scholarly journals The Promyelocytic Leukemia Zinc Finger Protein: Two Decades of Molecular Oncology

2012 ◽  
Vol 2 ◽  
Author(s):  
Bandar Ali Suliman ◽  
Dakang Xu ◽  
Bryan Raymond George Williams
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Promyelocytic Leukemia ◽  
Promyelocytic Leukemia Zinc Finger ◽  
Molecular Oncology ◽  
Finger Protein

scholarly journals Promyelocytic Leukemia Zinc Finger Protein Regulates Interferon-Mediated Innate Immunity

Immunity ◽  
2009 ◽  
Vol 30 (6) ◽  
pp. 802-816 ◽  
Author(s):  
Dakang Xu ◽  
Michelle Holko ◽  
Anthony J. Sadler ◽  
Bernadette Scott ◽  
Shigeki Higashiyama ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Promyelocytic Leukemia ◽  
Promyelocytic Leukemia Zinc Finger ◽  
Finger Protein

scholarly journals The GTPase domain of Galphao contributes to the functional interaction of Galphao with the promyelocytic leukemia zinc finger protein

2009 ◽  
Vol 14 (1) ◽  
Author(s):  
Jung Won ◽  
Sung Ghil
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Promyelocytic Leukemia ◽  
Functional Interaction ◽  
Gtpase Domain ◽  
Promyelocytic Leukemia Zinc Finger ◽  
Downstream Effector ◽  
Finger Protein ◽  
Family Based ◽  
G Protein Coupled

AbstractGo, one of the most abundant heterotrimeric G proteins in the brain, is classified as a member of the Gi/Go family based on its homology to Gi proteins. Recently, we identified promyelocytic leukemia zinc finger protein (PLZF) as a candidate downstream effector for the alpha subunit of Go (Gαo). Activated Gαo interacts with PLZF and augments its function as a repressor of transcription and cell growth. G protein-coupled receptor-mediated Gαo activation also enhanced PLZF function. In this study, we determined that the GTPase domain of Gαo contributes to Gαo:PLZF interaction. We also showed that the Gαo GTPase domain is important in modulating the function of PLZF. This data indicates that the GTPase domain of Gαo may be necessary for the functional interaction of Gαo with PLZF.

scholarly journals Sequence-specific DNA Binding and Transcriptional Regulation by the Promyelocytic Leukemia Zinc Finger Protein

1997 ◽  
Vol 272 (36) ◽  
pp. 22447-22455 ◽  
Author(s):  
Jia-Yuan Li ◽  
Milton A. English ◽  
Helen J. Ball ◽  
Patricia L. Yeyati ◽  
Samuel Waxman ◽  
...  
Keyword(s):  
Transcriptional Regulation ◽  
Dna Binding ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Promyelocytic Leukemia ◽  
Promyelocytic Leukemia Zinc Finger ◽  
Finger Protein

scholarly journals Regulation of epithelial sodium transport by promyelocytic leukemia zinc finger protein

2008 ◽  
Vol 295 (1) ◽  
pp. F18-F26 ◽  
Author(s):  
Anikó Náray-Fejes-Tóth ◽  
Cary Boyd ◽  
Géza Fejes-Tóth
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Promyelocytic Leukemia ◽  
Negative Regulator ◽  
Sodium Reabsorption ◽  
Target Cells ◽  
Mrna Levels ◽  
Na Transport ◽  
Promyelocytic Leukemia Zinc Finger ◽  
Finger Protein

Aldosterone is the principal regulator of Na homeostasis, and thereby blood pressure. One of the main targets of aldosterone is the epithelial Na channel (ENaC) located in the apical membrane of target cells. Previous studies identified several genes involved in the regulation of ENaC such as SGK1; however, SGK1 knockout mice have only a mild salt-losing phenotype, indicating that further genes must be involved in the action of aldosterone. In our search for further aldosterone-regulated genes, we discovered that aldosterone, at physiological concentrations, induces the expression of the promyelocytic leukemia zinc finger protein (PLZF) in renal cortical collecting duct (CCD) cell lines that stably express mineralocorticoid receptors (MRs). This effect is rapid and does not require de novo protein synthesis, suggesting a direct action. Surprisingly, stable overexpression of human or mouse PLZF isoforms significantly decreased transepithelial Na transport in CCD cells while having no effect on the integrity of the monolayers. In parallel with the decline in Na transport, PLZF suppressed the mRNA levels of β- and γ-ENaC subunits. These observations suggest that PLZF is a negative regulator of ENaC in renal epithelial cells and might be part of a negative feedback loop that limits aldosterone's stimulatory effects on sodium reabsorption.

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