anti-Zinc Finger Protein 521 (ZNF521) Antibodies

Human Zinc Finger Protein 521 (ZNF521) interaction partners

1. Examination of early adipogenic signals in subcutaneous adipose tissue identifies ZNF521 as a key regulator of maintaining human adipose stromal vascular fraction cells proliferative and uncommitted. Silencing ZNF521 increases BMP4 and nuclear import of the adipogenic marker and PPARgamma transcriptional activator ZNF423.

2. Together with our previous findings, these results show that ZNF521 inhibits both adipocytic and osteoblastic maturation in Human adipose-derived stem cells (hADSCs) and suggest that its expression may contribute to maintaining the immature properties of hADSCs

3. Performance metrics were used to select SNPs in stage 1, which were then genotyped to another dataset (stage 2). Four SNPs (CPXM2 rs2362967, APOC1 rs4420638, ZNF521 rs7230380, and rs12965520) were identified for LOAD by both traditional P-values (without correcting for multiple tests) and performance metrics.

4. IHC based post-Ki67 levels may have distinct predictive power compared with the naive IHC Ki67.

5. knockdown of ZNF521 reduced proliferation in human leukemia cell lines possessing MLL-AF9 translocations

6. two multi-zinc finger transcription cofactors named ZNF423 and ZNF521 have been characterised as potent inhibitors of EBF1 and are emerging as potentially relevant contributors to the development of B-cell leukaemias

7. Data show that zinc finger protein 521 (ZNF521) can function as a repressor of osteoblastic differentiation of bone marrow mesenchymal stem cells (bmMSCs).

8. Newly discovered ZNF521-molecular partners of potentially relevant functional role, such as ZNF423, Spt16, Spt5, were discovered and validated by Western blotting.

9. Data strongly support the notion that ZNF521, through the recruitment of the NuRD complex, contributes to the clonogenic growth, migration and tumorigenicity of medulloblastoma cells.

10. Data show that ZNF521 can antagonize B-cell development and support the notion that it may contribute to conserve the multipotency of primitive lympho-myeloid progenitors by preventing or delaying their EBF1-driven commitment toward the B-cell lineage.

11. Zinc finger protein 521, a new player in bone formation.

12. EHZF is likely to play a relevant role in the control of human hematopoiesis and might be implicated in the development of hematopoietic malignancies.

13. A review of possible roles for ZNF521 in development, stem cell regulation and oncogenesis.

14. ZNF521 modulates erythroid cell differentiation through direct binding with GATA-1.

15. Enhanced resistance of target cells to NK cell-mediated cytotoxicity was induced by enforced expression of EHZF in the cervical carcinoma cell line HeLa and in the B lymphoblastoid cell line IM9

Mouse (Murine) Zinc Finger Protein 521 (ZNF521) interaction partners

1. Report a novel role for ZFP521 in regulating the earliest stages of hematopoiesis and lymphoid cell development via a cell-extrinsic mechanism. Mice with inactivated Zfp521 genes (Zfp521(-/-)) possess reduced frequencies and numbers of hematopoietic stem and progenitor cells, common lymphoid progenitors, and B and T cell precursors.

2. 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.

3. these results identify ZNF521/ZFP521 as a critical regulator of HSC function, which facilitates MLL-AF9-mediated leukemic disease in mice.

4. links between dysregulated Zfp521 and B-cell survival

5. 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.

6. Data suggest a facilitated approach for establishing human neural stem cells (NSCs) through zinc finger protein 521 (Zfp521)-driven conversion of fibroblasts.

7. it is concluding that an enhanced expression of Fndc5 in neural progenitor cells is stimulated by Zfp521 overexpression in these cells

8. Data show that zinc finger protein 521 (ZNF521) overexpression repressed osteoblastic differentiation of C3H10T1/2 cells.

9. Runx1-dependent transcription factor gene Zfp521 is expressed in, and required for establishing molecular features that define, mechanoreceptors.

10. 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.

11. the interplay between Zfp521 and Ebf1 is identified as a novel rheostat for bone homeostasis.

12. Reduction of Zfp521 enhances adipogenic potential in vivo.

13. Zfp521 is a nuclear protein with 30 Kruppel-like zinc fingers mediating multiple protein-protein interactions, and regulates transcription in diverse tissues and organs.

14. 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.

15. This study provides the first genetic evidence that Zfp521 is required downstream of PTHR1 signaling to act on chondrocyte proliferation, differentiation, and cell death.

16. transition of ES cell differentiation from the epiblast state into neuroectodermal progenitors specifically depends on the cell-intrinsic expression and activator function of Zfp521

17. The balance and HDAC3-dependent molecular interplay between Zfp521 and Runx2 contribute to the control of osteoblast differentiation, skeletal development, and bone homeostasis.

18. Zfp521 is an important PTHrP target gene that regulates growth plate chondrocyte proliferation and differentiation.

19. 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.

20. Evi3 misexpression initiates tumorigenesis by perturbing B-cell development via an interaction with Early B-cell Factor (EBF).