ZNF342 antibody - C-terminal region (ARP31588_P050)
- Known as:
- ZNF342 (anti-) - C-terminal region (ARP31588_P050)
- Catalog number:
- arp31588_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF342 antibody - C-terminal region (ARP31588_P050)
Related genes to: ZNF342 antibody - C-terminal region (ARP31588_P050)
- Gene:
- ZNF296 NIH gene
- Name:
- zinc finger protein 296
- Previous symbol:
- ZNF342
- Synonyms:
- -
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-02
- Date modifiied:
- 2015-08-27
Related products to: ZNF342 antibody - C-terminal region (ARP31588_P050)
Related articles to: ZNF342 antibody - C-terminal region (ARP31588_P050)
- Gastric cancer prognosis remains poor, and neoadjuvant chemotherapy (NAC) is not widely used in Japan. While docetaxel-based regimens have shown promise internationally, the biological basis of their efficacy is not fully understood. - Source: PubMed
Tamura YukoOshi MasanoriKondo HirokiKasahara KoheiSato ShoKosaka TakashiAkiyama HirotoshiKunisaki ChikaraEndo Itaru - Resistance to immune-mediated destruction is a fundamental hallmark of cancer. Although several mechanisms have been identified that facilitate immune evasion, the transcriptional programs that orchestrate this process remain poorly understood. In this study, through a genome-wide CRISPR activation screen in human cancer cells subjected to NK cell-mediated killing, we identified ZNF296, a transcription factor highly expressed in epithelial cancers, as a key driver of tumor resistance to both NK and cytotoxic T-cell-mediated immunity. In mouse models, inhibition of ZNF296 significantly enhanced both NK and T-cell-mediated antitumor immunity, leading to a marked reduction in metastasis and increased infiltration of immune cells into the tumor microenvironment. Mechanistically, ZNF296 induced strong transcriptional repression of IFN-stimulated genes and key immunostimulatory ligands critical for NK and T-cell-mediated cytotoxicity. At the molecular level, ZNF296 directly interacted with and recruited the NuRD chromatin remodeling and deacetylase complex to the promoters of its target genes to suppress expression. Notably, treatment with low-dose romidepsin, an FDA-approved inhibitor targeting histone deacetylase 1, a core component of the NuRD complex, effectively restored NK and T-cell-mediated killing in cancer cells with high ZNF296 expression. Collectively, these findings establish ZNF296 as a key regulator of immune evasion, driving resistance to both NK and T-cell-mediated antitumor immunity, and highlight its potential as a therapeutic target to overcome immune resistance in epithelial cancers. - Source: PubMed
Wang HefeiZhao FangtingLi YaoWang PeiyuWang YixueRen PengfeiLi ChangheZheng HanqiuZeng ZexianPan Deng - - Source: PubMed
Publication date: 2025/05/27
Wang Wei JLin PeiStewart John MTang GuilinLi ShaoyingLoghavi SanamMedeiros L JeffreyXu Jie - Heart formation and function are tightly regulated at transcriptional and post-transcriptional levels. The dysfunction of cardiac cell-specific regulatory genes leads to various heart diseases. Heart failure is one of the most severe and complex cardiovascular diseases, which could be fatal if not treated promptly. However, the exact causes of heart failure are still unclear, especially at the level of single-gene causation. Here, an essential role was uncovered for the zinc finger protein Znf296 in heart development and cardiac contractile function. Specifically, znf296-deficient zebrafish embryos displayed heart defects characterized by decreased systolic and diastolic capacities of the ventricle and atrium. This was associated with reduced numbers and disrupted structural integrity of cardiomyocytes, including disorganized cytoskeleton and absence of sarcomeres. Mechanistically, the loss of Znf296 altered the alternative splicing of a subset of genes important for heart development and disease, such as mef2ca, sparc, tpm2, camk2g1, tnnt3b, and pdlim5b. Furthermore, Znf296 biochemically and functionally interacted with myelin transcription factor 1-like, a (Myt1la) in regulating cardiac-specific splicing and heart development. Importantly, ZNF296 also regulated alternative splicing in human cardiomyocytes to maintain structural integrity. These results suggest that Znf296 plays a conserved role for the differentiation of cardiomyocytes and the proper function of the cardiovascular system. - Source: PubMed
Publication date: 2025/03/22
Li XianpengYang ShuaiqiWang LuZhang XiangminZhang AilongWang YunchaoShi De-LiLi Hongyan - Hepatocellular carcinoma (HCC) is a prevalent malignancy with poor survival. Different cell types in the tumor microenvironment participate in the tumorigenesis and progression of HCC. This study aimed to analyze the immune microenvironment of HCC and its relationship with clinical outcomes. - Source: PubMed
Xu NanXiang XiaonanChen HuanChen YiyuanWang ShuaiGuo HaijunWei XuyongChen JunXu XiaoWei Qiang