scholarly journals Neuroprotection resulting from insufficiency of RANBP2 is associated with the modulation of protein and lipid homeostasis of functionally diverse but linked pathways in response to oxidative stress

2010 ◽  
Vol 3 (9-10) ◽  
pp. 595-604 ◽  
Author(s):  
K.-i. Cho ◽  
H. Yi ◽  
N. Tserentsoodol ◽  
K. Searle ◽  
P. A. Ferreira
Keyword(s):  
Oxidative Stress ◽  
Lipid Homeostasis ◽  
Functionally Diverse

scholarly journals Role of Pirin, an Oxidative Stress Sensor Protein, in Epithelial Carcinogenesis

Biology ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 116
Author(s):  
Francisco Perez-Dominguez ◽  
Diego Carrillo-Beltrán ◽  
Rancés Blanco ◽  
Juan P. Muñoz ◽  
Grettell León-Cruz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cancer Development ◽  
Biological Factors ◽  
Epithelial Cancers ◽  
Physical Chemical ◽  
Sensor Protein ◽  
Cupin Superfamily ◽  
Functionally Diverse ◽  
Light Chain Enhancer

Pirin is an oxidative stress (OS) sensor belonging to the functionally diverse cupin superfamily of proteins. Pirin is a suggested quercetinase and transcriptional activator of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. Its biological role in cancer development remains a novel area of study. This review presents accumulating evidence on the contribution of Pirin in epithelial cancers, involved signaling pathways, and as a suggested therapeutic target. Finally, we propose a model in which Pirin is upregulated by physical, chemical or biological factors involved in OS and cancer development.

scholarly journals Role of Pirin, an Oxidative Stress Sensor Protein, in Epithelial Carcinogenesis

2020 ◽  
Author(s):  
Francisco Perez-Dominguez ◽  
Diego Carrillo-Beltrán ◽  
Rancés Blanco ◽  
Juan P. Muñoz ◽  
Grettell León-Cruz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cancer Development ◽  
Biological Factors ◽  
Epithelial Cancers ◽  
Physical Chemical ◽  
Sensor Protein ◽  
Cupin Superfamily ◽  
Functionally Diverse ◽  
Light Chain Enhancer

Pirin is an oxidative stress (OS) sensor belonging to the functionally diverse cupin superfamily of proteins. Pirin is a suggested quercetinase and transcriptional activator of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. Its biological role in cancer development remains as a novel area of study. This review shows accumulating evidence on the contribution of Pirin in epithelial cancers, signaling pathways involved, and as a suggested therapeutic target. Finally, we propose a model in which Pirin is upregulated by physical, chemical or biological factors involved in OS and cancer development.

scholarly journals SAR1B GTPase is necessary to protect intestinal cells from disorders of lipid homeostasis, oxidative stress, and inflammation

2019 ◽  
Vol 60 (10) ◽  
pp. 1755-1764 ◽  
Author(s):  
Alain Sané ◽  
Lena Ahmarani ◽  
Edgard Delvin ◽  
Nikolas Auclair ◽  
Schohraya Spahis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Homeostasis ◽  
Intestinal Cells

scholarly journals The Transcriptional Response to a Peroxisome Proliferator-activated Receptor α Agonist Includes Increased Expression of Proteome Maintenance Genes

2004 ◽  
Vol 279 (50) ◽  
pp. 52390-52398 ◽  
Author(s):  
Steven P. Anderson ◽  
Paul Howroyd ◽  
Jie Liu ◽  
Xun Qian ◽  
Rainer Bahnemann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Responses ◽  
Transcriptional Response ◽  
Lipid Homeostasis ◽  
Peroxisome Proliferator ◽  
Wild Type ◽  
Peroxisome Proliferator Activated Receptor ◽  
Proteasomal Genes ◽  
Oxidative Stress Responses

