Zinc Finger Protein 278 Proteins (ZNF278)

Human Zinc Finger Protein 278 (ZNF278) interaction partners

1. The results of IHC and qPCR analyses showed that the expression of PATZ1 in cancerous tissue was significantly lower than that in non-cancerous tissues. Meanwhile, PATZ1 expression was significantly associated with tumor differentiation and LN metastasis.

2. ZNF278 played a prominent role in the pathogenesis of colorectal cancer (CRC), and promoted CRC cell proliferation via the ERK/MAPK pathway, suggesting that it may act as a potential target in the diagnosis or treatment of CRC

3. this study show that PATZ1 expression correlates positively with BAX and negatively with BCL6 and survival in human diffuse large B cell lymphomas

4. Our results suggest that PATZ1 and PP4R2 provide negative feedback on IKK/NF-kappaB signaling to prevent cancer cells from over-stimulation from cellular stimuli

5. The derived allele of rs174557, which is the common variant in most populations, diminishes binding of PATZ1, a transcription factor conferring allele-specific downregulation of FADS1.

6. Loss of PATZ1 expression is associated with thyroid cancer progression.

7. Results show that PATZ1 binds to p53 and inhibits p53-dependent transcription activation.

8. these results propose that Patz1 is important for ESC pluripotency.

9. The data support a PATZ1 tumour-suppressive function based on its ability to enhance p53-dependent transcription and apoptosis.

10. PATZ1 may have an important role in the regulation of EC senescence through an ROS-mediated p53-dependent pathway and contribute to vascular diseases associated with aging.

11. these results showed a potentially novel mechanism of cAMP signaling mediated through the interaction of RIalpha with PATZ1.

12. We report here the isolation and characterization of two novel nuclear BTB/POZ domain zinc finger isoformsthat are specifically expressed in early hippocampal neurons, cerebellar granule cells, and gliogenic progenitors as well as in differentiated glia

13. MAZR and MITF synergistically transactivated the mMCP-6 gene. MAZR appeared to play important roles in the normal phenotypic expression of mast cells in association with MITF

14. The results show that ZNF278 promotes cell growth, and its knockdown suppresses cell proliferation. ZNF278 could be a potential proto-oncogene in colorectal cancer.

15. The short isoform of the Zinc finger Sarcoma Gene (ZSG) was isolated as a RNF4 interacting protein.

Mouse (Murine) Zinc Finger Protein 278 (ZNF278) interaction partners

1. endothelial PATZ1 thus potently inhibits endothelial function and angiogenesis via inhibition of FABP4 expression, and abnormal induction of endothelial PATZ1 may contribute to multiple aspects of vascular dysfunction in diabetes

2. Together, these results suggest a novel mechanism regulating endothelial PATZ1 expression based on the down-regulation of miR-24 expression caused by hyperglycemia. Interfering with PATZ1 expression via miRNAs or miRNA mimics could potentially represent a new way to target endothelial PATZ1-dependent signaling of vascular dysfunction in diabetes.

3. the repression of ThPOK during CD8 lineage differentiation is mediated by the synergistic activity of the transcription factor MAZR and Runx/CBFbeta complexes.

4. Results show that PATZ1 binds to p53 and inhibits p53-dependent transcription activation.

5. The data support a PATZ1 tumour-suppressive function based on its ability to enhance p53-dependent transcription and apoptosis.

6. analysis of embryos in which Patz1 was disrupted revealed the presence of severe defects in the CNS and in the cardiac outflow tract, which eventually lead to a pre-mature in utero death during late gestation or soon after birth

7. PATZ1 may have an important role in the regulation of EC senescence through an ROS-mediated p53-dependent pathway and contribute to vascular diseases associated with aging.

8. controls the CD4 versus CD8 lineage fate of double-positive thymocytes

9. MAZR and MITF synergistically transactivated the mMCP-6 gene. MAZR appeared to play important roles in the normal phenotypic expression of mast cells in association with MITF

10. results demonstrate epigenetic control of the Cd8 loci and identify MAZR as an important regulator of Cd8 expression