Expression of RIZ1 protein (Retinoblastoma-interacting zinc-finger protein 1) in prostate cancer epithelial cells changes with cancer grade progression and is modulated in vitro by DHT and E2

2009 ◽  
Vol 221 (3) ◽  
pp. 771-777 ◽  
Author(s):  
Valentina Rossi ◽  
Stefania Staibano ◽  
Ciro Abbondanza ◽  
Daniela Pasquali ◽  
Caterina De Rosa ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Finger Protein ◽  
Grade Progression

scholarly journals Downregulation of zinc finger protein 132 in prostate cancer is associated with aberrant promoter hypermethylation and poor prognosis

2011 ◽  
Vol 130 (4) ◽  
pp. 885-895 ◽  
Author(s):  
Mette Opstrup Abildgaard ◽  
Michael Borre ◽  
Martin Mørck Mortensen ◽  
Benedicte P. Ulhøi ◽  
Niels Tørring ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Zinc Finger ◽  
Poor Prognosis ◽  
Zinc Finger Protein ◽  
Promoter Hypermethylation ◽  
Finger Protein

IL-7R–dependent survival and differentiation of early T-lineage progenitors is regulated by the BTB/POZ domain transcription factor Miz-1

Blood ◽  
2011 ◽  
Vol 117 (12) ◽  
pp. 3370-3381 ◽  
Author(s):  
Ingrid Saba ◽  
Christian Kosan ◽  
Lothar Vassen ◽  
Tarik Möröy
Keyword(s):  
T Cells ◽  
Transcription Factor ◽  
T Cell ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Strong Reduction ◽  
Expression Levels ◽  
Cell Numbers ◽  
Finger Protein

Abstract T cells originate from early T lineage precursors that have entered the thymus and differentiate through well-defined steps. Mice deficient for the BTB/POZ domain of zinc finger protein-1 (Miz-1) almost entirely lack early T lineage precursors and have a CD4−CD8− to CD4+CD8+ block causing a strong reduction in thymic cellularity. Miz-1ΔPOZ pro-T cells cannot differentiate in vitro and are unable to relay signals from the interleukin-7R (IL-7R). Both STAT5 phosphorylation and Bcl-2 up-regulation are perturbed. The high expression levels of SOCS1 found in Miz-1ΔPOZ cells probably cause these alterations. Moreover, Miz-1 can bind to the SOCS1 promoter, suggesting that Miz-1 deficiency causes a deregulation of SOCS1. Transgenic overexpression of Bcl-2 or inhibition of SOCS1 restored pro-T cell numbers and their ability to differentiate, supporting the hypothesis that Miz-1 is required for the regulation of the IL-7/IL-7R/STAT5/Bcl-2 signaling pathway by monitoring the expression levels of SOCS1.

The zinc finger protein GLI transforms primary cells in cooperation with adenovirus E1A

1991 ◽  
Vol 11 (3) ◽  
pp. 1724-1728 ◽  
Author(s):  
J M Ruppert ◽  
B Vogelstein ◽  
K W Kinzler
Keyword(s):  
Zinc Finger ◽  
Nude Mice ◽  
Zinc Finger Protein ◽  
Primary Cells ◽  
Adenovirus E1a ◽  
In Vitro Transformation ◽  
Finger Protein ◽  
Protein Functions

The GLI gene was previously isolated by virtue of its amplification in human glioblastomas. We have now found that GLI expression can result in the in vitro transformation of both primary and secondary rodent cells. When coexpressed with adenovirus E1A, the GLI protein functions analogously to RAS, resulting in the formation of dense foci of cells which are tumorigenic in nude mice.

scholarly journals Molecular Cloning and Characterization of a Zinc Finger Protein Involved in Id-1-stimulated Mammary Epithelial Cell Growth

2001 ◽  
Vol 276 (15) ◽  
pp. 11852-11858 ◽  
Author(s):  
Jarnail Singh ◽  
Yoko Itahana ◽  
Simona Parrinello ◽  
Kenji Murata ◽  
Pierre-Yves Desprez
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Mammary Epithelial Cells ◽  
Constitutive Expression ◽  
Mammary Epithelial ◽  
Protein Fusion ◽  
Degenerate Primers ◽  
Finger Protein

Id proteins are dominant negative regulators of basic helix-loop-helix transcription factors. Previous work in our laboratory has shown that constitutive expression of Id-1 in SCp2 mouse mammary epithelial cells inhibits their differentiation and induces proliferation, invasion, and migration. Id-1 expression also correlates with the invasive and aggressive potential of human breast cancer cells. However, little is known about Id-1 target genes that are important for regulating normal and transformed breast epithelial cell phenotypes. Now we report the cloning of a novel zinc finger protein, Zfp289, using degenerate primers to specifically amplify cDNAs from Id-1-transfected SCp2 cells. Zfp289 has homology with a yeast zinc finger protein, the GTPase-activating protein Gcs-1, which was initially identified as a gene required for the re-entry of cells into the cell cycle after stationary phase growth. Zfp289 mRNA expression pattern correlates with Id-1 expression in SCp2 mammary epithelial cells under various experimental conditions as well as in the mouse mammary gland at different stages of development. It is predominantly present in the cytoplasm of the cells as evident from green fluorescent protein fusion protein localization. SCp2 mammary epithelial cells with constitutive expression of Zfp289 have a higher S-phase index, compared with control cells, when cultured in a serum-free medium. We conclude that the novel zinc finger protein Zfp289, which may represent the mammalian homologue of Gcs-1, is potentially an important mediator of the Id-1-induced proliferation pathway in mammary epithelial cells.

