The in vitro modulatory effect of TNFα on the mRNA expression and protein levels of zinc finger protein ZNF334 in CD4+lymphocytes of healthy people

2015 ◽  
Vol 62 (1) ◽  
pp. 113-117
Author(s):  
Izabella Henc ◽  
Monika Soroczyńska-Cybula ◽  
Ewa Bryl ◽  
Jacek M. Witkowski
Keyword(s):  
Mrna Expression ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Healthy People ◽  
Protein Levels ◽  
Finger Protein ◽  
Cd4 Lymphocytes

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.

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 Decreased Expression of ZNF554 in Gliomas is Associated with the Activation of Tumor Pathways and Shorter Patient Survival

2020 ◽  
Vol 21 (16) ◽  
pp. 5762
Author(s):  
Andrea Balogh ◽  
Lilla Reiniger ◽  
Szabolcs Hetey ◽  
Peter Kiraly ◽  
Eszter Toth ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Malignant Tumors ◽  
Trophoblast Invasion ◽  
Normal Brain ◽  
Protein Levels ◽  
Finger Protein ◽  
Genome Wide ◽  
Transcriptomic Changes ◽  
The Brain

Zinc finger protein 554 (ZNF554), a member of the Krüppel-associated box domain zinc finger protein subfamily, is predominantly expressed in the brain and placenta in humans. Recently, we unveiled that ZNF554 regulates trophoblast invasion during placentation and its decreased expression leads to the early pathogenesis of preeclampsia. Since ZNF proteins are immensely implicated in the development of several tumors including malignant tumors of the brain, here we explored the pathological role of ZNF554 in gliomas. We examined the expression of ZNF554 at mRNA and protein levels in normal brain and gliomas, and then we searched for genome-wide transcriptomic changes in U87 glioblastoma cells transiently overexpressing ZNF554. Immunohistochemistry of brain tissues in our cohort (n = 62) and analysis of large TCGA RNA-Seq data (n = 687) of control, oligodendroglioma, and astrocytoma tissues both revealed decreased expression of ZNF554 towards higher glioma grades. Furthermore, low ZNF554 expression was associated with shorter survival of grade III and IV astrocytoma patients. Overexpression of ZNF554 in U87 cells resulted in differential expression, mostly downregulation of 899 genes. The “PI3K-Akt signaling pathway”, known to be activated during glioma development, was the most impacted among 116 dysregulated pathways. Most affected pathways were cancer-related and/or immune-related. Congruently, cell proliferation was decreased and cell cycle was arrested in ZNF554-transfected glioma cells. These data collectively suggest that ZNF554 is a potential tumor suppressor and its decreased expression may lead to the loss of oncogene suppression, activation of tumor pathways, and shorter survival of patients with malignant glioma.

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