter or enhancer region of the target gene and is responsible for initiating and sustaining the expression of genes associated with tumorigenesis. BRD4 expression is significantly elevated in various tumor types. Research has indicated that BRD4 plays a significant role in regulating various transcription factors and chromatin modification, as well as in repairing DNA damage and preserving telomere function, ultimately contributing to the survival of cancerous cells. The protein BRD4 has a significant impact on antitumor therapy, particularly in the management of lung cancer and hematological malignancies, and the promising potential of BRD4 inhibitors in the realm of cancer prevention and treatment is a topic of great interest. Therefore, BRD4 is considered a promising candidate for prophylaxis and therapy of neoplastic diseases. However, further research is required to fully comprehend the significance and indispensability of BRD4 in cancer and its potential as a therapeutic target.

Keywords: BRD4 protein, hematological cancer, lung cancer, mechanism, targeted therapy, neoplastic diseases.

Next »
Graphical Abstract
[1]
Aygun D, Bjornsson HT. Clinical epigenetics: A primer for the practitioner. Dev Med Child Neurol 2020; 62(2): 192-200.
[http://dx.doi.org/10.1111/dmcn.14398] [PMID: 31749156]
[2]
Nirmaladevi R, Paital B, Jayachandran P, Padma PR, Nirmaladevi R. Epigenetic alterations in cancer. Front Biosci 2020; 25(6): 1058-109.
[http://dx.doi.org/10.2741/4847] [PMID: 32114424]
[3]
Pérez-Salvia M, Esteller M. Bromodomain inhibitors and cancer therapy: From structures to applications. Epigenetics 2017; 12(5): 323-39.
[http://dx.doi.org/10.1080/15592294.2016.1265710] [PMID: 27911230]
[4]
Ghasemi S. Cancer’s epigenetic drugs: Where are they in the cancer medicines? Pharmacogenomics J 2020; 20(3): 367-79.
[http://dx.doi.org/10.1038/s41397-019-0138-5] [PMID: 31819161]
[5]
Liu K, Zhang Z, Ran T, Chen H, Lu T, Chen Y. Advances in BET bromodomain protein inhibitors. Zhongguo Yaoke Daxue Xuebao 2015; 264-71.
[6]
Duan Y, Guan Y, Qin W, Zhai X, Yu B, Liu H. Targeting Brd4 for cancer therapy: Inhibitors and degraders. MedChemComm 2018; 9(11): 1779-802.
[http://dx.doi.org/10.1039/C8MD00198G] [PMID: 30542529]
[7]
Shi J, Vakoc CR. The mechanisms behind the therapeutic activity of BET bromodomain inhibition. Mol Cell 2014; 54(5): 728-36.
[http://dx.doi.org/10.1016/j.molcel.2014.05.016] [PMID: 24905006]
[8]
Segura MF, Fontanals-Cirera B, Gaziel-Sovran A, et al. BRD4 sustains melanoma proliferation and represents a new target for epigenetic therapy. Cancer Res 2013; 73(20): 6264-76.
[http://dx.doi.org/10.1158/0008-5472.CAN-13-0122-T] [PMID: 23950209]
[9]
Goundiam O, Gestraud P, Popova T, et al. Histo-genomic stratification reveals the frequent amplification/overexpression of CCNE 1 and BRD 4 genes in non-BRCAness high grade ovarian carcinoma. Int J Cancer 2015; 137(8): 1890-900.
[http://dx.doi.org/10.1002/ijc.29568] [PMID: 25892415]
[10]
Ferri E, Petosa C, McKenna CE. Bromodomains: Structure, function and pharmacology of inhibition. Biochem Pharmacol 2016; 106: 1-18.
[http://dx.doi.org/10.1016/j.bcp.2015.12.005] [PMID: 26707800]
[11]
Luna-Peláez N, March-Díaz R, Ceballos-Chávez M, et al. The Cornelia de Lange Syndrome-associated factor NIPBL interacts with BRD4 ET domain for transcription control of a common set of genes. Cell Death Dis 2019; 10(8): 548.
