GSTO1 Antibody
- Known as:
- GSTO1 Antibody
- Catalog number:
- XW-7952
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- GSTO1 Antibody
Related genes to: GSTO1 Antibody
- 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 Antibody
Related articles to: GSTO1 Antibody
- The incorporation of water disinfectants into the main water supply has significantly decreased the incidence of waterborne diseases. However, the interaction between disinfectants and organic material generates water disinfection byproducts (DBPs) such as iodoacetic acid (IAA). IAA is an ovarian toxicant, but little is known about its mechanisms of toxicity. Thus, we tested the hypothesis that IAA exposure causes ovarian toxicity through oxidative stress pathways. Adult CD-1 mice were dosed with vehicle control (reverse osmosis water) or IAA (2.7- 2,695.7 μM) for 35 days. Then, whole ovaries or isolated antral follicles were collected for measurement of expression of several enzymes that regulate oxidative stress (Gpx1, Gpx2, Gsr, Gss, Gsta1, Gstm1, Gsto1, Gstp1 Gstt1, Sod1, Sod2, and Cat). In other experiments, antral follicles were cultured with vehicle control ± the antioxidant Trolox or IAA (2-15 μM) ± the antioxidant Trolox for 96 hours and follicle growth was measured every 24 hours. Media were collected for estradiol measurements. IAA decreased Cat, Sod1, Gss, Gsta1, Gstp1, and Gstt1 and increased Gstm1 expression in whole ovaries compared to control in vivo. IAA decreased Sod2 and Gpx2 and increased Gstp1 expression in antral follicles compared to control in vivo. IAA increased Gpx1 and Gsto1 expression in antral follicles compared to control in vitro. IAA inhibited follicle growth and reduced estradiol levels, whereas Trolox rescued follicles from IAA-induced inhibition of follicle growth and estrogen levels in vitro. Collectively, these data indicate that IAA exposure causes ovarian toxicity by altering oxidative stress pathways in the mouse ovary. - Source: PubMed
Publication date: 2026/04/08
Fields Audrey LGonsioroski Andressa VarellaMárquez Ramsés SantacruzLaws Mary JFlaws Jodi A - Glutathione S-transferase omega 1 (GSTO1) is overexpressed in a variety of cancers and plays an important role in the promotion of tumor proliferation and metastasis. Nevertheless, the function of GSTO1 in cervical cancer (CC) is unknown. Immunohistochemistry (IHC) was applied to observe GSTO1 protein levels in CC tissues. Cell proliferation, migration, and invasion capabilities were assessed using CCK8, EdU, plate cloning assays, and Transwell experiments in vitro. Flow cytometry was employed to analyze cell cycle progression and reactive oxygen species (ROS) levels. A subcutaneous xenograft model was utilized to observe cell growth in vivo. Cell stemness was assessed via sphere formation assay. Transcriptome sequencing and enrichment analysis were conducted to explore GSTO1-related signaling pathways. The proteins linked to cell cycle regulation, stemness, epithelial-mesenchymal transition (EMT), and the PI3K/AKT/mTOR signaling pathway were identified through western blotting and IHC. In this study, GSTO1 was highly expressed in CC tissues and associated with poor prognosis of patients. Knockdown of GSTO1 suppressed CC cell proliferation in vivo and in vitro and inhibited the cell cycle, stemness, migration, and EMT as in C1-27 treatment. Conversely, down-regulation of GSTO1 promoted ROS production in CC cells. RNA sequencing indicated that GSTO1 mediated the activation of the PI3K/AKT signaling pathway. In addition, silencing GSTO1 decreased the phosphorylation of PI3K, AKT, and mTOR proteins. Interestingly, 740 Y-P (PI3K activator) reversed the inhibitory effects of GSTO1-induced cell proliferation, cycle, stemness, and EMT via the PI3K/AKT/mTOR signaling axis. GSTO1 was important in CC progression through the PI3K/AKT/mTOR pathway and could serve as a promising therapeutic target. - Source: PubMed
Zhao ZouyuSun ChongfengLiu XingyanYu PanpanWang YanLi HongYang Ping - TRPV2 is the least studied member of the vanilloid TRP subfamily despite its emerging relevance in cancer metastasis, pain, and inflammation. Although several small-molecule TRPV2 modulators have been reported, including the natural products piperlongumine (PL) and cannabidiol, all lack selectivity, complicating the interpretation of phenotypic readouts and functional insights into the role of the channel in health and disease. Here, we report a series of PL-based derivatives rationally designed to maintain TRPV2 antagonism while eliminating covalent off-target activity associated with the electrophilic groups present in PL. Using electrophysiological and calcium fluorescence imaging assays in HEK293T cells and DRG nociceptors, we identified HKC54 as the most potent TRPV2 antagonist to date (IC = 0.4 μM), displaying ∼50-fold selectivity over TRPV1 and ∼70-fold selectivity over TRPA1. Cellular thermal shift assays demonstrated direct TRPV2 engagement, and molecular dynamics and docking studies suggest a near-identical binding mode of the derivatives to PL. To assess proteome-wide selectivity, we pursued an unbiased chemoproteomic strategy and developed photoaffinity probes derived from PL and noncovalent derivative HKC22. Whereas the PL-based probe labeled many established covalent and noncovalent PL targets (e.g., GSTP1, GSTO1, STAT3, and KEAP1), no off-targets were detected for HKC22, suggesting high selectivity for TRPV2. Finally, PL derivatives inhibited cancer cell migration in vitro and suppressed metastasis in vivo, underscoring the therapeutic potential of selective TRPV2 antagonists. - Source: PubMed
Publication date: 2026/03/25
Kiely-Collins HannahTang CongMarques Marta CButron LauraLamberti AngelaBossons NicholasOffensperger FabianBrennsteiner VincenthSousa BárbaraCarvalho LuísFerrer-Montiel AntonioCorzana FranciscoWinter Georg EFernandez-Carvajal AsiaBernardes Gonçalo J L - Hepatocellular carcinoma (HCC) ranks among the most prevalent cancers globally. Ferroptosis plays a vital role in the resistance of HCC to various cancer treatments. However, the specific molecular mechanisms that inhibit ferroptosis in HCC remain unknown. Therefore, this study aims to elucidate the role of 5, N6-adenosine (METTL5) in regulating HCC development and ferroptosis. - Source: PubMed
Publication date: 2026/01/20
Ji TaoMiao XiangzhuoFang YinghaoNie JianminZhu QingZhu PengyuLiao WeiYang Dinghua - Diabetic nephropathy (DN) is a major complication of diabetes mellitus and a leading cause of end-stage renal disease (ESRD). Glutathione S-transferase omega 1 (GSTO1) is implicated in redox regulation and inflammation, but its causal role in DN remains unclear. This study aimed to investigate the potential causal relationship between GSTO1 and DN risk. - Source: PubMed
Tan JiangLei SisiZhao LiangHu JiliangChen Yuqin