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)
- Transcription factors (TFs) are key players in eukaryotic gene regulation, but the DNA binding specificity of many TFs remains unknown. Here, we assay 284 mostly uncharacterized putative human TFs using selective microfluidics-based ligand enrichment followed by sequencing (SMiLE-seq), revealing 74 new DNA binding motifs. To investigate whether TFs lacking detectable motifs preferably bind epigenetically modified DNA, we develop methylation-sensitive SMiLE-seq (meSMiLE-seq), a microfluidic assay that simultaneously probes binding to methylated and unmethylated DNA. Using meSMiLE-seq, we assay 114 TFs and identify DNA-binding models for 48 proteins, including known methylation-sensitive binding modes for POU5F1 and RFX5. 11 TFs prefer methylated DNA or display alternative methylation-dependent motifs (e.g. PRDM13), while 13 show aversion to methylated sequences (e.g. USF3). Finally, we identify ZHX2 as a putative Z-DNA binder. Altogether, our study significantly expands the human TF codebook, while providing a versatile platform to quantitatively assay the impact of DNA modifications on TF binding. - Source: PubMed
Publication date: 2026/08/05
Gralak Antoni JFaltejskova KaterinaYang Ally W HSteiner ClemenceRusseil JulieGrenningloh NadiaInukai SachiDemir MustafaDainese RiccardoOwen CooperPankevich Eugenia V Hughes Timothy RKulakovskiy Ivan VKribelbauer-Swietek Judith Fvan Mierlo GuidoDeplancke Bart - Based on findings from human atherosclerotic arteries and mouse arterial injury models, where ZHX2 expression is significantly downregulated, this study identifies ZHX2 as a critical inhibitor of pathological vascular remodeling. Functionally, local adenoviral overexpression of ZHX2 in vivo attenuates neointima formation in a mouse carotid artery ligation model, while in vitro experiments demonstrate that ZHX2 impedes the proliferation and migration of primary Vascular Smooth Muscle Cells (VSMCs). Mechanistically, integrated RNA-seq and ChIP-seq analyses reveal that ZHX2 transcriptionally regulates GADD45G, directly binding to its promoter and activating its transcription. The essential role of this pathway is confirmed by the finding that knockdown of GADD45G counteracts the inhibitory effects of ZHX2 overexpression on VSMC proliferation, migration, and neointima formation. Consequently, the ZHX2/GADD45G signaling axis is highlighted as a potential regulatory pathway in injury-associated neointimal remodeling. - Source: PubMed
Fan SiyuanWu XuelianGui LinWu YichenQiao BaoruLi YueZheng ZheHuang Kai - 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