<i>C-jun</i>Inhibits Mammary Apoptosis In Vivo

Katiyar, Sanjay; Casimiro, Mathew C.; Dettin, Luis E.; Ju, Xiaoming; Wagner, Erwin F.; Tanaka, Hirokazu; Pestell, Richard G.

doi:10.1091/mbc.e10-08-0705

Cited by 22 publications

(26 citation statements)

References 48 publications

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“…JNK activation was found to be in parallel with phosphorylation of c-Jun. Previous studies have reported that c-Jun activation has pro-hypertrophic and pro-apoptotic effects (16,32,52). In this study, an increase in JNK-dependent phosphorylation of c-Jun in pressure-overloadinduced heart failure was significantly decreased by SUMO-1 overexpression.…”

Section: Sumo-1 Overexpression Contributes Toward Regulating Redox Sisupporting

confidence: 55%

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The Role of SUMO-1 in Cardiac Oxidative Stress and Hypertrophy

Lee

Jeong

Mitsuyama

et al. 2014

Antioxidants & Redox Signaling

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Aims: Small ubiquitin-like modifier type 1 (SUMO-1) has been shown to play a critical role in the dysfunction of the cardiac isoform of sarcoplasmic reticulum calcium ATPase (SERCA2a) pump in the setting of heart failure. In cardiac hypertrophy, the role of SUMO-1 has not been defined and our study's goals were to examine the effects of modulating SUMO-1 on the hypertrophic response both in vitro and in vivo and to examine whether oxidative stress (during cardiac hypertrophy) is abrogated by SUMO-1 gene transfer. Results: In mice undergoing transverse aortic constriction (TAC), SUMO-1 levels increased slightly during the compensated stage of hypertrophy and then dropped sharply during the transition to heart failure. In isolated cardiomyocytes, SUMO-1 gene transfer inhibited the hypertrophic response in the presence of phenylephrine. Adeno-associated vector type 9 (AAV9) gene transfer of SUMO-1 prevented the heart from undergoing hypertrophy after TAC and prevented the development of left ventricular dysfunction. Furthermore, SUMO-1 gene transfer blocked the negative effects of H 2 O 2 on SERCA2a activity in cardiac myocytes, while in vivo indices of oxidative stress were decreased by SUMO-1 in cardiac hypertrophy and heart failure. Innovation and Conclusion: The results of this study indicate that post-translational modifications of SERCA2a caused by the toxic environment of the hypertrophied and failing myocardium can be prevented by SUMO-1.

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Section: Sumo-1 Overexpression Contributes Toward Regulating Redox Sisupporting

confidence: 55%

“…c-Jun activity is also closely associated with MnSOD transcripts and its activity. Endogenous c-Jun represses ROSreducing genes such as MnSOD and catalase via mitochondrial complexes and Nox enzyme (32).…”

Section: Sumo-1 Overexpression Contributes Toward Regulating Redox Simentioning

confidence: 99%

The Role of SUMO-1 in Cardiac Oxidative Stress and Hypertrophy

Lee

Jeong

Mitsuyama

et al. 2014

Antioxidants & Redox Signaling

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“…In fact, the binding of AP-1 to cellular extracts progressively decreases in cells incubated with increasing concentrations of CAT, as well as the activity of 3TP-Lux construction, which specifically activates in response to AP-1. This was a rather expected result, as this factor seems to be one of the most relevant transcription factors involved in TGF-β1 regulation (16,30), and it is up-regulated by ROS over-production (14,21,30,38).…”

Section: Discussionmentioning

confidence: 71%

Intracellular redox equilibrium is essential for the constitutive expression of AP-1 dependent genes in resting cells: Studies on TGF-β1 regulation

González-Ramos

Mora

Garcı́a

et al. 2012

The International Journal of Biochemistry & Cell Biology

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“…Acetylation of MnSOD directs the enzymatic activity responding to cellular nutrient status or oxidative stress (157). JNK-mediated repression of MnSOD and catalase occur via mitochondrial complex I and NOX I (104). Among the main factors involved in the redox balancing in adaptive response to IR (119), ATM, NF-jB, and pre-inflammatory factors (134,135,224) may also be regulated via NOX (220).…”

Section: Fig 3 Cyclin D1 Interacts Withmentioning

confidence: 99%

Cell Cycle Regulators Guide Mitochondrial Activity in Radiation-Induced Adaptive Response

Alexandrou

2014

Antioxidants & Redox Signaling

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Significance: There are accruing concerns on potential genotoxic agents present in the environment including low-dose ionizing radiation (LDIR) that naturally exists on earth's surface and atmosphere and is frequently used in medical diagnosis and nuclear industry. Although its long-term health risk is being evaluated and remains controversial, LDIR is shown to induce temporary but significant adaptive responses in mammalian cells and animals. The mechanisms guiding the mitochondrial function in LDIR-induced adaptive response represent a unique communication between DNA damage and cellular metabolism. Elucidation of the LDIRregulated mitochondrial activity may reveal new mechanisms adjusting cellular function to cope with hazardous environmental stress. Recent Advances: Key cell cycle regulators, including Cyclin D1/CDK4 and Cyclin B1/ cyclin-dependent kinase 1 (CDK1) complexes, are actively involved in the regulation of mitochondrial functions via phosphorylation of their mitochondrial targets. Accumulating new evidence supports a concept that the Cyclin B1/CDK1 complex acts as a mediator in the cross talk between radiation-induced DNA damage and mitochondrial functions to coordinate cellular responses to low-level genotoxic stresses. Critical Issues: The LDIR-mediated mitochondrial activity via Cyclin B1/CDK1 regulation is an irreplaceable network that is able to harmonize vital cellular functions with adjusted mitochondrial metabolism to enhance cellular homeostasis. Future Directions: Further investigation of the coordinative mechanism that regulates mitochondrial activities in sublethal stress conditions, including LDIR, will reveal new insights of how cells cope with genotoxic injury and will be vital for future targeted therapeutic interventions that reduce environmental injury and cancer risk.

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C-junInhibits Mammary Apoptosis In Vivo

Abstract: c-Jun mediates ROS production and apoptosis.

Cited by 22 publications

References 48 publications

The Role of SUMO-1 in Cardiac Oxidative Stress and Hypertrophy

The Role of SUMO-1 in Cardiac Oxidative Stress and Hypertrophy

Intracellular redox equilibrium is essential for the constitutive expression of AP-1 dependent genes in resting cells: Studies on TGF-β1 regulation

Cell Cycle Regulators Guide Mitochondrial Activity in Radiation-Induced Adaptive Response

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