Identification of the nuclear localization signal of SALL4B, a stem cell transcription factor

Wu, Maomao; Yang, Fan; Ren, Zhihua; Jiang, Yongping; Ma, Yupo; Chen, Yan; Dai, Wei

doi:10.4161/cc.28418

Cited by 11 publications

(9 citation statements)

References 41 publications

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“…A “K to R” substitution at position 64 (K64R) results in impaired SALL4 translocation into the nucleus. This remains true for SALL4B mutants with large truncation of lysine-rich domains 7 . Our sequence alignment confirms that the KRLR sequence is also found in SALL4A.…”

supporting

confidence: 82%

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Nuclear localization of SALL4: A stemness transcription factor

Firor

Jares

2014

Cell Cycle

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supporting

confidence: 82%

“…In this study, Wu et al investigated the mechanism of SALL4B nuclear localization 7 . In order to identify the necessary SALL4B regions, Wu et al generated mutants of the SALL4 wild-type protein labeled with HA tags for a loss-of-function study.…”

mentioning

confidence: 99%

Nuclear localization of SALL4: A stemness transcription factor

Firor

Jares

2014

Cell Cycle

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“…In addition, nuclear receptor binding protein 1 (NRBP1) is involved in the regulation of SALL4 protein levels (14). In the nuclear localization signal (NLS) of SALL4, K64 is necessary for localization in the nucleus, and K64R mutation increases the cytoplasmic level of SALL4 (19). To determine whether SALL4…”

Section: Sall4 Has 4 Sumoylation Sites Andmentioning

confidence: 99%

Sal-like 4 protein levels in breast cancer cells are post-translationally down-regulated by tripartite motif–containing 21

Itou

Ito

et al. 2018

Journal of Biological Chemistry

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“…SALL4 is a nuclear protein and its subcellular localization is mediated through at least one conserved nuclear localization signal (NLS) at amino acids (AA) 64–67. A single mutation that changes lysine 64 into arginine (K64 into R64) is sufficient to disrupt its subcellular distribution and compromises its function in vivo 12 .…”

Section: Introductionmentioning

confidence: 99%

SALL4, the missing link between stem cells, development and cancer

Tatetsu

Kong

Gao

et al. 2016

Gene

109

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There is a growing body of evidence supporting that cancer cells share many similarities with embryonic stem cells (ESCs). For example, aggressive cancers and ESCs share a common gene expression signature that includes hundreds of genes. Since ESC genes are not present in most adult tissues, they could be ideal candidate targets for cancer-specific diagnosis and treatment. This is an exciting cancer-targeting model. The major hurdle to test this model is to identify the key factors/pathway(s) within ESCs that are responsible for the cancer phenotype. SALL4 is one of few genes that can establish this link. The first publication of SALL4 is on its mutation in a human inherited disorder with multiple developmental defects. Since then, over 300 papers have been published on various aspects of this gene in stem cells, development, and cancers. This review aims to summarize our current knowledge of SALL4, including a SALL4-based approach to classify and target cancers. Many questions about this important gene still remain unanswered, specifically, on how this gene regulates cell fates at a molecular level. Understanding SALL4’s molecular functions will allow development of specific targeted approaches in the future.

show abstract

Identification of the nuclear localization signal of SALL4B, a stem cell transcription factor

Cited by 11 publications

References 41 publications

Nuclear localization of SALL4: A stemness transcription factor

Nuclear localization of SALL4: A stemness transcription factor

Sal-like 4 protein levels in breast cancer cells are post-translationally down-regulated by tripartite motif–containing 21

SALL4, the missing link between stem cells, development and cancer

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