Zinc Finger Protein, Multitype 1 Proteins (ZFPM1)

Human Zinc Finger Protein, Multitype 1 (ZFPM1) interaction partners

1. Forced FOG1 protein expression in K562 erythroleukemia cells induced the expression of SLC4A1 protein, but repressed that of transcription factor PU.1.

2. GAB2, GSPT1, TFDP2 and ZFPM1 are four new susceptibility loci for testicular germ cell tumor.

3. FOG1 is a member of the PR domain containing, zinc finger protein family of transcriptional regulators.

4. Our results reveal that the protein structure does not affect ligand binding, and the top three TCM candidates Bittersweet alkaloid II, Eicosandioic acid, and Perivine might resolve the instability of the RbAp48-FOG1 complex

5. FOG1, FOG2 and GATA-6 modulate the transcriptional up-regulation of HAMP in hepatocytes during inflammation.

6. ZFPM1 that facilitates human Th1 differentiation via the downregulation of IL-4 is a potential target for the treatment of allergic diseases.

7. Anagrelide suppresses megakaryocytopoiesis by reducing the expression levels of GATA-1 and FOG-1 via a PDEIII-independent mechanism that is differentiation context-specific and does not involve inhibition of MPL-mediated early signal transduction events

8. The FOG-1 peptide contacts a negatively charged binding pocket on top of the RbAp48 beta-propeller that is distinct from the binding surface used by RpAp48 to contact histone H4

9. X-linked thrombocytopenia with thalassemia from a mutation in the amino finger of GATA-1 affects DNA binding but does not affect FOG-1 interaction.(FOG1, cofactor of GATA1)

10. Erythroid and megakaryocytic lineage differentiation and maturation are regulated via cooperation between transcription factor GATA1 and its essential cofactor FOG1. It depends on the binding of FOG1 to the N-terminalfinger of GATA1.

11. 3D structure of a complex comprising the interaction domains of FOG1 and GATA1 reveals how zinc fingers can act as protein recognition motifs and provides a molecular explanation for how GATA-1 mutations contribute to distinct, related genetic diseases.

12. Megakaryocytes from idiopathic myelofibrosis patients have reduced GATA-1 content, possibly contributing to disease pathogenesis as in the GATA-1(low) mice.

13. Data verified the function of Zfpm-1 during erythropoietic differentiation.

14. FOG-1 inhibits mast-cell differentiation in a differentiation stage-dependent manner, and its effects are produced via different molecular mechanisms.

15. two novel mechanisms for the regulation of GATA1 interaction with FOG1-dependent protein complexes through the production of two translational isoforms with differential interaction profiles and independent nuclear localization controls.

Mouse (Murine) Zinc Finger Protein, Multitype 1 (ZFPM1) interaction partners

1. FOG1 is a member of the PR domain containing, zinc finger protein family of transcriptional regulators.

2. the role of FOG-1 in B lymphocytes

3. FOG-1 is required for the formation of all committed Mk- and E-lineage progenitors. It mediates transcriptional megakaryocyte/erythrocyte programming of HSCs as well as their subsequent Mk/E-lineage commitment.

4. Disruption of the GATA1/FOG1/NuRD transcriptional system results in a complex, pleiotropic platelet defect beyond gray platelet syndrome-like macrothrombocytopenia.

5. These results implicate FOG1 and 2 and CTBPs as partners of GATA proteins in the control of adipocyte proliferation and differentiation.

6. role of the hematopoietic transcription factor GATA-1, its cofactor FOG-1, and the associated chromatin remodeling complex NuRD in the developmental silencing of HBG1 and HBG2 gene expression

7. The continuous presence of GATA1, FOG1, and NuRD is required to maintain lineage fidelity throughout megakaryocyte-erythroid ontogeny.

8. Data demonstrate that sumoylation of GATA-1 K137 promotes transcriptional activation only at target genes requiring the coregulator Friend of GATA-1 (FOG-1).

9. Gene expression analysis in primary mutant erythroid cells and megakaryocytes revealed an essential function for NuRD during both the repression and activation of select Gata-1/Fog1 target genes.

10. Homozygous Fog1(R3K5A) mice were found to have splenomegaly, extramedullary erythropoiesis, granulocytosis and thrombocytopaenia secondary to a block in megakaryocyte maturation.

11. Interaction between FOG-1 and the corepressor C-terminal binding protein is dispensable for normal erythropoiesis in vivo.

12. may modulate the fate of a bipotential erythroid/megakaryocytic precursor cell.

13. requires an interaction with either GATA-1 or -2 as part of its essential role in early megakaryopoiesis

14. FOG-2, in addition to GATA-4, has a role in early gonadal development and sexual differentiation, and FOG-1 at later fetal stages, while GATA-1 executes its action postnatally

15. plays a role in the control of megakaryocyte-specific gene expression with gata-1: Ets transcription factors also have a role

16. nonredundant requirement for FOG-1 in the outlet tract and atrioventricular valves of the heart that depend on expression in endothelial-derived tissue and presumably reflect cooperation with the GATA-4/5/6 subfamily

17. Transgene expression comparable to the endogenous GATA-1 level resulted in much lower frequency of rescue, indicating that the GATA-1-FOG-1 association is critical for normal embryonic hematopoiesis.

18. the alpha-helix of FOG-ZF3 recognizes a C-terminal portion of the TACC3 coiled-coil

19. Status of differentiation depends on FOG-1 protein.

20. GATA-1 and its cofactor FOG-1 are required for the physical interaction between the beta-globin locus control region (LCR) and the beta-major globin promoter.

Xenopus laevis Zinc Finger Protein, Multitype 1 (ZFPM1) interaction partners

1. a requirement for FOG and its interaction with NuRD during primitive erythropoiesis

Zebrafish Zinc Finger Protein, Multitype 1 (ZFPM1) interaction partners

1. Loss of zinc finger protein multitype 1 (Zfpm1) activity resulted in over-activation of Neuregulin-ErbB signaling and abnormally elevated cardiomyocyte proliferation.

2. we identified 2 cis-regulatory elements that control the tissue-specific gene expression of FOG-1.