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    Sall4 spalt like transcription factor 4 [ Mus musculus (house mouse) ]

    Gene ID: 99377, updated on 27-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Sall genes regulate hindlimb initiation in mouse embryos.

    Sall genes regulate hindlimb initiation in mouse embryos.
    Chen KQ, Kawakami H, Anderson A, Corcoran D, Soni A, Nishinakamura R, Kawakami Y.,

    06/3/2024
    Sall4 regulates posterior trunk mesoderm development by promoting mesodermal gene expression and repressing neural genes in the mesoderm.

    Sall4 regulates posterior trunk mesoderm development by promoting mesodermal gene expression and repressing neural genes in the mesoderm.
    Pappas MP, Kawakami H, Corcoran D, Chen KQ, Scott EP, Wong J, Gearhart MD, Nishinakamura R, Nakagawa Y, Kawakami Y., Free PMC Article

    03/11/2024
    SALL4 is a CRL3[REN/KCTD11] substrate that drives Sonic Hedgehog-dependent medulloblastoma.

    SALL4 is a CRL3(REN/KCTD11) substrate that drives Sonic Hedgehog-dependent medulloblastoma.
    Lospinoso Severini L, Loricchio E, Navacci S, Basili I, Alfonsi R, Bernardi F, Moretti M, Conenna M, Cucinotta A, Coni S, Petroni M, De Smaele E, Giannini G, Maroder M, Canettieri G, Mastronuzzi A, Guardavaccaro D, Ayrault O, Infante P, Bufalieri F, Di Marcotullio L., Free PMC Article

    02/12/2024
    Sall1 and Sall4 cooperatively interact with Myocd and SRF to promote cardiomyocyte proliferation by regulating CDK and cyclin genes.

    Sall1 and Sall4 cooperatively interact with Myocd and SRF to promote cardiomyocyte proliferation by regulating CDK and cyclin genes.
    Katano W, Mori S, Sasaki S, Tajika Y, Tomita K, Takeuchi JK, Koshiba-Takeuchi K.

    12/21/2023
    Sall4 restricts glycolytic metabolism in limb buds through transcriptional regulation of glycolytic enzyme genes.

    Sall4 restricts glycolytic metabolism in limb buds through transcriptional regulation of glycolytic enzyme genes.
    Kawakami H, Chen KQ, Zhang R, Pappas MP, Bailey A, Reisz JA, Corcoran D, Nishinakamura R, D'Alessandro A, Kawakami Y., Free PMC Article

    07/12/2023
    Sall4 Guides p53-Mediated Enhancer Interference upon DNA Damage in Mouse Embryonic Stem Cells.

    Sall4 Guides p53-Mediated Enhancer Interference upon DNA Damage in Mouse Embryonic Stem Cells.
    Wang L, Tan X, Chen L, Xu S, Huang W, Chen N, Wu Y, Wang C, Zhou D, Li M.

    12/3/2022
    Epigenetic control of melanoma cell invasiveness by the stem cell factor SALL4.

    Epigenetic control of melanoma cell invasiveness by the stem cell factor SALL4.
    Diener J, Baggiolini A, Pernebrink M, Dalcher D, Lerra L, Cheng PF, Varum S, Häusel J, Stierli S, Treier M, Studer L, Basler K, Levesque MP, Dummer R, Santoro R, Cantù C, Sommer L., Free PMC Article

    09/4/2021
    Development of the Proximal-Anterior Skeletal Elements in the Mouse Hindlimb Is Regulated by a Transcriptional and Signaling Network Controlled by Sall4.

    Development of the Proximal-Anterior Skeletal Elements in the Mouse Hindlimb Is Regulated by a Transcriptional and Signaling Network Controlled by Sall4.
    Chen KQ, Tahara N, Anderson A, Kawakami H, Kawakami S, Nishinakamura R, Pandolfi PP, Kawakami Y., Free PMC Article

    04/3/2021
    SALL4 controls cell fate in response to DNA base composition.

