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1 to 21 of 21  Show
  1. 1
    "NEDO human cDNA sequencing project focused on splicing variants."
    Wakamatsu A., Yamamoto J., Kimura K., Ishii S., Watanabe K., Sugiyama A., Murakawa K., Kaida T., Tsuchiya K., Fukuzumi Y., Kumagai A., Oishi Y., Yamamoto S., Ono Y., Komori Y., Yamazaki M., Kisu Y., Nishikawa T.
    Isogai T.
    Submitted (OCT-2007) to the EMBL/GenBank/DDBJ databases
    Cited for: NUCLEOTIDE SEQUENCE.
    Category: Sequences.
    Tissue: Thalamus.
    Source: UniProtKB/TrEMBL (unreviewed).
  2. 2
    "The adenovirus E1A binding protein BS69 is a corepressor of transcription through recruitment of N-CoR."
    Masselink H., Bernards R.
    Oncogene 19:1538-1546(2000) [PubMed] [Europe PMC] [Abstract]
    Category: Interaction.
    Annotation: The adenovirus E1A binding protein BS69 is a corepressor of transcription through recruitment of N-CoR.
    Source: GeneRIF:10771.

    This publication is mapped to 8 other entries.

  3. 3
    "The conserved Mynd domain of BS69 binds cellular and oncoviral proteins through a common PXLXP motif."
    Ansieau S., Leutz A.
    J. Biol. Chem. 277:4906-4910(2002) [PubMed] [Europe PMC] [Abstract]
    Category: Interaction.
    Annotation: 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.
    Source: GeneRIF:10771.

    This publication is cited by 2 and mapped to 8 other entries.

  4. 4
    "Ubiquitin-dependent degradation of adenovirus E1A protein is inhibited by BS69."
    Isobe T., Uchida C., Hattori T., Kitagawa K., Oda T., Kitagawa M.
    Biochem. Biophys. Res. Commun. 339:367-374(2006) [PubMed] [Europe PMC] [Abstract]
    Category: Interaction.
    Annotation: BS69 controls E1A stability via inhibition of ubiquitination.
    Source: GeneRIF:10771.

    This publication is mapped to 7 other entries.

  5. 5
    "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 K.W., Chui Y.L., Cui Y., Tao Q., Yamamoto M., Akira S., Wu Z.
    Mol. Cell. Biol. 26:448-456(2006) [PubMed] [Europe PMC] [Abstract]
    Category: Interaction.
    Annotation: The recruitment and aggregation of BS69 is a prerequisite for JNK activation by LMP1.
    Source: GeneRIF:10771.

    This publication is cited by 1 and mapped to 6 other entries.

  6. 6
    Category: Interaction.
    Annotation: BS69 has roles in gene repression and chromatin remodeling.
    Source: GeneRIF:10771.

    This publication is mapped to 12 other entries.

  7. 7
    "BS69 is involved in cellular senescence through the p53-p21Cip1 pathway."
    Zhang W., Chan H.M., Gao Y., Poon R., Wu Z.
    EMBO Rep. 8:952-958(2007) [PubMed] [Europe PMC] [Abstract]
    Category: Interaction.
    Annotation: Data indicate that BS69 is involved in cellular senescence mainly through the p53-p21Cip1 pathway.
    Source: GeneRIF:10771.

    This publication is mapped to 195 other entries.

  8. 8
    "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.
    Exp. Cell Res. 315:3543-3553(2009) [PubMed] [Europe PMC] [Abstract]
    Category: Function, Interaction.
    Annotation: 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.
    Source: GeneRIF:10771.

    This publication is mapped to 27 other entries.

  9. 9
    "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.
    Eur. J. Immunol. 39:3469-3476(2009) [PubMed] [Europe PMC] [Abstract]
    Category: Interaction.
    Annotation: 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.
    Source: GeneRIF:10771.

    This publication is mapped to 17 other entries.

  10. 10
    "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.
    FEBS Lett. 584:865-872(2010) [PubMed] [Europe PMC] [Abstract]
    Category: Interaction.
    Annotation: 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.
    Source: GeneRIF:10771.

    This publication is cited by 1 and mapped to 13 other entries.

  11. 11
    "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.
    Ann. Hematol. 89:959-964(2010) [PubMed] [Europe PMC] [Abstract]
    Category: Sequences.
    Annotation: Data show significant association between the copy number variations of BS69 and some hematological malignancies.
    Source: GeneRIF:10771.

    This publication is mapped to 7 other entries.

  12. 12
    "The MYND domain-containing protein BRAM1 inhibits lymphotoxin beta receptor-mediated signaling through affecting receptor oligomerization."
    Liu H.P., Chung P.J., Liang C.L., Chang Y.S.
    Cell. Signal. 23:80-88(2011) [PubMed] [Europe PMC] [Abstract]
    Category: Interaction.
    Annotation: BRAM1 acts as a negative signal regulator located at the very proximal end of lymphotoxin beta receptor complex assembly.
    Source: GeneRIF:10771.

