scholarly journals The GATA transcription factor/ MTA ‐1 homolog egr‐1 promotes longevity and stress resistance in C aenorhabditis elegans

Aging Cell ◽  
2013 ◽  
Vol 13 (2) ◽  
pp. 329-339 ◽  
Author(s):  
Stephanie M. Zimmerman ◽  
Stuart K. Kim
Keyword(s):  
Transcription Factor ◽  
Stress Resistance ◽  
Gata Transcription Factor

scholarly journals SREB, a GATA Transcription Factor That Directs Disparate Fates in Blastomyces dermatitidis Including Morphogenesis and Siderophore Biosynthesis

2010 ◽  
Vol 6 (4) ◽  
pp. e1000846 ◽  
Author(s):  
Gregory M. Gauthier ◽  
Thomas D. Sullivan ◽  
Sergio S. Gallardo ◽  
T. Tristan Brandhorst ◽  
Amber J. Vanden Wymelenberg ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Blastomyces Dermatitidis ◽  
Siderophore Biosynthesis ◽  
Gata Transcription Factor

scholarly journals Peroxiporins Are Induced Upon Oxidative Stress Insult and Are Associated with Oxidative Stress Resistance in Colon Cancer Cell Lines

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1856
Author(s):  
Ana Čipak Gašparović ◽  
Lidija Milković ◽  
Claudia Rodrigues ◽  
Monika Mlinarić ◽  
Graça Soveral
Keyword(s):  
Oxidative Stress ◽  
Colon Cancer ◽  
Transcription Factor ◽  
Cell Lines ◽  
Stress Resistance ◽  
Therapy Resistance ◽  
Colon Cancer Cell ◽  
Colon Cancer Cell Lines ◽  
Intracellular Ros ◽  
Ht 29

Oxidative stress can induce genetic instability and change cellular processes, resulting in colorectal cancer. Additionally, adaptation of oxidative defense causes therapy resistance, a major obstacle in successful cancer treatment. Peroxiporins are aquaporin membrane channels that facilitate H2O2 membrane permeation, crucial for regulating cell proliferation and antioxidative defense. Here, we investigated four colon cancer cell lines (Caco-2, HT-29, SW620, and HCT 116) for their sensitivity to H2O2, cellular antioxidative status, and ROS intracellular accumulation after H2O2 treatment. The expression of peroxiporins AQP1, AQP3, and AQP5 and levels of NRF2, the antioxidant transcription factor, and PPARγ, a transcription factor that regulates lipid metabolism, were evaluated before and after oxidative insult. Of the four tested cell lines, HT-29 was the most resistant and showed the highest expression of all tested peroxiporins and the lowest levels of intracellular ROS, without differences in GSH levels, catalase activity, nor NF2 and PPARγ levels. Caco-2 shows high expression of AQP3 and similar resistance as HT-29. These results imply that oxidative stress resistance can be obtained by several mechanisms other than the antioxidant defense system. Regulation of intracellular ROS through modulation of peroxiporin expression may represent an additional strategy to target the therapy resistance of cancer cells.

NG-monomethyl-l-arginine inhibits erythropoietin gene expression by stimulating GATA-2

Blood ◽  
2000 ◽  
Vol 96 (5) ◽  
pp. 1716-1722 ◽  
Author(s):  
Takahisa Tarumoto ◽  
Shigehiko Imagawa ◽  
Ken Ohmine ◽  
Tadashi Nagai ◽  
Masato Higuchi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Messenger Rna ◽  
Promoter Activity ◽  
Binding Activity ◽  
Guanosine Monophosphate ◽  
Mobility Shift ◽  
Enhancer Activity ◽  
Gata Transcription Factor ◽  
Hep3b Cells