[http://dx.doi.org/10.1038/s41419-019-1792-x] [PMID: 31320616]
[12]
Lee S, Liu H, Hill R, et al. JMJD6 cleaves MePCE to release positive transcription elongation factor b (P-TEFb) in higher eukaryotes. eLife 2020; 9: e53930.
[http://dx.doi.org/10.7554/eLife.53930] [PMID: 32048991]
[13]
Xiao R, Ran T, Huang Q, et al. A specific JMJD6 inhibitor potently suppresses multiple types of cancers both in vitro and in vivo. Proc Natl Acad Sci USA 2022; 119(34): e2200753119.
[http://dx.doi.org/10.1073/pnas.2200753119] [PMID: 35969736]
[14]
Jung M, Gelato KA, Fernández-Montalván A, Siegel S, Haendler B. Targeting BET bromodomains for cancer treatment. Epigenomics 2015; 7(3): 487-501.
[http://dx.doi.org/10.2217/epi.14.91] [PMID: 26077433]
[15]
Stathis A, Bertoni F. BET proteins as targets for anticancer treatment. Cancer Discov 2018; 8(1): 24-36.
[http://dx.doi.org/10.1158/2159-8290.CD-17-0605] [PMID: 29263030]
[16]
Doroshow DB, Eder JP, LoRusso PM. BET inhibitors: A novel epigenetic approach. Ann Oncol 2017; 28(8): 1776-87.
[http://dx.doi.org/10.1093/annonc/mdx157] [PMID: 28838216]
[17]
Mochizuki K, Nishiyama A, Jang MK, et al. The bromodomain protein Brd4 stimulates G1 gene transcription and promotes progression to S phase. J Biol Chem 2008; 283(14): 9040-8.
[http://dx.doi.org/10.1074/jbc.M707603200] [PMID: 18223296]
[18]
Zhu H, Bengsch F, Svoronos N, et al. BET bromodomain inhibition promotes anti-tumor immunity by suppressing PD-L1 expression. Cell Rep 2016; 16(11): 2829-37.
[http://dx.doi.org/10.1016/j.celrep.2016.08.032] [PMID: 27626654]
[19]
Hsu JM, Li CW, Lai YJ, Hung MC. Posttranslational modifications of PD-L1 and their applications in cancer therapy. Cancer Res 2018; 78(22): 6349-53.
[http://dx.doi.org/10.1158/0008-5472.CAN-18-1892] [PMID: 30442814]
[20]
Zuber J, Shi J, Wang E, et al. RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukaemia. Nature 2011; 478(7370): 524-8.
[http://dx.doi.org/10.1038/nature10334] [PMID: 21814200]
[21]
Drusbosky LM, Vidva R, Gera S, et al. Predicting response to BET inhibitors using computational modeling: A BEAT AML project study. Leuk Res 2019; 77: 42-50.
[http://dx.doi.org/10.1016/j.leukres.2018.11.010] [PMID: 30642575]
[22]
Döhner K, Schlenk RF, Habdank M, et al. Mutant nucleophosmin (NPM1) predicts favorable prognosis in younger adults with acute myeloid leukemia and normal cytogenetics: interaction with other gene mutations. Blood 2005; 106(12): 3740-6.
[http://dx.doi.org/10.1182/blood-2005-05-2164] [PMID: 16051734]
[23]
Zhang S, Zhao Y, Heaster TM, et al. BET inhibitors reduce cell size and induce reversible cell cycle arrest in AML. J Cell Biochem 2019; 120(5): 7309-22.
[http://dx.doi.org/10.1002/jcb.28005] [PMID: 30417424]
[24]
Huang M, Zhu L, Garcia JS, Li MX, Gentles AJ, Mitchell BS. Brd4 regulates the expression of essential autophagy genes and Keap1 in AML cells. Oncotarget 2018; 9(14): 11665-76.
[http://dx.doi.org/10.18632/oncotarget.24432] [PMID: 29545928]
[25]
Burslem GM, Smith BE, Lai AC, et al. The advantages of targeted protein degradation over inhibition: An RTK case study. Cell Chem Biol 2018; 25(1): 67-77.e3.
