Please use this identifier to cite or link to this item: https://doi.org/10.1111/j.1537-2995.2012.03888.x
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dc.titleSALL4 is a key transcription regulator in normal human hematopoiesis
dc.contributor.authorGao, C.
dc.contributor.authorKong, N.R.
dc.contributor.authorLi, A.
dc.contributor.authorTatetu, H.
dc.contributor.authorUeno, S.
dc.contributor.authorYang, Y.
dc.contributor.authorHe, J.
dc.contributor.authorYang, J.
dc.contributor.authorMa, Y.
dc.contributor.authorKao, G.S.
dc.contributor.authorTenen, D.G.
dc.contributor.authorChai, L.
dc.date.accessioned2016-09-06T08:42:11Z
dc.date.available2016-09-06T08:42:11Z
dc.date.issued2013-05
dc.identifier.citationGao, C., Kong, N.R., Li, A., Tatetu, H., Ueno, S., Yang, Y., He, J., Yang, J., Ma, Y., Kao, G.S., Tenen, D.G., Chai, L. (2013-05). SALL4 is a key transcription regulator in normal human hematopoiesis. Transfusion 53 (5) : 1037-1049. ScholarBank@NUS Repository. https://doi.org/10.1111/j.1537-2995.2012.03888.x
dc.identifier.issn00411132
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/126852
dc.description.abstractBACKGROUND: Stem cell factor SALL4 is a zinc finger transcription factor. It plays vital roles in the maintenance of embryonic stem cell properties, functions as an oncogene in leukemia, and has been recently proposed to use for cord blood expansion. The mechanism(s) by which SALL4 functions in normal human hematopoiesis, including identification of its target genes, still need to be explored. STUDY DESIGN AND METHODS: Chromatin immunoprecipitation followed by microarray hybridization (ChIP-chip) was used for mapping SALL4 global gene targets in normal primary CD34+ cells. The results were then correlated with SALL4 functional studies in the CD34+ cells. RESULTS: More than 1000 potential SALL4 downstream target genes have been identified, and validation of binding by ChIP-quantitative polymerase chain reaction was performed for 5% of potential targets. These include genes that are involving in hematopoietic differentiation and self-renewal, such as HOXA9, RUNX1, CD34, and PTEN. Down regulation of SALL4 expression using small-hairpin RNA in these cells led to decreased in vitro myeloid colony-forming abilities and impaired in vivo engraftment. Furthermore, HOXA9 was identified to be a major SALL4 target in normal human hematopoiesis and the loss of either SALL4 or HOXA9 expression in CD34+ cells shared a similar phenotype. CONCLUSION: Taken together, SALL4 is a key regulator in normal human hematopoiesis and the mechanism of its function is at least in part through the HOXA9. Future study will determine whether modulating the SALL4/HOXA9 pathway can be used in cellular therapy such as cord blood expansion and/or myeloid engraftment. © 2012 American Association of Blood Banks.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1111/j.1537-2995.2012.03888.x
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentMEDICINE
dc.description.doi10.1111/j.1537-2995.2012.03888.x
dc.description.sourcetitleTransfusion
dc.description.volume53
dc.description.issue5
dc.description.page1037-1049
dc.description.codenTRANA
dc.identifier.isiut000318657200016
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