Abstract NG-monomethyl-l-arginine (L-NMMA) has been reported to be elevated in uremic patients. Based on the hypothesis that the pathogenesis of the anemia of renal disease might be due to the perturbation of transcription factors of the erythropoietin (Epo) gene by L-NMMA, the present study was designed to investigate the effect of L-NMMA on Epo gene expression through the GATA transcription factor. L-NMMA caused decreased levels of NO, cyclic guanosine monophosphate (cGMP), and Epo protein in Hep3B cells. L-NAME (analogue of L-NMMA) also inhibited Epo production in anemic mice. Transfection of the Epo promoter-luciferase gene into Hep3B cells revealed that L-NMMA inhibited the Epo promoter activity. However, L-NMMA did not inhibit the Epo promoter activity when mutated Epo promoter (GATA to TATA) was transfected, and L-NMMA did not affect the enhancer activity. Electrophoretic mobility shift assays demonstrated the stimulation of GATA binding activity by L-NMMA. However, L-NMMA had no effect on the binding activity of hepatic nuclear factor-4, COUP-TF1, hypoxia-inducing factor-1, or NF-κB. Furthermore, cGMP inhibited the L-NMMA–induced GATA binding activity. L-NMMA also increased GATA-2 messenger RNA expression. These results demonstrate that L-NMMA suppresses Epo gene expression by up-regulation of the GATA transcription factor and support the hypothesis that L-NMMA is one of the candidate substances that underlie the pathogenesis of renal anemia.

scholarly journals TORC1 Regulates Developmental Responses to Nitrogen Stress via Regulation of the GATA Transcription Factor Gaf1

mBio ◽  
2015 ◽  
Vol 6 (4) ◽  
Author(s):  
Dana Laor ◽  
Adiel Cohen ◽  
Martin Kupiec ◽  
Ronit Weisman
Keyword(s):  
Transcription Factor ◽  
Sexual Development ◽  
Nitrogen Availability ◽  
Stress Conditions ◽  
Nitrogen Stress ◽  
Content Type ◽  
Downstream Target ◽  
Gata Transcription Factor ◽  
Novel Target ◽  
Developmental Responses

ABSTRACT The TOR (target of rapamycin [sirolimus]) is a universally conserved kinase that couples nutrient availability to cell growth. TOR complex 1 (TORC1) in Schizosaccharomyces pombe positively regulates growth in response to nitrogen availability while suppressing cellular responses to nitrogen stress. Here we report the identification of the GATA transcription factor Gaf1 as a positive regulator of the nitrogen stress-induced gene isp7 +, via three canonical GATA motifs. We show that under nitrogen-rich conditions, TORC1 positively regulates the phosphorylation and cytoplasmic retention of Gaf1 via the PP2A-like phosphatase Ppe1. Under nitrogen stress conditions when TORC1 is inactivated, Gaf1 becomes dephosphorylated and enters the nucleus. Gaf1 was recently shown to negatively regulate the transcription induction of ste11 +, a major regulator of sexual development. Our findings support a model of a two-faceted role of Gaf1 during nitrogen stress. Gaf1 positively regulates genes that are induced early in the response to nitrogen stress, while inhibiting later responses, such as sexual development. Taking these results together, we identify Gaf1 as a novel target for TORC1 signaling and a step-like mechanism to modulate the nitrogen stress response. IMPORTANCE TOR complex 1 (TORC1) is an evolutionary conserved protein complex that positively regulates growth and proliferation, while inhibiting starvation responses. In fission yeast, the activity of TORC1 is downregulated in response to nitrogen starvation, and cells reprogram their transcriptional profile and prepare for sexual development. We identify Gaf1, a GATA-like transcription factor that regulates transcription and sexual development in response to starvation, as a downstream target for TORC1 signaling. Under nitrogen-rich conditions, TORC1 positively regulates the phosphorylation and cytoplasmic retention of Gaf1 via the PP2A-like phosphatase Ppe1. Under nitrogen stress conditions when TORC1 is inactivated, Gaf1 becomes dephosphorylated and enters the nucleus. Budding yeast TORC1 regulates GATA transcription factors via the phosphatase Sit4, a structural homologue of Ppe1. Thus, the TORC1-GATA transcription module appears to be conserved in evolution and may also be found in higher eukaryotes.

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