| MicroRNA-196b promotes cell growth and metastasis of ovarian cancer by targeting ZMYND11. | MicroRNA-196b promotes cell growth and metastasis of ovarian cancer by targeting ZMYND11.
Zhang Z, Xu L, Hu Z, Yang B, Xu J. | 08/6/2022 |
| Oncogenic ZMYND11-MBTD1 fusion protein anchors the NuA4/TIP60 histone acetyltransferase complex to the coding region of active genes. | Oncogenic ZMYND11-MBTD1 fusion protein anchors the NuA4/TIP60 histone acetyltransferase complex to the coding region of active genes.
Devoucoux M, Fort V, Khelifi G, Xu J, Alerasool N, Galloy M, Wong N, Bourriquen G, Fradet-Turcotte A, Taipale M, Hope K, Hussein SMI, Côté J. | 07/2/2022 |
| ZMYND11 variants are a novel cause of centrotemporal and generalised epilepsies with neurodevelopmental disorder. | ZMYND11 variants are a novel cause of centrotemporal and generalised epilepsies with neurodevelopmental disorder.
Oates S, Absoud M, Goyal S, Bayley S, Baulcomb J, Sims A, Riddett A, Allis K, Brasch-Andersen C, Balasubramanian M, Bai R, Callewaert B, Hüffmeier U, Le Duc D, Radtke M, Korff C, Kennedy J, Low K, Møller RS, Nielsen JEK, Popp B, Quteineh L, Rønde G, Schönewolf-Greulich B, Shillington A, Taylor MR, Todd E, Torring PM, Tümer Z, Vasileiou G, Yates TM, Zweier C, Rosch R, Basson MA, Pal DK. | 02/5/2022 |
| ZMYND11-related syndromic intellectual disability: 16 patients delineating and expanding the phenotypic spectrum. | ZMYND11-related syndromic intellectual disability: 16 patients delineating and expanding the phenotypic spectrum.
Yates TM, Drucker M, Barnicoat A, Low K, Gerkes EH, Fry AE, Parker MJ, O'Driscoll M, Charles P, Cox H, Marey I, Keren B, Rinne T, McEntagart M, Ramachandran V, Drury S, Vansenne F, Sival DA, Herkert JC, Callewaert B, Tan WH, Balasubramanian M. | 07/24/2021 |
| ZMYND11-MBTD1 induces leukemogenesis through hijacking NuA4/TIP60 acetyltransferase complex and a PWWP-mediated chromatin association mechanism. | ZMYND11-MBTD1 induces leukemogenesis through hijacking NuA4/TIP60 acetyltransferase complex and a PWWP-mediated chromatin association mechanism.
Li J, Galbo PM Jr, Gong W, Storey AJ, Tsai YH, Yu X, Ahn JH, Guo Y, Mackintosh SG, Edmondson RD, Byrum SD, Farrar JE, He S, Cai L, Jin J, Tackett AJ, Zheng D, Wang GG., Free PMC Article | 02/27/2021 |
| Our data indicate that increased association with BS69 restricts the function of type 2 EBNA2 as a transcriptional activator and driver of B cell growth and may contribute to reduced B-cell transformation by type 2 EBV. | Increased association between Epstein-Barr virus EBNA2 from type 2 strains and the transcriptional repressor BS69 restricts EBNA2 activity.
Ponnusamy R, Khatri R, Correia PB, Wood CD, Mancini EJ, Farrell PJ, West MJ., Free PMC Article | 01/4/2020 |
| the E1A proteins from HAdV-C5 and -A12 bind the cellular repressor protein BS69. This occurs via a SLiM containing a conserved PXLXP motif, which is present in CR2 of E1A. This SLiM confers interaction with the MYND domain of BS69. | The Transcriptional Repressor BS69 is a Conserved Target of the E1A Proteins from Several Human Adenovirus Species.
Zhang A, Tessier TM, Galpin KJC, King CR, Gameiro SF, Anderson WW, Yousef AF, Qin WT, Li SSC, Mymryk JS., Free PMC Article | 02/16/2019 |
| The ZMYND11 gene has important functions in epigenetic regulation. | Phenotype comparison confirms ZMYND11 as a critical gene for 10p15.3 microdeletion syndrome.
Tumiene B, Čiuladaitė Ž, Preikšaitienė E, Mameniškienė R, Utkus A, Kučinskas V. | 02/3/2018 |
| Taken together, ZMYND11 was demonstrated to be a potential and extremely promising suppressor of GBM, while miRNA-196a-5p was quite an important target of treatment of GBM. | Downregulation of ZMYND11 induced by miR-196a-5p promotes the progression and growth of GBM.
Yang JP, Yang JK, Li C, Cui ZQ, Liu HJ, Sun XF, Geng SM, Lu SK, Song J, Guo CY, Jiao BH. | 11/25/2017 |
| Interaction with ZMYND11 mediates opposing roles of Ras-responsive ETS1 and ETS2. | Interaction with ZMYND11 mediates opposing roles of Ras-responsive transcription factors ETS1 and ETS2.
Plotnik JP, Hollenhorst PC., Free PMC Article | 09/9/2017 |
| In this study, we show that this translocation results in an in-frame translocation fusing exon 12 of the tumor suppressor gene ZMYND11 to exon 3 of the chromatin protein MBTD1, encoding a protein of 1,054 amino acids | Recurrent translocation t(10;17)(p15;q21) in minimally differentiated acute myeloid leukemia results in ZMYND11/MBTD1 fusion.
de Rooij JD, van den Heuvel-Eibrink MM, Kollen WJ, Sonneveld E, Kaspers GJ, Beverloo HB, Fornerod M, Pieters R, Zwaan CM. | 10/8/2016 |
| ZMYND11 represses gene expression by binding H3.3K36me3 and preventing transcription elongation. | The putative tumor suppressor ZMYND11 recognizes H3.3K36me3.
| 12/19/2015 |
| We propose that BS69 specifically associates with H3K36me3-enriched chromatin through the PWWP domain, which facilitates the recruitment of MYND-bound transcription and chromatin remodeling factors | Crystal structure of human BS69 Bromo-ZnF-PWWP reveals its role in H3K36me3 nucleosome binding.
