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The pre-B-cell receptor (pre-BCR) signaling molecules BLNK, BTK and BANK1 were positively regulated by the ZFP521 gene, leading to enhancement of the pre-BCR signaling pathway.
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these results identify ZNF521/ZFP521 as a critical regulator of HSC function, which facilitates MLL-AF9-mediated leukemic disease in mice.
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links between dysregulated Zfp521 and B-cell survival
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Here we demonstrate that the transcription factors SPI1 (PU.1) and HOXC13 synergistically regulate Zfp521 expression, and identify the regions of the Zfp521 promoter required for this transcriptional activity. We also show that SPI1 and HOXC13 activate Zfp521 in a dose-dependent manner.
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Data suggest a facilitated approach for establishing human neural stem cells (NSCs) through zinc finger protein 521 (Zfp521)-driven conversion of fibroblasts.
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it is concluding that an enhanced expression of Fndc5 in neural progenitor cells is stimulated by Zfp521 overexpression in these cells
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Data show that zinc finger protein 521 (ZNF521) overexpression repressed osteoblastic differentiation of C3H10T1/2 cells.
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Runx1-dependent transcription factor gene Zfp521 is expressed in, and required for establishing molecular features that define, mechanoreceptors.
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the data suggest that Zfp521 is a cell fate switch critical for BMP-induced osteoblast commitment and identify Zfp521 as the intrinsic repressor of Zfp423 and hence of adipocyte commitment during BMP-induced mesenchymal precursor differentiation.
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the interplay between Zfp521 and Ebf1 is identified as a novel rheostat for bone homeostasis.
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Reduction of Zfp521 enhances adipogenic potential in vivo.
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Zfp521 is a nuclear protein with 30 Kruppel-like zinc fingers mediating multiple protein-protein interactions, and regulates transcription in diverse tissues and organs.
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we found the expression of Zfp521 declined with the neural differentiation of bone marrow mesenchymal stem cells, and miR-9 could promote the neural differentiation via targeting Zfp521.
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This study provides the first genetic evidence that Zfp521 is required downstream of PTHR1 signaling to act on chondrocyte proliferation, differentiation, and cell death.
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transition of ES cell differentiation from the epiblast state into neuroectodermal progenitors specifically depends on the cell-intrinsic expression and activator function of Zfp521
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The balance and HDAC3-dependent molecular interplay between Zfp521 and Runx2 contribute to the control of osteoblast differentiation, skeletal development, and bone homeostasis.
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Zfp521 is an important PTHrP target gene that regulates growth plate chondrocyte proliferation and differentiation.
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Evi3 encodes an EBFAZ-related Kruppel-like zinc finger protein. Evi3 expression could be detected at all stages of B-cell development. EVI3, not EBFAZ, is the member of this protein family that interacts with and regulates early b-cell factor in B cells.
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Evi3 misexpression initiates tumorigenesis by perturbing B-cell development via an interaction with Early B-cell Factor (EBF).
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ZNF521 modulates erythroid cell differentiation through direct binding with GATA-1.