    This publication is mapped to 11 other entries.

  13. 13
    "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 M.C., Li W., Li H., Shi X.
    Nature 508:263-268(2014) [PubMed] [Europe PMC] [Abstract]
    Category: Function.
    Annotation: identification of ZMYND11 as an H3.3-specific reader of H3K36me3 that links the histone-variant-mediated transcription elongation control to tumor suppression.
    Source: GeneRIF:10771.

    This publication is cited by 2 and mapped to 27 other entries.

  14. 14
    "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.
    Cell Res. 24:890-893(2014) [PubMed] [Europe PMC] [Abstract]
    Category: Structure.
    Annotation: 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.
    Source: GeneRIF:10771.

    This publication is mapped to 6 other entries.

  15. 15
    "The putative tumor suppressor ZMYND11 recognizes H3.3K36me3."
    Cancer Discov 4:OF12-OF12(2014) [PubMed] [Europe PMC] [Abstract]
    Category: Function.
    Annotation: ZMYND11 represses gene expression by binding H3.3K36me3 and preventing transcription elongation.
    Source: GeneRIF:10771.

    This publication is mapped to 7 other entries.

  16. 16
    "BS69/ZMYND11 reads and connects histone H3.3 lysine 36 trimethylation-decorated chromatin to regulated pre-mRNA processing."
    Guo R., Zheng L., Park J.W., 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 Y.G., Xing Y., Lan F., Shi Y.
    Mol. Cell 56:298-310(2014) [PubMed] [Europe PMC] [Abstract]
    Category: Interaction.
    Annotation: 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.
    Source: GeneRIF:10771.

    This publication is mapped to 10 other entries.

  17. 17
    "Recurrent translocation t(10;17)(p15;q21) in minimally differentiated acute myeloid leukemia results in ZMYND11/MBTD1 fusion."
    de Rooij J.D., van den Heuvel-Eibrink M.M., Kollen W.J., Sonneveld E., Kaspers G.J., Beverloo H.B., Fornerod M., Pieters R., Zwaan C.M.
    Genes Chromosomes Cancer 55:237-241(2016) [PubMed] [Europe PMC] [Abstract]
    Category: Sequences.
    Annotation: 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.
    Source: GeneRIF:10771.

    This publication is mapped to 9 other entries.

  18. 18
    "Interaction with ZMYND11 mediates opposing roles of Ras-responsive transcription factors ETS1 and ETS2."
    Plotnik J.P., Hollenhorst P.C.
    Nucleic Acids Res. 45:4452-4462(2017) [PubMed] [Europe PMC] [Abstract]
    Category: Interaction.
    Annotation: Interaction with ZMYND11 mediates opposing roles of Ras-responsive ETS1 and ETS2.
    Source: GeneRIF:10771.

    This publication is mapped to 14 other entries.

  19. 19
    "Phenotype comparison confirms ZMYND11 as a critical gene for 10p15.3 microdeletion syndrome."
    Tumiene B., Ciuladaite Z., Preiksaitiene E., Mameniskiene R., Utkus A., Kucinskas V.
    J. Appl. Genet. 58:467-474(2017) [PubMed] [Europe PMC] [Abstract]
    Category: Pathology & Biotech, Sequences.
    Annotation: The ZMYND11 gene has important functions in epigenetic regulation.
    Source: GeneRIF:10771.

    This publication is mapped to 7 other entries.

  20. 20
    "Downregulation of ZMYND11 induced by miR-196a-5p promotes the progression and growth of GBM."
    Yang J.P., Yang J.K., Li C., Cui Z.Q., Liu H.J., Sun X.F., Geng S.M., Lu S.K., Song J., Guo C.Y., Jiao B.H.
    Biochem. Biophys. Res. Commun. 494:674-680(2017) [PubMed] [Europe PMC] [Abstract]
    Category: Expression.
    Annotation: 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.
    Source: GeneRIF:10771.

    This publication is mapped to 7 other entries.

  21. 21
    "The Transcriptional Repressor BS69 is a Conserved Target of the E1A Proteins from Several Human Adenovirus Species."
    Zhang A., Tessier T.M., Galpin K.J.C., King C.R., Gameiro S.F., Anderson W.W., Yousef A.F., Qin W.T., Li S.S.C., Mymryk J.S.
    Viruses 10:0-0(2018) [PubMed] [Europe PMC] [Abstract]
    Category: Function, Interaction.
    Annotation: 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.
    Source: GeneRIF:10771.

    This publication is mapped to 7 other entries.

1 to 21 of 21  Show
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