Abstract 19212: The Zinc-finger Protein 148(zfp148) Attenuates Aortic Aneurysm Formation and is a Novel Smooth Muscle Cell Regulator

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Morgan Salmon ◽  
Nicolas H Pope ◽  
William F Johnston ◽  
John P Davis ◽  
Gary K Owens ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Aortic Aneurysm ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Marker Genes ◽  
Aortic Dilation ◽  
Aneurysm Formation ◽  
Finger Protein

Objective: Previously, we found that the zinc-finger protein 148(ZFP148) binds to smooth muscle(SMC) genes following ligation injury; however, it has no known role in aortic aneurysm formation. The study objective was to determine whether ZFP148 is important in AA formation. Methods: ZFP148 was examined via qPCR in human aortic aneurysms(n=12/group). 8-12 week male C57/B6 mice (n=6/group) underwent elastase perfusion and were harvested at 3, 7, and 14 days for qPCR for ZFP148. Separately, 8-12 week male (n=10/group) ZFP flx/flx Myh11 Cre+(SMC tamoxifen ZFP148 KO), Myh11 ZFP148 flx/wt Cre+ and Myh11 ZFP wt/wt Cre+ underwent elastase perfusion. At 14 days, maximal aortic dilation was measured with video micrometry. ZFP148 flx/flx ERT Cre+ (n=10/group) and ZFP148 flx/flx ERT Cre-(WT) mice also underwent elastase perfusion. A separate set of mice were bred to an ApoE-/- background and administered Angiotensin II via osmotic pump. Aortic samples were evaluated with histology for α-actin, macrophages, neutrophils, T lymphocytes, caspase3, Ki67, and elastin. In vitro ZFP148 was knocked down using siRNA in smooth muscle cells and stimulated with elastase, or IL-1β. Results: ZFP148 expression was elevated in human and murine AA. Maximal aortic dilation was significantly reduced in SMC ZFP148 KO mice compared with controls (55.7 ± 6.32% versus 106.4 ± 8.43%, p<0.05). Maximal aortic dilation of ERT Cre+ ZFP148 mice was significantly decreased versus WT controls (50.4± 8.65% versus 101.3± 9.43%, p<0.05). Knock-out of ZFP148 in both elastase models demonstrated reduced macrophage, T-cell, Ki-67, Caspase3 and neutrophil staining. Kaplan-Meier curves demonstrated increased survival in SM-MHC ZFP148 flx/flx (Chi2=4.357, p=0.0421) and flx/wt mice (Chi2=4.169, p=0.0476) compared to their WT controls following Angiotensin II infusion. Knock-down of ZFP148 followed by treatment with elastase or IL-1β in SMCs attenuated the down-regulation of SM22α, SM-MHC, and SMαA. ZFP148 bound via ChIP analysis to SMC marker genes in vitro and in vivo and was found to bind within the proximal promoter region of SmαA and SM22α. Conclusions: ZFP148 KO attenuates AA formation and binds to smooth muscle marker genes. ZFP148 could represent a novel regulator of vascular disease.

TcZFP1: a CCCH zinc finger protein of Trypanosoma cruzi that binds poly-C oligoribonucleotides in vitro

2004 ◽  
Vol 319 (1) ◽  
pp. 169-177 ◽  
Author(s):  
Patrı́cia A Mörking ◽  
Bruno M Dallagiovanna ◽  
Leonardo Foti ◽  
Beatriz Garat ◽  
Gisele F.A Picchi ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Ccch Zinc Finger ◽  
Finger Protein

scholarly journals Structure, expression and in vitro functional characterization of a novel RNA binding zinc finger protein from Xenopus.

1991 ◽  
Vol 10 (10) ◽  
pp. 3087-3093 ◽  
Author(s):  
M. Köster ◽  
U. Kühn ◽  
T. Bouwmeester ◽  
W. Nietfeld ◽  
T. el-Baradi ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Rna Binding ◽  
Zinc Finger Protein ◽  
Functional Characterization ◽  
Finger Protein

scholarly journals A Gene for a Novel Zinc-finger Protein Expressed in Differentiated Epithelial Cells and Transiently in Certain Mesenchymal Cells

1996 ◽  
Vol 271 (49) ◽  
pp. 31384-31390 ◽  
Author(s):  
Lee Ann Garrett-Sinha ◽  
Heidi Eberspaecher ◽  
Michael F. Seldin ◽  
Benoit de Crombrugghe
Keyword(s):  
Epithelial Cells ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Mesenchymal Cells ◽  
Finger Protein
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