[http://dx.doi.org/10.1016/j.chembiol.2017.09.009] [PMID: 29129716]
[26]
Wu F, Zhang Y, Li K, Heng J, Yang N. Advance in anti-tumor mechanism study of bromodomain-containing protein 4 inhibitors. Anti-Tumor Pharm 2019; 9: 177-83.
[27]
Winter GE, Buckley DL, Paulk J, et al. Phthalimide conjugation as a strategy for in vivo target protein degradation. Science 2015; 348(6241): 1376-81.
[http://dx.doi.org/10.1126/science.aab1433] [PMID: 25999370]
[28]
Zhou B, Hu J, Xu F, et al. Discovery of a small-molecule degrader of bromodomain and extra-terminal (BET) proteins with picomolar cellular potencies and capable of achieving tumor regression. J Med Chem 2018; 61(2): 462-81.
[http://dx.doi.org/10.1021/acs.jmedchem.6b01816] [PMID: 28339196]
[29]
Qin C, Hu Y, Zhou B, et al. Discovery of QCA570 as an exceptionally potent and efficacious proteolysis targeting chimera (PROTAC) degrader of the bromodomain and extra-terminal (BET) proteins capable of inducing complete and durable tumor regression. J Med Chem 2018; 61(15): 6685-704.
[http://dx.doi.org/10.1021/acs.jmedchem.8b00506] [PMID: 30019901]
[30]
Kelm JM, Pandey DS, Malin E, et al. PROTAC’ing oncoproteins: Targeted protein degradation for cancer therapy. Mol Cancer 2023; 22(1): 62.
[http://dx.doi.org/10.1186/s12943-022-01707-5] [PMID: 36991452]
[31]
Lu J, Qian Y, Altieri M, et al. Hijacking the E3 ubiquitin ligase cereblon to efficiently target BRD4. Chem Biol 2015; 22(6): 755-63.
[http://dx.doi.org/10.1016/j.chembiol.2015.05.009] [PMID: 26051217]
[32]
Sun B, Fiskus W, Qian Y, et al. BET protein proteolysis targeting chimera (PROTAC) exerts potent lethal activity against mantle cell lymphoma cells. Leukemia 2018; 32(2): 343-52.
[http://dx.doi.org/10.1038/leu.2017.207] [PMID: 28663582]
[33]
Bai L, Zhou B, Yang CY, et al. Targeted degradation of BET proteins in triple-negative breast cancer. Cancer Res 2017; 77(9): 2476-87.
[http://dx.doi.org/10.1158/0008-5472.CAN-16-2622] [PMID: 28209615]
[34]
Piya S, Yang Y, Bhattacharya S, et al. Targeting the NOTCH1-MYC-CD44 axis in leukemia-initiating cells in T-ALL. Leukemia 2022; 36(5): 1261-73.
[http://dx.doi.org/10.1038/s41375-022-01516-1] [PMID: 35173274]
[35]
Bleichert F, Baserga SJ. Ribonucleoprotein multimers and their functions. Crit Rev Biochem Mol Biol 2010; 45(5): 331-50.
[http://dx.doi.org/10.3109/10409238.2010.496772] [PMID: 20572804]
[36]
Contieri B, Duarte BKL, Lazarini M. Updates on DNA methylation modifiers in acute myeloid leukemia. Ann Hematol 2020; 99(4): 693-701.
[http://dx.doi.org/10.1007/s00277-020-03938-2] [PMID: 32025842]
[37]
Pericole FV, Lazarini M, de Paiva LB, et al. BRD4 inhibition enhances azacitidine efficacy in acute myeloid leukemia and myelodysplastic syndromes. Front Oncol 2019; 9: 16.
[http://dx.doi.org/10.3389/fonc.2019.00016] [PMID: 30761268]
[38]
Bakshi HA, Mishra V, Satija S, et al. Dynamics of prolyl hydroxylases levels during disease progression in experimental colitis. Inflammation 2019; 42(6): 2032-6.
[http://dx.doi.org/10.1007/s10753-019-01065-3] [PMID: 31377947]
[39]
Erber L, Luo A, Chen Y. Targeted and interactome proteomics revealed the role of PHD2 in regulating BRD4 proline hydroxylation. Mol Cell Proteomics 2019; 18(9): 1772-81.
