Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.celrep.2020.108574
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dc.titleZinc Finger Protein SALL4 Functions through an AT-Rich Motif to Regulate Gene Expression
dc.contributor.authorKong, Nikki R.
dc.contributor.authorBassal, Mahmoud A.
dc.contributor.authorTan, Hong Kee
dc.contributor.authorKurland, Jesse, V
dc.contributor.authorYong, Kol Jia
dc.contributor.authorYoung, John J.
dc.contributor.authorYang, Yang
dc.contributor.authorLi, Fudong
dc.contributor.authorLee, Jonathan D.
dc.contributor.authorLiu, Yue
dc.contributor.authorWu, Chan-Shuo
dc.contributor.authorStein, Alicia
dc.contributor.authorLuo, Hongbo R.
dc.contributor.authorSilberstein, Leslie E.
dc.contributor.authorBulyk, Martha L.
dc.contributor.authorTenen, Daniel G.
dc.contributor.authorChai, Li
dc.date.accessioned2022-10-26T09:17:28Z
dc.date.available2022-10-26T09:17:28Z
dc.date.issued2021-01-01
dc.identifier.citationKong, Nikki R., Bassal, Mahmoud A., Tan, Hong Kee, Kurland, Jesse, V, Yong, Kol Jia, Young, John J., Yang, Yang, Li, Fudong, Lee, Jonathan D., Liu, Yue, Wu, Chan-Shuo, Stein, Alicia, Luo, Hongbo R., Silberstein, Leslie E., Bulyk, Martha L., Tenen, Daniel G., Chai, Li (2021-01-01). Zinc Finger Protein SALL4 Functions through an AT-Rich Motif to Regulate Gene Expression. Cell Reports 34 (1) : 108574. ScholarBank@NUS Repository. https://doi.org/10.1016/j.celrep.2020.108574
dc.identifier.issn2211-1247
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/233809
dc.description.abstractThe zinc finger transcription factor SALL4 is highly expressed in embryonic stem cells, downregulated in most adult tissues, but reactivated in many aggressive cancers. This unique expression pattern makes SALL4 an attractive therapeutic target. However, whether SALL4 binds DNA directly to regulate gene expression is unclear, and many of its targets in cancer cells remain elusive. Here, through an unbiased screen of protein binding microarray (PBM) and cleavage under targets and release using nuclease (CUT&RUN) experiments, we identify and validate the DNA binding domain of SALL4 and its consensus binding sequence. Combined with RNA sequencing (RNA-seq) analyses after SALL4 knockdown, we discover hundreds of new SALL4 target genes that it directly regulates in aggressive liver cancer cells, including genes encoding a family of histone 3 lysine 9-specific demethylases (KDMs). Taken together, these results elucidate the mechanism of SALL4 DNA binding and reveal pathways and molecules to target in SALL4-dependent tumors. © 2020 The Author(s)In this paper, Kong et al. elucidate the DNA binding mechanisms of the transcription factor SALL4 and an epigenetic pathway that it regulates. Due to its important role in driving aggressive cancers, better understanding of SALL4 function will lead to strategies to target this protein in cancer. © 2020 The Author(s)
dc.publisherElsevier B.V.
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/
dc.sourceScopus OA2021
dc.subjectCUT&RUN
dc.subjectheterochromatin
dc.subjectKDM
dc.subjectliver cancer
dc.subjectprotein binding microarray
dc.subjectSALL4
dc.subjecttranscription
dc.typeArticle
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.contributor.departmentMEDICINE
dc.description.doi10.1016/j.celrep.2020.108574
dc.description.sourcetitleCell Reports
dc.description.volume34
dc.description.issue1
dc.description.page108574
dc.published.statePublished
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