Zhx2 Antibody - C-terminal region (ARP37944_P050)
- Known as:
- Zhx2 Antibody - C-terminal region (ARP37944_P050)
- Catalog number:
- arp37944_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Zhx2 Antibody - C-terminal region (ARP37944_P050)
Related genes to: Zhx2 Antibody - C-terminal region (ARP37944_P050)
- Gene:
- ZHX2 NIH gene
- Name:
- zinc fingers and homeoboxes 2
- Previous symbol:
- -
- Synonyms:
- KIAA0854
- Chromosome:
- 8q24.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-22
- Date modifiied:
- 2015-08-24
Related products to: Zhx2 Antibody - C-terminal region (ARP37944_P050)
Related articles to: Zhx2 Antibody - C-terminal region (ARP37944_P050)
- Neuroblastoma (NB) is the most common malignant extracranial solid tumor in children, with poor prognosis, inadequate therapeutic responses, and high recurrence rates. Zinc fingers and homeoboxes protein 2 (ZHX2) functions in various cancers, but its role in NB remains unclear. Retinoic acid (RA) has been used as a pro-differentiation agent in NB, but its limited response rate necessitates novel combinations. This study aims to explore key transcription factors (TFs) in improving RA efficacy and NB prognosis. - Source: PubMed
Publication date: 2026/05/02
Wang YanLiu WeiweiLi DongMa HuixianLiu LinghongZhang AijunJu Xiuli - Colorectal cancer (CRC) is the most prevalent digestive system malignancy worldwide. The development of targeted therapeutics specifically effective for CRC is currently in dire need. Preclinical studies showed that CDK4/6 inhibitor palbociclib suppressed the growth of CRC, but whether this effect is durable is unclear. In this study, we aimed to evaluate the roles of palbociclib-induced senescence and find a new strategy to maximize its effectiveness in CRC treatment. Animal and cellular experiments revealed that palbociclib-induced senescence and the senescence-associated secretory phenotype (SASP) caused drug resistance, anti-apoptosis, PD-L1 upregulation and inhibition of CD8 T cells' function. Using CRISPR/Cas9 screening, we identified MCL1 as a senolytic target to eliminate palbociclib-induced senescent CRC cells in the presence of palbociclib. Mechanically, palbociclib-induced senescent cells upregulated ZHX2 and its transcriptional target MCL1, rendered their resistance to apoptosis and T cell-mediated cytotoxicity, whereases combining palbociclib with MCL1 inhibitor markedly induced apoptosis in senescent cells by activating both extrinsic and intrinsic apoptotic pathways. Lastly, we proposed a seno-therapy consisting of a palbociclib pre-treatment plus a combination treatment of palbociclib and MCL1 inhibitor and found it effectively inhibited tumor growth and improved the survival of CRC xenografted mice. Besides its senolytic effect, seno-therapy also reduced PD-L1-positive cells and enhancing the cytotoxic functions of CD8 T cells. In conclusion, co-targeting CDK4/6 and MCL1 efficiently eliminates palbociclib-induced senescent CRC cells and offers a promising CDK4/6 inhibitor-based strategy for CRC treatment, ensuring prolonged tumor suppression and reducing the risk of progression or recurrence. - Source: PubMed
Publication date: 2026/03/24
Wang HaiyangShen TianqiYang SuisuiZhou XiaohuiCao PingpingYu HongHe KexinFu MinYu HanyangLiu XiaorongZhou TingtingWang JingHuang MingdeQian XuWang XiuxingWang QianghuLiu LiFan ZhiningZhang YingjianLin Fan - The extremely complex, multivariate, and systemic pathophysiology of diabetic nephropathy is brought on by prolonged exposure to hyperglycemia, making the quest for the best therapeutic approach crucial and urgent. Accumulating evidence suggests that pyroptosis and inflammation contribute to the development of diabetic nephropathy. Zinc fingers and homeoboxes 2 (ZHX2) were recently discovered to be a new regulator of inflammatory response. However, the role and potential molecular mechanisms of ZHX2 in diabetic nephropathy remain unclear. Exosomes derived from gingival mesenchymal stem cells (GMSCs-Exo) were successfully isolated and characterized. GMSCs-Exo reversed high glucose-induced podocyte pyroptosis and inflammation. ZHX2 was highly expressed in GMSCs-Exo. Furthermore, ZHX2 derived from GMSCs-Exo reversed podocyte pyroptosis and inflammation induced by HG. Additionally, ZHX2 was enriched in the FABP4 promoter region and transcriptionally inhibited the mRNA and protein levels of FABP4. GMSCs-Exo-derived ZHX2 abolished HG-induced podocyte pyroptosis and inflammation by inhibiting FABP4 and blocking the advanced glycation endproducts/the receptor of advanced glycation endproducts/NOD-like receptor family pyrin domain-containing 3 (AGEs/RAGE/NLRP3) pathway. Similarly, GMSCs-Exo-derived ZHX2 alleviated renal injury, pyroptosis, and inflammation in diabetic nephropathy mice. In conclusion, our findings demonstrated that ZHX2 protects against diabetic nephropathy by binding to the FABP4 promoter and reducing the expression of FABP4. We also showed that GMSCs-Exo-derived ZHX2 reversed HG-induced podocyte pyroptosis and inflammation by inhibiting the AGEs/RAGE/NLRP3 pathway. ZHX2 derived from GMSCs-Exo also alleviated tubular injury, pyroptosis, and inflammation in diabetic nephropathy mice. The therapeutic potential of targeting ZHX2 to treat diabetic nephropathy is clarified by these findings. - Source: PubMed
Wang ShaoboCai XueWeng ChanyanSu MiaozhuYang QunfengChen BoZeng Jincheng - Identification of cancer biomarkers for early detection is required. However, little is known about which candidate cell signaling pathway markers can be identified and which pathways may serve as therapeutic targets. We focused on the disulfidptosis among numerous signaling pathways, because it is a mechanism that causes cell death and is associated with iron-dependent cell death or ferroptosis, the tricarboxylic acid cycle, energy metabolism, and glucose uptake. The aim of the study was to detect the disulfidptosis-linked gene signatures associated with stage-specific makers and prognosis. - Source: PubMed
Publication date: 2025/10/30
Takashima YasuoYoshii KengoTanaka MasamiTashiro Kei - The transcription factor ZHX2 exerts paradoxical roles in cancer, acting as either an oncogene or tumor suppressor in a context-dependent manner. This duality stems from ZHX2's regulation of key processes including cell cycle, apoptosis, EMT, stemness, and metabolism. Consequently, ZHX2 may impacts tumor cell growth, migration, and immune evasion, positioning it as a promising therapeutic target. This short communication synthesizes current understanding of ZHX2's molecular structure, transcriptional regulation, and its critical modulation of oncogenic and tumor-suppressive pathways across various cancers. We highlight its potential utility as a prognostic biomarker and its implications for precision medicine, chemotherapy, targeted therapy, and immunotherapy. However, translating ZHX2-targeting strategies faces significant hurdles, particularly concerning tissue-specific restoration and integration with existing treatments. Future research should prioritize overcoming these barriers and exploring ZHX2's epigenetic regulatory potential. - Source: PubMed
Publication date: 2025/09/20
Wei YifanGuo HaiyangZhou JingjieShi DaHao Liqiang