[http://dx.doi.org/10.1074/mcp.RA119.001535] [PMID: 31239290]
[40]
Xie J, Wang J, Cheng S, et al. Expression of immune checkpoints in T cells of esophageal cancer patients. Oncotarget 2016; 7(39): 63669-78.
[http://dx.doi.org/10.18632/oncotarget.11611] [PMID: 27577071]
[41]
Zhou G, Sprengers D, Boor PPC, et al. Antibodies against immune checkpoint molecules restore functions of tumor-infiltrating T cells in hepatocellular carcinomas. Gastroenterology 2017; 153(4): 1107-1119.e10.
[http://dx.doi.org/10.1053/j.gastro.2017.06.017] [PMID: 28648905]
[42]
Shi X, Li CW, Tan LC, et al. Immune co-inhibitory receptors PD-1, CTLA-4, TIM-3, LAG-3, and TIGIT in medullary thyroid cancers: A large cohort study. J Clin Endocrinol Metab 2021; 106(1): 120-32.
[http://dx.doi.org/10.1210/clinem/dgaa701] [PMID: 33000173]
[43]
Cao Z, Budinich KA, Huang H, et al. ZMYND8-regulated IRF8 transcription axis is an acute myeloid leukemia dependency. Mol Cell 2021; 81(17): 3604-3622.e10.
[http://dx.doi.org/10.1016/j.molcel.2021.07.018] [PMID: 34358447]
[44]
Xing Y, Wei X, Liu Y, et al. Autophagy inhibition mediated by MCOLN1/TRPML1 suppresses cancer metastasis via regulating a ROS-driven TP53/p53 pathway. Autophagy 2022; 18(8): 1932-54.
[http://dx.doi.org/10.1080/15548627.2021.2008752] [PMID: 34878954]
[45]
Imai S, Ooki T, Murata-Kamiya N, et al. Helicobacter pylori CagA elicits BRCAness to induce genome instability that may underlie bacterial gastric carcinogenesis. Cell Host Microbe 2021; 29(6): 941-958.e10.
[http://dx.doi.org/10.1016/j.chom.2021.04.006] [PMID: 33989515]
[46]
Moily NS, Ormsby AR, Stojilovic A, et al. Transcriptional profiles for distinct aggregation states of mutant Huntingtin exon 1 protein unmask new Huntington’s disease pathways. Mol Cell Neurosci 2017; 83: 103-12.
[http://dx.doi.org/10.1016/j.mcn.2017.07.004] [PMID: 28743452]
[47]
Reyes-Gutierrez P, Carrasquillo-Rodríguez JW, Imbalzano AN. Promotion of adipogenesis by JMJD6 requires the AT hook-like domain and is independent of its catalytic function. PLoS One 2019; 14(8): e0216015.
[http://dx.doi.org/10.1371/journal.pone.0216015] [PMID: 31430278]
[48]
Churcher I. Protac-induced protein degradation in drug discovery: Breaking the rules or just making new ones? J Med Chem 2018; 61(2): 444-52.
[http://dx.doi.org/10.1021/acs.jmedchem.7b01272] [PMID: 29144739]
[49]
Noblejas-López MM, Nieto-Jimenez C, Burgos M, et al. Activity of BET-proteolysis targeting chimeric (PROTAC) compounds in triple negative breast cancer. J Exp Clin Cancer Res 2019; 38(1): 383.
[http://dx.doi.org/10.1186/s13046-019-1387-5] [PMID: 31470872]
[50]
Górecki M, Kozioł I, Kopystecka A, Budzyńska J, Zawitkowska J, Lejman M. Updates in KMT2A gene rearrangement in pediatric acute lymphoblastic leukemia. Biomedicines 2023; 11(3): 821.
[http://dx.doi.org/10.3390/biomedicines11030821] [PMID: 36979800]
[51]
Saenz DT, Fiskus W, Qian Y, et al. Novel BET protein proteolysis-targeting chimera exerts superior lethal activity than bromodomain inhibitor (BETi) against post-myeloproliferative neoplasm secondary (s) AML cells. Leukemia 2017; 31(9): 1951-61.
