Molecular mechanisms of transcriptional regulation by the nuclear zinc-finger protein Zfat in T cells

2016 ◽  
Vol 1859 (11) ◽  
pp. 1398-1410 ◽  
Author(s):  
Shuhei Ishikura ◽  
Toshiyuki Tsunoda ◽  
Kazuhiko Nakabayashi ◽  
Keiko Doi ◽  
Midori Koyanagi ◽  
...  
Keyword(s):  
T Cells ◽  
Transcriptional Regulation ◽  
Zinc Finger ◽  
Molecular Mechanisms ◽  
Zinc Finger Protein ◽  
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.

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 The Tristetraprolin Family of RNA-Binding Proteins in Cancer: Progress and Future Prospects

Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1539 ◽  
Author(s):  
Yogesh Saini ◽  
Jian Chen ◽  
Sonika Patial
Keyword(s):  
Gene Expression ◽  
Transcriptional Regulation ◽  
Zinc Finger ◽  
Binding Proteins ◽  
Rna Binding ◽  
Zinc Finger Protein ◽  
Rna Binding Proteins ◽  
Regulation Of Gene Expression ◽  
Finger Protein ◽  
Post Transcriptional Regulation

Post-transcriptional regulation of gene expression plays a key role in cellular proliferation, differentiation, migration, and apoptosis. Increasing evidence suggests dysregulated post-transcriptional gene expression as an important mechanism in the pathogenesis of cancer. The tristetraprolin family of RNA-binding proteins (RBPs), which include Zinc Finger Protein 36 (ZFP36; commonly referred to as tristetraprolin (TTP)), Zinc Finger Protein 36 like 1 (ZFP36L1), and Zinc Finger Protein 36 like 2 (ZFP36L2), play key roles in the post-transcriptional regulation of gene expression. Mechanistically, these proteins function by binding to the AU-rich elements within the 3′-untranslated regions of their target mRNAs and, in turn, increasing mRNA turnover. The TTP family RBPs are emerging as key regulators of multiple biological processes relevant to cancer and are aberrantly expressed in numerous human cancers. The TTP family RBPs have tumor-suppressive properties and are also associated with cancer prognosis, metastasis, and resistance to chemotherapy. Herein, we summarize the various hallmark molecular traits of cancers that are reported to be regulated by the TTP family RBPs. We emphasize the role of the TTP family RBPs in the regulation of trait-associated mRNA targets in relevant cancer types/cell lines. Finally, we highlight the potential of the TTP family RBPs as prognostic indicators and discuss the possibility of targeting these TTP family RBPs for therapeutic benefits.

scholarly journals RhoH participates in a multi-protein complex with the zinc finger protein kaiso that regulates both cytoskeletal structures and chemokine-induced T cells

Small GTPases ◽  
2016 ◽  
Vol 9 (3) ◽  
pp. 260-273 ◽  
Author(s):  
Akihisa Mino ◽  
Anja Troeger ◽  
Christian Brendel ◽  
Alan Cantor ◽  
Chad Harris ◽  
...  
Keyword(s):  
T Cells ◽  
Zinc Finger ◽  
Protein Complex ◽  
Zinc Finger Protein ◽  
Finger Protein

scholarly journals KRAB zinc finger protein diversification drives mammalian interindividual methylation variability

2020 ◽  
Vol 117 (49) ◽  
pp. 31290-31300 ◽  
Author(s):  
Tessa M. Bertozzi ◽  
Jessica L. Elmer ◽  
Todd S. Macfarlan ◽  
Anne C. Ferguson-Smith
Keyword(s):  
Dna Methylation ◽  
Zinc Finger ◽  
Histone Modifications ◽  
Molecular Mechanisms ◽  
Zinc Finger Protein ◽  
Large Family ◽  
Epigenetic Inheritance ◽  
Evolutionary Origins ◽  
Finger Protein ◽  
Genetic Background Effects

Most transposable elements (TEs) in the mouse genome are heavily modified by DNA methylation and repressive histone modifications. However, a subset of TEs exhibit variable methylation levels in genetically identical individuals, and this is associated with epigenetically conferred phenotypic differences, environmental adaptability, and transgenerational epigenetic inheritance. The evolutionary origins and molecular mechanisms underlying interindividual epigenetic variability remain unknown. Using a repertoire of murine variably methylated intracisternal A-particle (VM-IAP) epialleles as a model, we demonstrate that variable DNA methylation states at TEs are highly susceptible to genetic background effects. Taking a classical genetics approach coupled with genome-wide analysis, we harness these effects and identify a cluster of KRAB zinc finger protein (KZFP) genes that modifies VM-IAPs intransin a sequence-specific manner. Deletion of the cluster results in decreased DNA methylation levels and altered histone modifications at the targeted VM-IAPs. In some cases, these effects are accompanied by dysregulation of neighboring genes. We find that VM-IAPs cluster together phylogenetically and that this is linked to differential KZFP binding, suggestive of an ongoing evolutionary arms race between TEs and this large family of epigenetic regulators. These findings indicate that KZFP divergence and concomitant evolution of DNA binding capabilities are mechanistically linked to methylation variability in mammals, with implications for phenotypic variation and putative paradigms of mammalian epigenetic inheritance.

Short Communication: C2H2-546: A zinc finger protein differentially expressed in HTLV-1 infected T cells

1997 ◽  
Vol 3 (6) ◽  
pp. 455-459
Author(s):  
Paul D Drew ◽  
Ameer M Gado ◽  
Rachel D Canning ◽  
James W Nagle ◽  
Anindya M Dehejia ◽  
...  
Keyword(s):  
T Cells ◽  
Zinc Finger ◽  
Short Communication ◽  
Zinc Finger Protein ◽  
Differentially Expressed ◽  
Finger Protein
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