The Writers, Readers and Erasers in Redox Regulation of GAPDH

Tossounian, Maria; Zhang, Bruce; Gout, Ivan

doi:10.20944/preprints202012.0024.v1

Cited by 14 publications

(2 citation statements)

References 136 publications

(229 reference statements)

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“…On the contrary, DNA-activated protein kinase (DNA-PK), which is involved in DNA repair, is activated by S-nitrosylation with the participation of GAPDH-SNO [ 88 , 97 ]. In response to stress, GAPDH is translocated into the mitochondria, where it transnitrosylates Hsp60, acetyl-CoA thiolase, and VDAC1, thus affecting membrane permeability, the regulation of mitochondrial function, and cell death [ 98 , 99 ].…”

Section: Protein S-nitrosylation and Denitrosylationmentioning

confidence: 99%

Glutathione in Protein Redox Modulation through S-Glutathionylation and S-Nitrosylation

Калинина

Novichkova

2021

Molecules

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S-glutathionylation and S-nitrosylation are reversible post-translational modifications on the cysteine thiol groups of proteins, which occur in cells under physiological conditions and oxidative/nitrosative stress both spontaneously and enzymatically. They are important for the regulation of the functional activity of proteins and intracellular processes. Connecting link and “switch” functions between S-glutathionylation and S-nitrosylation may be performed by GSNO, the generation of which depends on the GSH content, the GSH/GSSG ratio, and the cellular redox state. An important role in the regulation of these processes is played by Trx family enzymes (Trx, Grx, PDI), the activity of which is determined by the cellular redox status and depends on the GSH/GSSG ratio. In this review, we analyze data concerning the role of GSH/GSSG in the modulation of S-glutathionylation and S-nitrosylation and their relationship for the maintenance of cell viability.

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Section: Protein S-nitrosylation and Denitrosylationmentioning

confidence: 99%

Glutathione in Protein Redox Modulation through S-Glutathionylation and S-Nitrosylation

Калинина

Novichkova

2021

Molecules

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“…Actin beta (ACTB) is involved in cell structure, motility, and integrity, and, as it is essential to multiple cell functions, the gene is highly abundant in many cell lines (39). Glyceraldehyde 3-phosphate dehydrogenase (GAPDH), although it is reported to be involved in cellular survival, apoptosis and DNA repair, is mainly known to express a cellular energy enzyme determinant to the glycolytic process, functioning as a catalyzer of triose phosphate oxidation and, for this reason, ubiquitously distributed in all cell types (40,41).…”

Section: Discussionmentioning

confidence: 99%

Reference genes for mesangial cell and podocyte qPCR gene expression studies under high-glucose and renin-angiotensin-system blocker conditions

Hosni

Anauate

Boim

2021

Preprint

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BackgroundReal-time PCR remains currently the gold standard method for gene expression studies. Identification of the best reference gene is a key point in performing high quality qPCR, providing strong support for results, as well as performing as a source of bias when inappropriately chosen. Mesangial cells and podocytes, as essential cell lines to study diabetic kidney disease (DKD) physiopathology, demand accurate analysis of the reference genes used so far to enhance validity of gene expression studies, especially regarding high glucose (HG) and DKD treatments, with angiotensin II receptor blockers (e.g. Losartan) being the most commonly used. This study aimed to evaluate the suitability and define the most stable reference gene for mesangial cells and podocytes studies of an in vitro DKD model of disease and its treatment.MethodsFive software packages (RefFinder, NormFinder, GeNorm, Bestkeeper, and DataAssist) and the comparative ΔCt method were selected to analyze six different candidate genes: HPRT, ACTB, PGAM-1, GAPDH, PPIA, and B2M. RNA was extracted and cDNA was synthesized from immortalized mouse mesangial cells and podocytes cultured in 4 groups: control (n=5; 5mM glucose), mannitol (n=5; 30mM, as osmotic control), HG (n=5; 30mM glucose), and HG + losartan (n=5; 30mM glucose and 10-4 mM of losartan). Real-time PCR was performed according to MIQE guidelines.ResultsWe identified that the use of 2 genes is the best combination for qPCR normalization for both mesangial cell and podocytes. For mesangial cells, the combination of HPRT and ACTB presented higher stability values. For podocytes, HPRT and GAPDH showed the best results.ConclusionThis analysis provides support for the use of HPRT and ACTB as reference genes in mouse mesangial cell studies of gene expression via real-time PCR technique, while for podocytes, HPRT and GAPDH should be chosen.

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Sp1 S-Sulfhydration Induced by Hydrogen Sulfide Inhibits Inflammation via HDAC6/MyD88/NF-κB Signaling Pathway in Adjuvant-Induced Arthritis

Wang

et al. 2022

Antioxidants

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Histone deacetylase 6 (HDAC6) acts as a regulator of the nuclear factor kappa-B (NF-κB) signaling pathway by deacetylating the non-histone protein myeloid differentiation primary response 88 (MyD88) at lysine residues, which is an adapter protein for the Toll-like receptor (TLR) and interleukin (IL)-1β receptor. Over-activated immune responses, induced by infiltrated immune cells, excessively trigger the NF-κB signaling pathway in other effector cells and contribute to the development of rheumatoid arthritis (RA). It has also been reported that HDAC6 can promote the activation of the NF-κB signaling pathway. In the present study, we showed that HDAC6 protein level was increased in the synovium tissues of adjuvant-induced arthritis rats. In addition, hydrogen sulfide (H2S) donor S-propargyl-cysteine (SPRC) can inhibit HDAC6 expression and alleviate inflammatory response in vivo. In vitro study revealed that HDAC6 overexpression activated the NF-κB signaling pathway by deacetylating MyD88. Meanwhile, sodium hydrosulfide (NaHS) or HDAC6 inhibitor tubastatin A (tubA) suppressed the pro-inflammatory function of HDAC6. Furthermore, the reduced expression of HDAC6 appeared to result from transcriptional inhibition by S-sulfhydrating specificity protein 1 (Sp1), which is a transcription factor of HDAC6. Our results demonstrate that Sp1 can regulate HDAC6 expression, and S-sulfhydration of Sp1 by antioxidant molecular H2S ameliorates RA progression via the HDAC6/MyD88/NF-κB signaling pathway.

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The Writers, Readers and Erasers in Redox Regulation of GAPDH

Cited by 14 publications

References 136 publications

Glutathione in Protein Redox Modulation through S-Glutathionylation and S-Nitrosylation

Glutathione in Protein Redox Modulation through S-Glutathionylation and S-Nitrosylation

Reference genes for mesangial cell and podocyte qPCR gene expression studies under high-glucose and renin-angiotensin-system blocker conditions

Sp1 S-Sulfhydration Induced by Hydrogen Sulfide Inhibits Inflammation via HDAC6/MyD88/NF-κB Signaling Pathway in Adjuvant-Induced Arthritis

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