Ask about this productRelated genes to: NDRG2 Blocking Peptide
- Gene:
- NDRG2 NIH gene
- Name:
- NDRG family member 2
- Previous symbol:
- -
- Synonyms:
- KIAA1248, SYLD
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-24
- Date modifiied:
- 2015-09-01
Related products to: NDRG2 Blocking Peptide
Related articles to: NDRG2 Blocking Peptide
- ATL is an aggressive T-cell malignancy with a poor prognosis that is caused by HTLV-1 infection. We previously demonstrated that NDRG2 is significantly downregulated in ATL, resulting in aberrant activation of the signal transduction pathways through the dissociation of serine/threonine phosphatase PP2A. To identify potential targets of NDRG2, we performed comprehensive mass spectrometry of differentially phosphorylated peptides in ATL cells with overexpression of NDRG2 using a TiO-based enrichment method. KEGG and GO analysis revealed that the downregulated phosphopeptides correlated with signaling pathways, T-cell differentiation, and proliferation. Our results identified STAT5B as a novel NDRG2-regulated protein that is dephosphorylated at serine 193 and tyrosine 699. Although enforced expression of NDRG2 in ATL cell lines does not change the phosphorylation of JAK3, an upstream regulator of STAT5, phosphorylated STAT5 at tyrosine and serine is significantly suppressed by the direct binding to STAT5 with NDRG2 leading to the inhibition of STAT5 downstream gene expression. Furthermore, NDRG2 binds to STAT5B with alanine replacement of Y699 (Y699A) but only weakly is associated with S193A, suggesting that NDRG2 is directly involved in serine phosphorylation through the recruitment of PP2A to STAT5. Because S193A remarkably induces reduced phosphorylation of Y699 and subsequent transcriptional activity, the induction of serine phosphorylation through the loss of NDRG2 expression is dispensable for STAT5 tyrosine phosphorylation and activity. Since the loss of NDRG2 expression is essential factor to maintenance of ATL cells by STAT5 activity through phosphorylation of serine and tyrosine, targeting STAT5 becomes a feasible and effective strategy in NDRG2-deficient ATL. - Source: PubMed
Publication date: 2026/04/27
Ichikawa TomonagaNakahata ShingoShimoda KazuyaMurakami TakashiMorishita Kazuhiro - Pulmonary hypertension (PH) is a progressive disease characterized by obstructive pulmonary vascular remodeling, for which no curative therapies effectively reverse disease progression. This study investigated whether N-myc downstream-regulated gene 2 () drives PH pathogenesis by regulating mitochondrial dynamics. - Source: PubMed
Luo JiayongChang JinyuLiu YiShao YusangZhang YanyanZheng YingruXiao EnfangXie YanqingTu ShuangshuangLu HaoxuanHe Wenming - Breast cancer (BC) incidence continues to rise, and recurrence and metastasis remain major contributors to mortality. The epithelial-mesenchymal transition (EMT), associated with the acquisition of invasive functions by epithelial cells, also promotes resistance to anticancer therapies. Here, an EMT-based prognostic model was developed to enhance BC outcome prediction. - Source: PubMed
Publication date: 2026/03/15
Wu ZizhengZheng JieMen ShuaiSui ShuangruiYan WeitaoLiu YinfengHan Meng - Hepatocellular carcinoma (HCC) is a malignant tumor characterized by high metabolic dependence. In particular, it relies on dysregulated lipid synthesis. N-myc downstream regulated gene 2 (NDRG2) acts as a tumor suppressor in HCC, yet its underlying mechanisms remain unclear. This study aimed to elucidate the role of NDRG2 in HCC progression through the regulation of lipid metabolism. We established NDRG2-overexpressing and knockout HCC cell lines, and a hepatocellular-specific Ndrg2 mouse model of induced HCC. Metabolomics, Co-IP, and bioinformatics prediction were used to investigate the regulatory mechanisms and biological functions of NDRG2 on lipogenesis and the activity of the lipogenic enzyme, acetyl-CoA carboxylase 1 (ACC1). Interestingly, compared with wild-type mice, Ndrg2 knockout mice exhibited significantly enhanced hepatic lipogenesis and hepatocarcinogenesis. Mechanistically, NDRG2 functions as a scaffold protein that specifically recruits the E3 ubiquitin ligase constitutive photomorphogenic protein 1 (COP1), forming an NDRG2-COP1-ACC1 ternary complex, and thereby promoting ACC1 degradation via the ubiquitin-proteasome pathway. Furthermore, the accelerated degradation of ACC1 leads to decreases in de novo lipogenesis (DNL) and lipid droplet formation, thereby reducing the proliferation and progression of HCC cells. Notably, NDRG2-mediated ACC1 degradation significantly synergized with sorafenib to suppress tumor growth and angiogenesis. Our study revealed that NDRG2 mediates the ubiquitination and degradation of ACC1 through recruiting COP1. Thus, targeting the NDRG2-ACC1 axis or its combination with sorafenib may be a novel potential strategy for HCC therapy. - Source: PubMed
Publication date: 2026/04/17
Shi QianqianBai YuWang JiayuanRu MengyaoZhang KunGuo YanBai ZhantaoShen Lan - Triple-negative breast cancer (TNBC) is an aggressive subtype lacking estrogen and progesterone receptors and HER2 amplification. Representing 10-15% of breast cancer cases, TNBC disproportionately affects Black and pre-menopausal women and is associated with poorer outcomes. With chemotherapy as the primary systemic treatment option, achieving a pathological complete response (pCR) to neoadjuvant chemotherapy (NAC) is a key prognostic factor. However, TNBC biological heterogeneity complicates treatment response prediction. This study aimed to identify transcriptomic biomarkers predictive of NAC response in TNBC patients and evaluate machine-learning models for response classification. - Source: PubMed
Publication date: 2026/03/26
Amniouel SoukainaJafri Mohsin Saleet