The effect of menadione on glutathione S-transferase A1 (GSTA1): c-Jun N-terminal kinase (JNK) complex dissociation in human colonic adenocarcinoma Caco-2 cells

Adnan, Humaira; Antenos, Monica; Kirby, Gordon M.

doi:10.1016/j.toxlet.2012.08.007

Cited by 21 publications

(16 citation statements)

References 27 publications

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“…It is acknowledged that the undifferentiated Caco-2 cell is similar to the crypt enterocyte, whereas the well-differentiated cell is analogous to the villus enterocyte (2,15,31). Previous reports have shown that the undifferentiated Caco-2 cell was more prone to acquire JNK activation than the well-differentiated cell when exposed to the same stresses (1,34). Hence the undifferentiated Caco-2 cell is predisposed to suffer JNK-mediated apoptosis.…”

Section: Discussionmentioning

confidence: 93%

miR-200b inhibits TNF-α-induced IL-8 secretion and tight junction disruption of intestinal epithelial cells in vitro

Shen

Zhou

Yan

et al. 2017

American Journal of Physiology-Gastrointestinal and Liver Physi

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This was the first time that the inhibitory role of miR-200b on intestinal epithelial inflammation and paracellular permeability has been reported. Moreover, we further divided the intestinal epithelial cells (IECs) into two differentiated conditions and investigated the distinct impacts of miR-200b. Finally, we put forward and proved that myosin light chain kinase (MLCK) was a novel target of miR-200b.

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Section: Discussionmentioning

confidence: 93%

miR-200b inhibits TNF-α-induced IL-8 secretion and tight junction disruption of intestinal epithelial cells in vitro

Shen

Zhou

Yan

et al. 2017

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…GSTA1-1 forms complexes with c-Jun N -terminal kinase (JNK) and modifies JNK activation during cellular stress, but the factors that influence complex association and dissociation are unknown. Very recently, it has been suggested that the mechanism of menadione-induced JNK activation involves the production of reactive oxygen species, likely superoxide anion, and intracellular GSH levels play an important role in preventing GSTA1-1-JNK complex dissociation, subsequent JNK activation, and induction of cytotoxicity [40]. Having in mind the presence of pro-oxidant OTA derivatives, as well as increased oxidative stress in BEN, such mechanisms might also take place in the case of BEN progression.…”

Section: Resultsmentioning

confidence: 99%

Is Increased Susceptibility to Balkan Endemic Nephropathy in Carriers of Common GSTA1 (A/B) Polymorphism Linked with the Catalytic Role of GSTA1 in Ochratoxin A Biotransformation? Serbian Case Control Study and In Silico Analysis

Reljic

Zlatović

Savić-Radojević

et al. 2014

Toxins

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Although recent data suggest aristolochic acid as a putative cause of Balkan endemic nephropathy (BEN), evidence also exists in favor of ochratoxin A (OTA) exposure as risk factor for the disease. The potential role of xenobiotic metabolizing enzymes, such as the glutathione transferases (GSTs), in OTA biotransformation is based on OTA glutathione adducts (OTHQ-SG and OTB-SG) in blood and urine of BEN patients. We aimed to analyze the association between common GSTA1, GSTM1, GSTT1, and GSTP1 polymorphisms and BEN susceptibility, and thereafter performed an in silico simulation of particular GST enzymes potentially involved in OTA transformations. GSTA1, GSTM1, GSTT1 and GSTP1 genotypes were determined in 207 BEN patients and 138 non-BEN healthy individuals from endemic regions by polymerase chain reaction (PCR). Molecular modeling in silico was performed for GSTA1 protein. Among the GST polymorphisms tested, only GSTA1 was significantly associated with a higher risk of BEN. Namely, carriers of the GSTA1*B gene variant, associated with lower transcriptional activation, were at a 1.6-fold higher BEN risk than those carrying the homozygous GSTA1*A/*A genotype (OR = 1.6; p = 0.037). In in silico modeling, we found four structures, two OTB-SG and two OTHQ-SG, bound in a GSTA1 monomer. We found that GSTA1 polymorphism was associated with increased risk of BEN, and suggested, according to the in silico simulation, that GSTA1-1 might be involved in catalyzing the formation of OTHQ-SG and OTB-SG conjugates.

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“…At least three factors impact specificity of oxidation, i.e., localized high activity generation of H 2 O 2 , catalytic mediators of oxidation, and generation of alternative low-molecular weight chemical oxidants. Enzymes with high reactivity with H 2 O 2 [e.g., members of the Prx and GSH S -transferase(GST)] may act as special carriers of the oxidative signal to interacting proteins [150]. Alternatively, H 2 O 2 is used to generate other oxidants with altered kinetics (e.g., hypohalous acids) [151], which in turn can form further derivative oxidizing species (e.g., haloamines).…”

Section: Protein Cys Redox Regulationmentioning

confidence: 99%

The cysteine proteome

Chandler

Jones

2015

Free Radical Biology and Medicine

315

243

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The cysteine (Cys) proteome is a major component of the adaptive interface between the genome and the exposome. The thiol moiety of Cys undergoes a range of biologic modifications enabling biological switching of structure and reactivity. These biological modifications include sulfenylation and disulfide formation, formation of higher oxidation states, S-nitrosylation, persulfidation, metallation, and other modifications. Extensive knowledge about these systems and their compartmentalization now provides a foundation to develop advanced integrative models of Cys proteome regulation. In particular, detailed understanding of redox signaling pathways and sensing networks is becoming available to discriminate network structures. This research focuses attention on the need for atlases of Cys modifications to develop systems biology models. Such atlases will be especially useful for integrative studies linking the Cys proteome to imaging and other omics platforms, providing a basis for improved redox-based therapeutics. Thus, a framework is emerging to place the Cys proteome as a complement to the quantitative proteome in the omics continuum connecting the genome to the exposome.

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The effect of menadione on glutathione S-transferase A1 (GSTA1): c-Jun N-terminal kinase (JNK) complex dissociation in human colonic adenocarcinoma Caco-2 cells

Cited by 21 publications

References 27 publications

miR-200b inhibits TNF-α-induced IL-8 secretion and tight junction disruption of intestinal epithelial cells in vitro

miR-200b inhibits TNF-α-induced IL-8 secretion and tight junction disruption of intestinal epithelial cells in vitro

Is Increased Susceptibility to Balkan Endemic Nephropathy in Carriers of Common GSTA1 (A/B) Polymorphism Linked with the Catalytic Role of GSTA1 in Ochratoxin A Biotransformation? Serbian Case Control Study and In Silico Analysis

The cysteine proteome

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The effect of menadione on glutathione S-transferase A1 (GSTA1): c-Jun N-terminal kinase (JNK) complex dissociation in human colonic adenocarcinoma Caco-2 cells

Cited by 21 publications

References 27 publications

miR-200b inhibits TNF-α-induced IL-8 secretion and tight junction disruption of intestinal epithelial cells in vitro

miR-200b inhibits TNF-α-induced IL-8 secretion and tight junction disruption of intestinal epithelial cells in vitro

Is Increased Susceptibility to Balkan Endemic Nephropathy in Carriers of Common GSTA1 (*A/*B) Polymorphism Linked with the Catalytic Role of GSTA1 in Ochratoxin A Biotransformation? Serbian Case Control Study and In Silico Analysis

The cysteine proteome

Contact Info

Product

Resources

About

Is Increased Susceptibility to Balkan Endemic Nephropathy in Carriers of Common GSTA1 (A/B) Polymorphism Linked with the Catalytic Role of GSTA1 in Ochratoxin A Biotransformation? Serbian Case Control Study and In Silico Analysis