Ask about this productRelated genes to: DHRS2 Blocking Peptide
- Gene:
- DHRS2 NIH gene
- Name:
- dehydrogenase/reductase 2
- Previous symbol:
- -
- Synonyms:
- HEP27, SDR25C1
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-04-26
- Date modifiied:
- 2016-05-27
Related products to: DHRS2 Blocking Peptide
Related articles to: DHRS2 Blocking Peptide
- Breast cancer is the most common malignancy among women, and metastatic cases have a significantly poorer prognosis than non-metastatic disease. Epithelial-mesenchymal transition (EMT), characterized by the acquisition of mesenchymal features and enhanced migratory capacity by epithelial cells, is a key mechanism underlying cancer metastasis. DHRS2 has recently gained attention for its role in proliferation, invasion, and apoptosis in breast cancer. This study aimed to investigate the relationship between DHRS2 and EMT-related genes in breast cancer. - Source: PubMed
Publication date: 2026/08/10
Karaca HümeyraYaylaz Burcu SalmanZarerajabi VahidehPunar ŞeymaEkmekci Sema SirmaAbaci Neslihan - The precise contribution of basophils to cancer development and advancement remains undefined. Our research sought to delineate the immune subtypes of basophils in head and neck squamous cell carcinoma (HNSCC) and to develop a robust prognostic model. - Source: PubMed
Publication date: 2026/07/27
Zhao XinyuWang HongfaHuang HuangGuo YuminMei Xiangyang - Radiation Therapy (RT) in Head and Neck Squamous Cell Carcinoma (HNSCC) often induces inflammation. Here, we examined the relationship between mitophagy and inflammation in HNSCC. - Source: PubMed
Publication date: 2026/07/01
Wu YinghuiYao QingwenLi YangSong ZixiaoGan MeiZhong JinghuaLiang Leifeng - Intestinal fibroblast senescence contributes to gut aging and the development of related diseases, yet the regulatory mechanisms governing this process remain largely elusive. In this study, we identify the RNA N4-acetylcytidine (acC) modification and its cognate writer, N-acetyltransferase 10 (NAT10), as key modulators of human colonic fibroblast senescence. Through a series of loss- and gain-of-function assays, we demonstrate that NAT10-mediated mRNA acC modification is functionally involved in controlling intestinal fibroblast senescence. Suppression of this modification diminishes senescence-associated markers and attenuates replicative, oxidative (HO), and DNA damage-induced (doxorubicin) senescence in intestinal fibroblasts. Mechanistically, NAT10-driven acC deposition enhances DHRS2 mRNA stability, thereby promoting fibroblast senescence. Collectively, our findings establish the NAT10/acC/DHRS2 regulatory axis as a critical player in intestinal fibroblast senescence and suggest its potential as a therapeutic target for age-related intestinal disorders. - Source: PubMed
Publication date: 2026/06/30
Zhong JingZhu JianingXue MengChen Jingyu - Fibroblast growth factor receptor 1 (FGFR1) is a cell surface receptor tyrosine kinase implicated in cellular signaling and homeostasis. Several reports indicate that N-glycosylation of FGFR1 is critical for the FGFR1 trafficking to the cell surface, as glycosylation-deficient mutant of FGFR1 (FGFR1.GF) is trapped inside the cell, in the endoplasmic reticulum (ER), and in the nuclear envelope. Our recent mass spectrometry analyses revealed dehydrogenase/reductase 2 (DHRS2) as a putative binding partner of the intracellular FGFR1.GF. Here, we identified a peroxisomal targeting signal 1 (PTS1) at the C-terminus of DHRS2 and demonstrated that DHRS2 is dually targeted to peroxisomes and mitochondria. Furthermore, we determined that knockdown of DHRS2 results in increased number of peroxisomes, implicating the role of DHRS2 in peroxisome biogenesis. Using proximity ligation assay (PLA), we confirmed the interaction between FGFR1.GF and DHRS2 and demonstrated that FGFR1.GF/DHRS2 complexes are predominantly detected in peroxisomes. In agreement, we detected a small fraction of FGFR1.GF in peroxisomes. Taken together our data indicate that accumulation of FGFR1.GF in the ER may result in FGFR1.GF targeting to peroxisomes. Furthermore, we reveal interconnection between FGFR1 and DHRS2 and their role in peroxisome biogenesis. - Source: PubMed
Działek PaulinaChorążewska AleksandraBiaduń MartynaQiu JianPorębska NataliaOpaliński Łukasz