The nuclear receptor peroxisome proliferator-activated receptor α (PPARα), in addition to regulating lipid homeostasis, controls the level of tissue damage after chemical or physical stress. To determine the role of PPARα in oxidative stress responses, we examined damage after exposure to chemicals that increase oxidative stress in wild-type or PPARα-null mice. Primary hepatocytes from wild-type but not PPARα-null mice pretreated with the PPAR pan-agonist WY-14,643 (WY) were protected from damage to cadmium and paraquat. The livers from intact wild-type but not PPARα-null mice were more resistant to damage after carbon tetrachloride treatment. To determine the molecular basis of the protection by PPARα, we identified by transcript profiling genes whose expression was altered by a 7-day exposure to WY in wild-type and PPARα-null mice. Of the 815 genes regulated by WY in wild-type mice (p≤ 0.001; ≥1.5-fold or ≤-1.5-fold), only two genes were regulated similarly by WY in PPARα-null mice. WY increased expression of stress modifier genes that maintain the health of the proteome, including those that prevent protein aggregation (heat stress-inducible chaperones) and eliminate damaged proteins (proteasome components). Although the induction of proteasomal genes significantly overlapped with those regulated by 1,2-dithiole-3-thione, an activator of oxidant-inducible Nrf2, WY increased expression of proteasomal genes independently of Nrf2. Thus, PPARα controls the vast majority of gene expression changes after exposure to WY in the mouse liver and protects the liver from oxidant-induced damage, possibly through regulation of a distinct set of proteome maintenance genes.

scholarly journals CBMT-29. PROMOTING FATTY ACID STORAGE BY DIACYLGLYCEROL-ACYLTRANSFERASE 1 PROTECTS GLIOBLASTOMA AGAINST OXIDATIVE STRESS AND MAINTAINS LIPID HOMEOSTASIS FOR RAPID TUMOR GROWTH

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi39-vi39
Author(s):  
Xiang Cheng ◽  
Feng Geng ◽  
Yaogang Zhong ◽  
Zhihua Tian ◽  
Meixia Pan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Tumor Growth ◽  
Tumor Cells ◽  
Energy Resource ◽  
Building Blocks ◽  
Diacylglycerol Acyltransferase ◽  
Lipid Homeostasis ◽  
Normal Brain

Abstract Fatty acids are essential building blocks and energy substrates of lipids in cells. They constitute the major structural components of membrane lipids, i.e., glycerophospholipids and sphingolipids, and also serve as an important energy resource. Whereas excess fatty acids or dysregulation of fatty acid metabolism causes lipotoxicity, leading to severe cell damage. We previously identified that lipid metabolism is dramatically altered in glioblastoma (GBM), especially fatty acid synthesis, which is greatly elevated in various types of cancers. However, how tumor cells prevent excessive fatty acids accumulation from inducing lipotoxicity has rarely been studied. We recently identified that GBM greatly upregulates diacylglycerol-acyltransferase 1 (DGAT1) to direct excess fatty acids into triglycerides and lipid droplets to prevent oxidative stress. Inhibiting DGAT1 disrupts lipid homeostasis and shifts excessive fatty acids moving into mitochondria for oxidation, resulting in a high level of reactive oxygen species (ROS), mitochondrial damage, cytochrome c release and apoptosis. Inhibiting carnitine palmitoyltransferase to reduce fatty acids shuttling into mitochondria significantly decreases ROS and rescues cell death caused by DGAT1 inhibition. Xenograft models show that genetic or pharmacological inhibition of DGAT1 blocks lipid droplet formation, induces tumor cell apoptosis and markedly suppresses GBM tumor growth. Together, our study demonstrates that DGAT1 upregulation protects GBM from oxidative damage and maintains lipid homeostasis by facilitating excess fatty acids storage. Our data further show that targeting DGAT1 specifically induces lipotoxicity in tumor cells, while sparing normal brain, which is a very promising therapeutic strategy antagonizing GBM and has a high potential to shift current paradigm in treating GBM.

Tu1750 Inflammation and Oxidative Stress in the Small Intestine Are Associated With Insulin Resistance and Alterations in Lipid Homeostasis in Obese Subjects

2013 ◽  
Vol 144 (5) ◽  
pp. S-836-S-837
Author(s):  
Alain Veilleux ◽  
Emilie Grenier ◽  
Picard Marceau ◽  
André C. Carpentier ◽  
Denis Richard ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Small Intestine ◽  
Lipid Homeostasis ◽  
Obese Subjects ◽  
And Oxidative Stress
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