    SALL4 controls cell fate in response to DNA base composition.
    Pantier R, Chhatbar K, Quante T, Skourti-Stathaki K, Cholewa-Waclaw J, Alston G, Alexander-Howden B, Lee HY, Cook AG, Spruijt CG, Vermeulen M, Selfridge J, Bird A., Free PMC Article

    03/6/2021
    A role of Sall4 in regulating Neuromesodermal progenitor cells and their descendants in mouse embryos.

    Sall4 regulates neuromesodermal progenitors and their descendants during body elongation in mouse embryos.
    Tahara N, Kawakami H, Chen KQ, Anderson A, Yamashita Peterson M, Gong W, Shah P, Hayashi S, Nishinakamura R, Nakagawa Y, Garry DJ, Kawakami Y., Free PMC Article

    07/11/2020
    changes of Sall4 lineage contribution in developing embryos and the contribution of Sall4-lineages to postnatal germ cells in mice

    Temporal changes of Sall4 lineage contribution in developing embryos and the contribution of Sall4-lineages to postnatal germ cells in mice.
    Tahara N, Kawakami H, Zhang T, Zarkower D, Kawakami Y., Free PMC Article

    10/26/2019
    Findings indicate that SALL4 critically contributes to MLL-AF9-induced leukemia, unraveling the underlying transcriptional and epigenetic mechanisms in this disease.

    The stem cell factor SALL4 is an essential transcriptional regulator in mixed lineage leukemia-rearranged leukemogenesis.
    Yang L, Liu L, Gao H, Pinnamaneni JP, Sanagasetti D, Singh VP, Wang K, Mathison M, Zhang Q, Chen F, Mo Q, Rosengart T, Yang J., Free PMC Article

    06/16/2018
    SALL4 associated with the NuRD co-repressor and repressed expression of the tumor suppressor genes Foxl1 and Dusp4.

    Germline Stem Cell Activity Is Sustained by SALL4-Dependent Silencing of Distinct Tumor Suppressor Genes.
    Chan AL, La HM, Legrand JMD, Mäkelä JA, Eichenlaub M, De Seram M, Ramialison M, Hobbs RM., Free PMC Article

    05/19/2018
    Study propose a model whereby enhancer binding by Sall4 and other pluripotency-associated transcription factors is responsible for maintaining the balance between transcriptional programmes in pluripotent cells.

    Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex.
    Miller A, Ralser M, Kloet SL, Loos R, Nishinakamura R, Bertone P, Vermeulen M, Hendrich B., Free PMC Article

    09/9/2017
    SALL4 has a negative impact in DNA damage repair, and support the model of dual functional properties of SALL4 in leukemogenesis through inhibiting DNA damage repair and promoting cell survival.

    Leukemic survival factor SALL4 contributes to defective DNA damage repair.
    Wang F, Gao C, Lu J, Tatetsu H, Williams DA, Müller LU, Cui W, Chai L., Free PMC Article

    09/9/2017
    these data reveal the full profile of PLZF and SALL4 regulatory targets in undifferentiated spermatogonia.

    The regulatory repertoire of PLZF and SALL4 in undifferentiated spermatogonia.
    Lovelace DL, Gao Z, Mutoji K, Song YC, Ruan J, Hermann BP., Free PMC Article

    09/2/2017
    study explores a pivotal role of Sall4 in regulating epigenetic maturation of mouse oocytes.

