scholarly journals Targeted Disruption of Mouse Yin Yang 1 Transcription Factor Results in Peri-Implantation Lethality

1999 ◽  
Vol 19 (10) ◽  
pp. 7237-7244 ◽  
Author(s):  
Mary E. Donohoe ◽  
Xiaolin Zhang ◽  
Lynda McGinnis ◽  
John Biggers ◽  
En Li ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Gene Targeting ◽  
Mouse Embryo ◽  
Mammalian Development ◽  
Targeted Disruption ◽  
Viral Oncoproteins ◽  
Yin Yang 1 ◽  
Yin Yang ◽  
Essential Function

ABSTRACT Yin Yang 1 (YY1) is a zinc finger-containing transcription factor and a target of viral oncoproteins. To determine the biological role of YY1 in mammalian development, we generated mice deficient for YY1 by gene targeting. Homozygosity for the mutated YY1 allele results in embryonic lethality in the mouse. YY1 mutants undergo implantation and induce uterine decidualization but rapidly degenerate around the time of implantation. A subset of YY1 heterozygote embryos are developmentally retarded and exhibit neurulation defects, suggesting that YY1 may have additional roles during later stages of mouse embryogenesis. Our studies demonstrate an essential function for YY1 in the development of the mouse embryo.

scholarly journals Role of the Transcription Factor Yin Yang 1 and Its Selectively Identified Target Survivin in High-Grade B-Cells Non-Hodgkin Lymphomas: Potential Diagnostic and Therapeutic Targets

2020 ◽  
Vol 21 (17) ◽  
pp. 6446
Author(s):  
Silvia Vivarelli ◽  
Luca Falzone ◽  
Giovanni Ligresti ◽  
Saverio Candido ◽  
Adriana Garozzo ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Therapeutic Targets ◽  
Gene Expression Omnibus ◽  
Drug Induced ◽  
Apoptotic Pathway ◽  
Yin Yang 1 ◽  
Yin Yang ◽  
Induced Apoptosis ◽  
Transcriptional Target

B-cell non-Hodgkin lymphomas (B-NHLs) are often characterized by the development of resistance to chemotherapeutic drugs and/or relapse. During drug-induced apoptosis, Yin Yang 1 (YY1) transcription factor might modulate the expression of apoptotic regulators genes. The present study was aimed to: (1) examine the potential oncogenic role of YY1 in reversing drug resistance in B-NHLs; and (2) identify YY1 transcriptional target(s) that regulate the apoptotic pathway in B-NHLs. Predictive analyses coupled with database-deposited data suggested that YY1 binds the promoter of the BIRC5/survivin anti-apoptotic gene. Gene Expression Omnibus (GEO) analyses of several B-NHL repositories revealed a conserved positive correlation between YY1 and survivin, both highly expressed, especially in aggressive B-NHLs. Further validation experiments performed in Raji Burkitt’s lymphomas cells, demonstrated that YY1 silencing was associated with survivin downregulation and sensitized the cells to apoptosis. Overall, our results revealed that: (1) YY1 and survivin are positively correlated and overexpressed in B-NHLs, especially in BLs; (2) YY1 strongly binds to the survivin promoter, hence survivin may be suggested as YY1 transcriptional target; (3) YY1 silencing sensitizes Raji cells to drug-induced apoptosis via downregulation of survivin; (4) both YY1 and survivin are potential diagnostic markers and therapeutic targets for the treatment of resistant/relapsed B-NHLs.

scholarly journals Interplay Between Heme Oxygenase-1 and the Multifunctional Transcription Factor Yin Yang 1 in the Inhibition of Intimal Hyperplasia

2010 ◽  
Vol 107 (12) ◽  
pp. 1490-1497 ◽  
Author(s):  
Konstanze Beck ◽  
Ben J. Wu ◽  
Jun Ni ◽  
Fernando S. Santiago ◽  
Kristine P. Malabanan ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Heme Oxygenase ◽  
Intimal Hyperplasia ◽  
Heme Oxygenase 1 ◽  
Yin Yang 1 ◽  
Yin Yang ◽  
Multifunctional Transcription Factor

scholarly journals The transcription factor Yin Yang 1 is an activator of BACE1 expression

2006 ◽  
Vol 96 (6) ◽  
pp. 1696-1707 ◽  
Author(s):  
Katrin Nowak ◽  
Christine Lange-Dohna ◽  
Ulrike Zeitschel ◽  
Albrecht Günther ◽  
Bernhard Lüscher ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Yin Yang 1 ◽  
Bace1 Expression ◽  
Yin Yang

scholarly journals Astrocyte-specific deletion of the transcription factor Yin Yang 1 in murine substantia nigra mitigates manganese-induced dopaminergic neurotoxicity

2020 ◽  
Vol 295 (46) ◽  
pp. 15662-15676 ◽  
Author(s):  
Edward Pajarillo ◽  
James Johnson ◽  
Asha Rizor ◽  
Ivan Nyarko-Danquah ◽  
Getinet Adinew ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Substantia Nigra ◽  
Critical Role ◽  
Conditional Knockout ◽  
Motor Functions ◽  
Mn Toxicity ◽  
Protein Levels ◽  
Yin Yang 1 ◽  
Yin Yang

