GSTO1, 1_241aa, Human, E.coli
- Known as:
- GSTO1, 1_241aa, Human, E.coli
- Catalog number:
- ATGP0474
- Product Quantity:
- 0.5mg
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- GSTO1 1_241aa Human .coli
Related genes to: GSTO1, 1_241aa, Human, E.coli
- Gene:
- FCN2 NIH gene
- Name:
- ficolin 2
- Previous symbol:
- -
- Synonyms:
- P35, FCNL, EBP-37, ficolin-2
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-11
- Date modifiied:
- 2016-10-05
- Gene:
- GSTO1 NIH gene
- Name:
- glutathione S-transferase omega 1
- Previous symbol:
- -
- Synonyms:
- GSTTLp28, P28
- Chromosome:
- 10q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-01
- Date modifiied:
- 2015-09-11
Related products to: GSTO1, 1_241aa, Human, E.coli
Related articles to: GSTO1, 1_241aa, Human, E.coli
- Sepsis-associated coagulopathy contributes to organ dysfunction and mortality. Macrophage-mediated inflammation disrupts anticoagulant homeostasis, but the role of glutathione S-transferase omega 1 (GSTO1) in this process remains unclear. Clinical samples from sepsis patients were analyzed for correlations among GSTO1, ANXA5, and coagulation parameters were evaluated using Spearman rank correlation analysis. In vitro, loss- and gain-of-function approaches were employed in macrophages to examine the regulatory axis among GSTO1, ANXA5, and HUWE1. Protein interactions, post-translational modifications (S-glutathionylation and ubiquitination), and protein stability were assessed using co-immunoprecipitation, Western blotting, and cycloheximide chase assays. Macrophage polarization and tissue factor activity were detected with a commercial assay kit and flow cytometry. Coagulation function was assessed by incubating macrophage-conditioned media with human plasma and measuring APTT, PT, and TT. In vivo, myeloid-specific GSTO1 knockout mice and pharmacological GSTO1 inhibition were utilized to dissect the function of GSTO1 in a cecal ligation and puncture (CLP)-induced septic mouse model. The results indicated that upregulation of GSTO1 was associated with coagulation abnormalities in sepsis, where it promoted macrophage-mediated coagulopathy. GSTO1 reduced ANXA5 protein stability by facilitating its S-glutathionylation at Cys314 in a catalytic activity-dependent manner. Additionally, GSTO1 promoted HUWE1-dependent ubiquitination and subsequent degradation of ANXA5. ANXA5 overexpression rescued the loss of anticoagulant function caused by GSTO1-induced inflammation in macrophages. In vivo, knockout or inhibition of GSTO1 reduced the incidence of coagulopathy in a CLP-induced septic mouse model. GSTO1 facilitated ANXA5 degradation via S-glutathionylation and HUWE1-mediated ubiquitination, promoting macrophage inflammation and anticoagulation impairment, identifying GSTO1 as a candidate for translational exploration in sepsis-associated coagulopathy. - Source: PubMed
Peng JiapeiHu ChangmeiFu XiaoLi ShujunLiu WeiPeng Jie - Perioperative neurocognitive disorders (PND) are common and devastating perioperative neurological complications that markedly hinder postoperative rehabilitation and impair long-term quality of life in elderly surgical patients. Oxidative stress and neuroinflammation are well-established core pathogenic drivers of PND, whereas the key molecular mediators bridging perioperative stress and cognitive dysfunction remain poorly elucidated. Glutathione S-transferase Omega 1 (GSTO1) is a multifunctional deglutathionylase that centrally governs intracellular redox homeostasis and inflammatory signal transduction. Notably, no direct clinical or preclinical perioperative evidence has validated the modulatory effects of surgical trauma or anesthetic exposure on GSTO1 expression and catalytic activity, identifying GSTO1 as a promising yet unverified molecular linker between perioperative oxidative/inflammatory insults and PND progression. Accumulating indirect mechanistic evidence from chronic neurodegenerative disease models confirms the essential regulatory function of GSTO1 in conserved oxidative and inflammatory cascades shared by chronic cognitive degeneration and acute perioperative brain injury. This narrative review systematically elaborates the structural characteristics, enzymatic properties, and multifaceted biological functions of GSTO1, and clarifies the potential mechanistic correlation between anesthetic/surgical stress-induced redox imbalance, neuroinflammation, and PND pathogenesis. We propose a verifiable three-axis regulatory framework centered on the Nrf2 antioxidant pathway, NF-κB inflammatory cascade, and NLRP3 inflammasome signaling. Circulating GSTO1 in serum and platelets, detectable via ELISA and enzymatic activity assays, is proposed as a novel minimally invasive peripheral biomarker for preoperative cognitive risk stratification and central redox status evaluation. Furthermore, we differentiate context-dependent GSTO1-targeted intervention strategies, replacing vague universal modulator concepts with stage-specific therapeutic regimens for acute perioperative injury and chronic neurodegeneration. This review provides innovative theoretical foundations and targeted translational prospects for mechanistic research and clinical neuroprotective strategies against PND. - Source: PubMed
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