    Maternal Sall4 Is Indispensable for Epigenetic Maturation of Mouse Oocytes.
    Xu K, Chen X, Yang H, Xu Y, He Y, Wang C, Huang H, Liu B, Liu W, Li J, Kou X, Zhao Y, Zhao K, Zhang L, Hou Z, Wang H, Wang H, Li J, Fan H, Wang F, Gao Y, Zhang Y, Chen J, Gao S., Free PMC Article

    06/3/2017
    JARID2 physically interacts with ESRRB, SALL4A, and PRDM14

    Combined Overexpression of JARID2, PRDM14, ESRRB, and SALL4A Dramatically Improves Efficiency and Kinetics of Reprogramming to Induced Pluripotent Stem Cells.
    Iseki H, Nakachi Y, Hishida T, Yamashita-Sugahara Y, Hirasaki M, Ueda A, Tanimoto Y, Iijima S, Sugiyama F, Yagami K, Takahashi S, Okuda A, Okazaki Y.

    11/5/2016
    As SALL4A is known to impair ZBTB16-mediated Kit repression [14], our study provides novel insights into the molecular mechanism by which ATRA could control KIT expression, and thereby the differentiation of Aal into A1 spermatogonia in vivo.

    Retinoic Acid Receptors Control Spermatogonia Cell-Fate and Induce Expression of the SALL4A Transcription Factor.
    Gely-Pernot A, Raverdeau M, Teletin M, Vernet N, Féret B, Klopfenstein M, Dennefeld C, Davidson I, Benoit G, Mark M, Ghyselinck NB., Free PMC Article

    05/7/2016
    In differentiated ESCs, Sall4 bound to these somatic cell program gene loci, which are reportedly occupied by Prdm1 in embryonic carcinoma cells.

    Sall4 is essential for mouse primordial germ cell specification by suppressing somatic cell program genes.
    Yamaguchi YL, Tanaka SS, Kumagai M, Fujimoto Y, Terabayashi T, Matsui Y, Nishinakamura R.

    09/26/2015
    This study identified a critical role of the Sall4-Gli3 system at the early steps of limb development for proper development of the appendicular skeletal elements.

    Sall4-Gli3 system in early limb progenitors is essential for the development of limb skeletal elements.
    Akiyama R, Kawakami H, Wong J, Oishi I, Nishinakamura R, Kawakami Y., Free PMC Article

    07/4/2015
    Sall4 also interacts with Baf60a, a member of the SWI/SNF (switch/sucrose nonfermentable) ATP-dependent chromatin-remodeling complex, which is responsible for recruiting Sall4 to the site of DNA DSB damage.

    Stemness factor Sall4 is required for DNA damage response in embryonic stem cells.
    Xiong J, Todorova D, Su NY, Kim J, Lee PJ, Shen Z, Briggs SP, Xu Y., Free PMC Article

    05/2/2015
    SALL4b is the major isoform in hematopoietic stem cells. Overexpression of either isoform impairs hematopoietic colony formation. Lineage-negative bone marrow overexpressing SALL4b fails to engraft. SALL4a or SALL4b overexpression impairs hematopoiesis.

    Sall4 overexpression blocks murine hematopoiesis in a dose-dependent manner.
    Milanovich S, Peterson J, Allred J, Stelloh C, Rajasekaran K, Fisher J, Duncan SA, Malarkannan S, Rao S., Free PMC Article

    02/14/2015
    our data revealed that histone demethylase LSD1 may negatively regulate SALL4-mediated transcription, and the dynamic regulation of SALL4-associated epigenetic factors cooperatively modulates early hematopoietic precursor proliferation.

    Histone lysine-specific demethylase 1 (LSD1) protein is involved in Sal-like protein 4 (SALL4)-mediated transcriptional repression in hematopoietic stem cells.
    Liu L, Souto J, Liao W, Jiang Y, Li Y, Nishinakamura R, Huang S, Rosengart T, Yang VW, Schuster M, Ma Y, Yang J., Free PMC Article

    02/22/2014
    Oct4, Sall4, and Nanog form a robust and integrated network to govern mammalian pre-implantation development.

    An Oct4-Sall4-Nanog network controls developmental progression in the pre-implantation mouse embryo.
    Tan MH, Au KF, Leong DE, Foygel K, Wong WH, Yao MW., Free PMC Article

    09/21/2013
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