Manganese (Mn)-induced neurotoxicity resembles Parkinson's disease (PD), but the mechanisms underpinning its effects remain unknown. Mn dysregulates astrocytic glutamate transporters, GLT-1 and GLAST, and dopaminergic function, including tyrosine hydroxylase (TH). Our previous in vitro studies have shown that Mn repressed GLAST and GLT-1 via activation of transcription factor Yin Yang 1 (YY1). Here, we investigated if in vivo astrocytic YY1 deletion mitigates Mn-induced dopaminergic neurotoxicity, attenuating Mn-induced reduction in GLAST/GLT-1 expression in murine substantia nigra (SN). AAV5-GFAP-Cre-GFP particles were infused into the SN of 8-week–old YY1flox/flox mice to generate a region-specific astrocytic YY1 conditional knockout (cKO) mouse model. 3 weeks after adeno-associated viral (AAV) infusion, mice were exposed to 330 μg of Mn (MnCl2 30 mg/kg, intranasal instillation, daily) for 3 weeks. After Mn exposure, motor functions were determined in open-field and rotarod tests, followed by Western blotting, quantitative PCR, and immunohistochemistry to assess YY1, TH, GLAST, and GLT-1 levels. Infusion of AAV5-GFAP-Cre-GFP vectors into the SN resulted in region-specific astrocytic YY1 deletion and attenuation of Mn-induced impairment of motor functions, reduction of TH-expressing cells in SN, and TH mRNA/protein levels in midbrain/striatum. Astrocytic YY1 deletion also attenuated the Mn-induced decrease in GLAST/GLT-1 mRNA/protein levels in midbrain. Moreover, YY1 deletion abrogated its interaction with histone deacetylases in astrocytes. These results indicate that astrocytic YY1 plays a critical role in Mn-induced neurotoxicity in vivo, at least in part, by reducing astrocytic GLAST/GLT-1. Thus, YY1 might be a potential target for treatment of Mn toxicity and other neurological disorders associated with dysregulation of GLAST/GLT-1.

Inhibition of the transcription factor Yin Yang 1 activity by S-nitrosation

2005 ◽  
Vol 336 (2) ◽  
pp. 692-701 ◽  
Author(s):  
Fumiya Hongo ◽  
Hermes Garban ◽  
Sara Huerta-Yepez ◽  
Mario Vega ◽  
Ali R. Jazirehi ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Yin Yang 1 ◽  
Yin Yang

scholarly journals Regulation of Transcription Factor Yin Yang 1 by SET7/9-mediated Lysine Methylation

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Wen-juan Zhang ◽  
Xiao-nan Wu ◽  
Tao-tao Shi ◽  
Huan-teng Xu ◽  
Jia Yi ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Regulation Of Transcription ◽  
Lysine Methylation ◽  
Yin Yang 1 ◽  
Yin Yang

scholarly journals Essential Dosage-Dependent Functions of the Transcription Factor Yin Yang 1 in Late Embryonic Development and Cell Cycle Progression

2006 ◽  
Vol 26 (9) ◽  
pp. 3565-3581 ◽  
Author(s):  
El Bachir Affar ◽  
Frédérique Gay ◽  
Yujiang Shi ◽  
Huifei Liu ◽  
Maite Huarte ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Transcription Factor ◽  
Cell Cycle Progression ◽  
Target Genes ◽  
Eukaryotic Cell ◽  
Dependent Manner ◽  
Phenotypic Analysis ◽  
Yin Yang 1 ◽  
Yin Yang

ABSTRACT Constitutive ablation of the Yin Yang 1 (YY1) transcription factor in mice results in peri-implantation lethality. In this study, we used homologous recombination to generate knockout mice carrying yy1 alleles expressing various amounts of YY1. Phenotypic analysis of yy1 mutant embryos expressing ∼75%, ∼50%, and ∼25% of the normal complement of YY1 identified a dosage-dependent requirement for YY1 during late embryogenesis. Indeed, reduction of YY1 levels impairs embryonic growth and viability in a dose-dependent manner. Analysis of the corresponding mouse embryonic fibroblast cells also revealed a tight correlation between YY1 dosage and cell proliferation, with a complete ablation of YY1 inducing cytokinesis failure and cell cycle arrest. Consistently, RNA interference-mediated inhibition of YY1 in HeLa cells prevents cytokinesis, causes proliferative arrest, and increases cellular sensitivity to various apoptotic agents. Genome-wide expression profiling identified a plethora of YY1 target genes that have been implicated in cell growth, proliferation, cytokinesis, apoptosis, development, and differentiation, suggesting that YY1 coordinates multiple essential biological processes through a complex transcriptional network. These data not only shed new light on the molecular basis for YY1 developmental roles and cellular functions, but also provide insight into the general mechanisms controlling eukaryotic cell proliferation, apoptosis, and differentiation.

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