Wang J, Qin S, Li F, Li S, Zhang W, Peng J, Zhang Z, Gong Q, Wu J, Shi Y., Free PMC Article | 02/28/2015 |
| this study identifies an H3.3K36me3-specific reader and a regulator of intron retention and reveals that BS69 connects histone H3.3K36me3 to regulated RNA splicing, providing significant, important insights into chromatin regulation of pre-mRNA processing. | BS69/ZMYND11 reads and connects histone H3.3 lysine 36 trimethylation-decorated chromatin to regulated pre-mRNA processing.
Guo R, Zheng L, Park JW, Lv R, Chen H, Jiao F, Xu W, Mu S, Wen H, Qiu J, Wang Z, Yang P, Wu F, Hui J, Fu X, Shi X, Shi YG, Xing Y, Lan F, Shi Y., Free PMC Article | 01/10/2015 |
| identification of ZMYND11 as an H3.3-specific reader of H3K36me3 that links the histone-variant-mediated transcription elongation control to tumor suppression | ZMYND11 links histone H3.3K36me3 to transcription elongation and tumour suppression.
Wen H, Li Y, Xi Y, Jiang S, Stratton S, Peng D, Tanaka K, Ren Y, Xia Z, Wu J, Li B, Barton MC, Li W, Li H, Shi X., Free PMC Article | 05/17/2014 |
| BRAM1 acts as a negative signal regulator located at the very proximal end of lymphotoxin beta receptor complex assembly. | The MYND domain-containing protein BRAM1 inhibits lymphotoxin beta receptor-mediated signaling through affecting receptor oligomerization.
Liu HP, Chung PJ, Liang CL, Chang YS. | 02/26/2011 |
| Data show significant association between the copy number variations of BS69 and some hematological malignancies. | Analysis of copy number variations of BS69 in multiple types of hematological malignancies.
Yang H, Zhang C, Zhao X, Wu Q, Fu X, Yu B, Shao Y, Guan M, Zhang W, Wan J, Huang X. | 09/27/2010 |
| Data found that BS69 directly interacted with TRAF3, a negative regulator of NF-kappaB activation. Results revealed that TRAF3 was involved in the BS69-mediated suppression of LMP1/CTAR1-induced NF-kappaB activation. | BS69 cooperates with TRAF3 in the regulation of Epstein-Barr virus-derived LMP1/CTAR1-induced NF-kappaB activation.
Ikeda O, Miyasaka Y, Yoshida R, Mizushima A, Oritani K, Sekine Y, Kuroda M, Yasui T, Fujimuro M, Muromoto R, Nanbo A, Matsuda T. | 03/22/2010 |
| BS69 forms oligomers. The PHD and MYND domains are important for the cellular localization of BS69. PIAS1 and Ubc9 interact with BS69 and promote the sumoylation of BS69. BS69 plays inhibitory roles in both muscle and neuron differentiation. | BS69 undergoes SUMO modification and plays an inhibitory role in muscle and neuronal differentiation.
Yu B, Shao Y, Zhang C, Chen Y, Zhong Q, Zhang J, Yang H, Zhang W, Wan J. | 01/21/2010 |
| Knockdown of BS69 resulted in a decrease of IFN-beta induction, suggesting that BS69 is a positive regulator for the TLR3-TICAM-1 pathway and negative regulatory properties in NF-kappaB activation. | Oligomerized TICAM-1 (TRIF) in the cytoplasm recruits nuclear BS69 to enhance NF-kappaB activation and type I IFN induction.
Takaki H, Oshiumi H, Sasai M, Kawanishi T, Matsumoto M, Seya T. | 01/21/2010 |
| Data indicate that BS69 is involved in cellular senescence mainly through the p53-p21Cip1 pathway. | BS69 is involved in cellular senescence through the p53-p21Cip1 pathway.
Zhang W, Chan HM, Gao Y, Poon R, Wu Z., Free PMC Article | 01/21/2010 |
| the C-terminal Mynd domain of BS69 (amino acids 516-561) or Mynd domains of the Caenorhabditis elegans proteins Bra-1 and Bra-2 bind not only to E1A but also to the Epstein-Barr virus EBNA2 oncoprotein and the Myc-related cellular protein MGA | The conserved Mynd domain of BS69 binds cellular and oncoviral proteins through a common PXLXP motif.
Ansieau S, Leutz A. | 01/21/2010 |
| The recruitment and aggregation of BS69 is a prerequisite for JNK activation by LMP1. | BS69, a specific adaptor in the latent membrane protein 1-mediated c-Jun N-terminal kinase pathway.
Wan J, Zhang W, Wu L, Bai T, Zhang M, Lo KW, Chui YL, Cui Y, Tao Q, Yamamoto M, Akira S, Wu Z., Free PMC Article | 01/21/2010 |
| BS69 has roles in gene repression and chromatin remodeling | New insights into BS69 functions.
Velasco G, Grkovic S, Ansieau S. | 01/21/2010 |
| BS69 controls E1A stability via inhibition of ubiquitination. | Ubiquitin-dependent degradation of adenovirus E1A protein is inhibited by BS69.
Isobe T, Uchida C, Hattori T, Kitagawa K, Oda T, Kitagawa M. | 01/21/2010 |