[http://dx.doi.org/10.1038/leu.2016.393] [PMID: 28042144]
[52]
Wood L, Huang M, Zeki J, et al. Combining inhibitors of Brd4 and cyclin-dependent kinase can decrease tumor growth in neuroblastoma with MYCN amplification. J Pediatr Surg 2021; 56(7): 1199-202.
[http://dx.doi.org/10.1016/j.jpedsurg.2021.03.037] [PMID: 33838899]
[53]
Dehnhardt CM, Venkatesan AM, Chen Z, et al. Identification of 2-oxatriazines as highly potent pan-PI3K/mTOR dual inhibitors. Bioorg Med Chem Lett 2011; 21(16): 4773-8.
[http://dx.doi.org/10.1016/j.bmcl.2011.06.063] [PMID: 21763134]
[54]
Canella A, Van Belle S, Brouns T, et al. LEDGF/p75-mediated chemoresistance of mixed-lineage leukemia involves cell survival pathways and super enhancer activators. Cancer Gene Ther 2022; 29(2): 133-40.
[http://dx.doi.org/10.1038/s41417-021-00319-3] [PMID: 33795806]
[55]
Liedtke V, Schröder C, Roggenbuck D, et al. LEDGF/p75 is required for an efficient DNA damage response. Int J Mol Sci 2021; 22(11): 5866.
[http://dx.doi.org/10.3390/ijms22115866] [PMID: 34070855]
[56]
He L, Chen C, Gao G, Xu K, Ma Z. ARV-825-induced BRD4 protein degradation as a therapy for thyroid carcinoma. Aging (Albany NY) 2020; 12(5): 4547-57.
[http://dx.doi.org/10.18632/aging.102910] [PMID: 32163373]
[57]
Zoine JT, Moore SE, Velasquez MP. Leukemia’s next top model? syngeneic models to advance adoptive cellular therapy. Front Immunol 2022; 13: 867103.
[http://dx.doi.org/10.3389/fimmu.2022.867103] [PMID: 35401520]
[58]
Bose P, Vachhani P, Cortes JE. Treatment of relapsed/refractory acute myeloid leukemia. Curr Treat Options Oncol 2017; 18(3): 17.
[http://dx.doi.org/10.1007/s11864-017-0456-2] [PMID: 28286924]
[59]
Siegel RL, Miller KD, Jemal A. Cancer statistics, 2019. CA Cancer J Clin 2019; 69(1): 7-34.
[http://dx.doi.org/10.3322/caac.21551] [PMID: 30620402]
[60]
Bray F, Ferlay J, Soerjomataram I, Siegel RL, Torre LA, Jemal A. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin 2018; 68(6): 394-424.
[http://dx.doi.org/10.3322/caac.21492] [PMID: 30207593]
[61]
Liu Y, Li Y, Liu S, et al. NK cells mediate synergistic antitumor effects of combined inhibition of HDAC6 and BET in a SCLC preclinical model. Cancer Res 2018; 78(13): 3709-17.
[http://dx.doi.org/10.1158/0008-5472.CAN-18-0161] [PMID: 29760044]
[62]
Sun D, Nikonova AS, Zhang P, et al. Evaluation of the small-molecule BRD4 degrader CFT-2718 in small-cell lung cancer and pancreatic cancer models. Mol Cancer Ther 2021; 20(8): 1367-77.
[http://dx.doi.org/10.1158/1535-7163.MCT-20-0831] [PMID: 34045230]
[63]
Rittmeyer A, Barlesi F, Waterkamp D, et al. Atezolizumab versus docetaxel in patients with previously treated non-small-cell lung cancer (OAK): A phase 3, open-label, multicentre randomised controlled trial. Lancet 2017; 389(10066): 255-65.
[http://dx.doi.org/10.1016/S0140-6736(16)32517-X] [PMID: 27979383]
[64]
Lv Y, Lv X, Zhang J, et al. BRD4 Targets the KEAP1-Nrf2-G6PD axis and suppresses redox metabolism in small cell lung cancer. Antioxidants 2022; 11(4): 661.
[http://dx.doi.org/10.3390/antiox11040661] [PMID: 35453346]
[65]
Fu Y, Liu L, Wu H, Zheng Y, Zhan H, Li L. LncRNA GAS5 regulated by FTO-mediated m6A demethylation promotes autophagic cell death in NSCLC by targeting UPF1/BRD4 axis. Mol Cell Biochem 2023.
