anti-Zinc Finger Protein 423 (104125) Antibodies

Mouse (Murine) Zinc Finger Protein 423 (104125) interaction partners

1. In vivo, vitamin A supplementation prevents obesity, downregulates Gadd45a expression, and reduces GADD45A binding and DNA demethylation in the Zfp423 promoter.

2. ZFP423 to be expressed in the developing cortex and promote RA-dependent neuronal differentiation.

3. Zfp423/ZNF423 has a role in regulating cell cycle progression, the mode of cell division and the DNA-damage response in Purkinje neuron progenitors

4. These data identify Zfp423 as a molecular brake on adipocyte thermogenesis.

5. loss of Zfp423 alters expression of several genes encoding key cilium components, including increased expression of Tulp3. Tulp3 is a direct binding target of Zfp423 and reducing the overexpression of Tulp3 in Zfp423-deficient cells suppresses Smoothened translocation defects.

6. Data show that the expression of miR-195a is regulated during adipocyte differentiation and identified Zfp423 as its novel target.

7. the antiadipogenic function of Zfp521 is mostly exerted through repression of Zfp423 and the downstream target PPAR-gamma gene.

8. Zfp423 binds autoregulatory sites in a developmental cell culture model.

9. Maternal obesity enhanced Zfp423 expression and adipogenic differentiation during fetal development, at least partially through reducing DNA methylation in the Zfp423 promoter.

10. Constitutive expression of a C-terminal mutant OAZ that selectively disrupts OAZ-O/E interaction while retaining other activities, exhibits apparently normal OSN differentiation.

11. Zfp423 expression identifies committed preadipocytes and localizes to adipose endothelial and perivascular cells.

12. Zfp423(-/-) hemisphere malformations are shaped by both genetic and non-genetic factors to produce distinct phenotypes.

13. ZFP423 coordinates Notch1 and bone morphogenetic protein signaling, selectively up-regulating Hes5 gene expression.

14. Zfp423 as a transcriptional regulator of preadipocyte determination

15. Ebfaz can substitute for the upregulated expression of Evi3 in B-cell disease and has a role in hematopoietic cancer

16. Homozygous Zfp423 null mice are runted and ataxic, the cerebellum is underdeveloped, and the vermis is severely reduced. In the remaining cerebellar structures, the Purkinje cells are poorly developed and mislocalized.

17. Neural precursor proliferation is reduced in Zfp423 null cerebellum, especially near the midline. Radial glia are morphologically abnormal. Cell layers appear nearly normal to grossly disorganized.

18. these experiments suggest that OAZ participates in a developmental switch regulating the transition from differentiation to maturation in ORNs.

19. Enhanced expression of p210BCR/ABL and aberrant expression of Zfp423/ZNF423 induce blast crisis of chronic myelogenous leukemia.

Xenopus laevis Zinc Finger Protein 423 (104125) interaction partners

1. ZFP423 coordinates Notch1 and bone morphogenetic protein signaling, selectively up-regulating Hes5 gene expression.

Human Zinc Finger Protein 423 (104125) interaction partners

1. We identified calmodulin-like protein 3 (CALML3) as a key sensor of this SNP and a coregulator of ERalpha, which contributes to differential gene transcription regulation in an estrogen and SERM-dependent fashion. Furthermore, using CRISPR/Cas9-engineered ZR75-1 breast cancer cells with different ZNF423 SNP genotypes, striking differences in cellular responses to SERMs and PARP inhibitors, alone or in combination

2. We report that CTSO reduces the protein levels of BRCA1 and ZNF423 through cysteine proteinase-mediated degradation. We also have identified a series of transcription factors of BRCA1 that are regulated by CTSO at the protein level.

3. 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

4. ZNF423 expression is associated with poor outcome of ETV6-RUNX1-negative B precursor acute lymphoblastic leukemia patients.

5. OAZ gene expression was highly enriched in mesenchymal stem cells (MSCs) compared with peripheral blood leukocytes and was increased in patients with systemic lupus erythematosus (SLE) compared with control subjects.

6. These findings suggest that expression of UBR5-ZNF423 protein might contribute to the transformation of a subset of Nasopharyngeal carcinoma

7. Study identifies by whole-exome resequencing, mutations of MRE11, ZNF423, and CEP164 as causing Nephronophthisis-related ciliopathies.

8. Elevated expression of OAZ transcripts in systemic lupus erythematosus PBLs were strongly correlated with disease activity.

9. The expression level of OAZ mRNA in the bone marrow and peripheral blood of SLE patients was significantly increased than those observed in normal controls.

10. Low ZNF423 expression is associated with neuroblastoma.

Cow (Bovine) Zinc Finger Protein 423 (104125) interaction partners

1. Zfp423 is a critical regulator of adipogenesis in stromal vascular cells of bovine muscle.