Ask about this productRelated genes to: GSTM3 antibody
- Gene:
- GSTM3 NIH gene
- Name:
- glutathione S-transferase mu 3
- Previous symbol:
- -
- Synonyms:
- GST5
- Chromosome:
- 1p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-06
- Date modifiied:
- 2016-06-27
- Gene:
- GSTM3P1 NIH gene
- Name:
- glutathione S-transferase mu 3 pseudogene 1
- Previous symbol:
- GSTM3P
- Synonyms:
- dJ984P4.2
- Chromosome:
- 20p11.22
- Locus Type:
- pseudogene
- Date approved:
- 2001-09-17
- Date modifiied:
- 2014-11-19
Related products to: GSTM3 antibody
Related articles to: GSTM3 antibody
- Long noncoding RNAs are emerging as critical regulators of acute kidney injury (AKI). In this study, the pathologic role of pseudogene-derived long noncoding RNAs GSTM3P1 (human)/Gstm2-ps1 (mouse) in sepsis-associated AKI (SA-AKI) was investigated. Glutathione S-transferase mu 3, pseudogene 1 (GSTM3P1)/glutathione S-transferase mu 2, pseudogene 1 (Gstm2-ps1) were transiently up-regulated in kidney proximal tubular cells at the early stage of SA-AKI in mice treated with lipopolysaccharide (LPS) or cecal ligation and puncture, as well as in LPS-treated proximal tubular cells. Functionally, overexpression of GSTM3P1/Gstm2-ps1 exacerbated LPS-induced proximal tubular cell apoptosis and oxidative stress. In contrast, proximal tubule-specific Gstm2-ps1 knockout mice were significantly protected from LPS-induced AKI, as evidenced by improved renal function and reduced apoptosis, kidney injury markers, and reactive oxygen species. Similarly, these mice showed renal protective effects against cecal ligation and puncture-induced AKI. Mechanistically, overexpression of GSTM3P1/Gstm2-ps1 in proximal tubular cells markedly suppressed parent gene GSTM3/GSTM2 protein but not mRNA expression, indicating a translational repression. Restoration of GSTM3/GSTM2 rescued proximal tubular cells from LPS-induced apoptosis. Furthermore, an RNA pulldown assay revealed that Gstm2-ps1 binds to human antigen R (HuR), a known post-transcriptional regulator for mRNA stability and translation. Overexpression of HuR antagonized Gstm2-ps1-mediated repression of GSTM2, associated with increased cell survival after LPS injury. In conclusion, the early induction of GSTM3P1/Gstm2-ps1 in SA-AKI exacerbates kidney injury by a novel mechanism to sequester HuR and inhibit the translation of parent gene GSTM3/gstm2 for oxidative stress detoxification. - Source: PubMed
Publication date: 2026/02/01
Huang JingDong ZhengWei Qingqing