[http://dx.doi.org/10.1007/s11010-023-04748-6] [PMID: 37120495]
[66]
Gao Z, Yuan T, Zhou X, et al. Targeting BRD4 proteins suppresses the growth of NSCLC through downregulation of eIF4E expression. Cancer Biol Ther 2018; 19(5): 407-15.
[http://dx.doi.org/10.1080/15384047.2018.1423923] [PMID: 29333921]
[67]
Abolfathi H, Arabi M, Sheikhpour M. A literature review of microRNA and gene signaling pathways involved in the apoptosis pathway of lung cancer. Respir Res 2023; 24(1): 55.
[http://dx.doi.org/10.1186/s12931-023-02366-w] [PMID: 36800962]
[68]
Zhang HT, Peng R, Chen S, et al. Versatile nano-PROTAC-induced epigenetic reader degradation for efficient lung cancer therapy. Adv Sci 2022; 9(29): 2202039.
[http://dx.doi.org/10.1002/advs.202202039] [PMID: 35988145]
[69]
Ma D, Qin Y, Li S, et al. circDENND4C promotes proliferation and metastasis of lung cancer by upregulating BRD4 signaling pathway. J Oncol 2021; 2021: 1-11.
[http://dx.doi.org/10.1155/2021/2469691] [PMID: 34876902]
[70]
Cho H, Jeon SI, Shim MK, Ahn CH, Kim K. In situ albumin-binding and esterase-specifically cleaved BRD4-degrading PROTAC for targeted cancer therapy. Biomaterials 2023; 295: 122038.
[http://dx.doi.org/10.1016/j.biomaterials.2023.122038] [PMID: 36787659]
[71]
Zong D, Gu J, Cavalcante GC, et al. BRD4 levels determine the response of human lung cancer cells to BET degraders that potently induce apoptosis through suppression of Mcl-1. Cancer Res 2020; 80(11): 2380-93.
[http://dx.doi.org/10.1158/0008-5472.CAN-19-3674] [PMID: 32156781]
[72]
Wang J, Xu Y, Rao X, et al. BRD4-IRF1 axis regulates chemoradiotherapy-induced PD-L1 expression and immune evasion in non-small cell lung cancer. Clin Transl Med 2022; 12(1): e718.
[http://dx.doi.org/10.1002/ctm2.718] [PMID: 35083874]
[73]
Xu W, Sun D, Wang Y, et al. Inhibitory effect of microRNA-608 on lung cancer cell proliferation, migration, and invasion by targeting BRD4 through the JAK2/STAT3 pathway. Bosn J Basic Med Sci 2020; 20(3): 347-56.
[PMID: 31621555]
[74]
Zhou Y, Li S, Li J, Wang D, Li Q. Effect of microRNA-135a on cell proliferation, migration, invasion, apoptosis and tumor angiogenesis through the IGF-1/PI3K/Akt signaling pathway in non-small cell lung cancer. Cell Physiol Biochem 2017; 42(4): 1431-46.
[http://dx.doi.org/10.1159/000479207] [PMID: 28715819]
[75]
Yang C, Yang Y, Li Y, Ni Q, Li J. Radiotherapy-triggered proteolysis targeting chimera prodrug activation in tumors. J Am Chem Soc 2023; 145(1): 385-91.
[http://dx.doi.org/10.1021/jacs.2c10177] [PMID: 36542856]
[76]
Costa FA, Amano MT, Asprino PF, et al. Revealing the BRD4-NOTCH3 fusion: A novel hill in the cancer landscape. Lung Cancer 2021; 154: 146-50.
[http://dx.doi.org/10.1016/j.lungcan.2021.02.016] [PMID: 33676359]
[77]
Shi Y, Liao Y, Liu Q, et al. BRD4-targeting PROTAC as a unique tool to study biomolecular condensates. Cell Discov 2023; 9(1): 47.
[http://dx.doi.org/10.1038/s41421-023-00544-0] [PMID: 37156794]

Rights & Permissions Print Cite
© 2024 Bentham Science Publishers | Privacy Policy