Ask about this productRelated genes to: ZNF768 Blocking Peptide
- Gene:
- ZNF768 NIH gene
- Name:
- zinc finger protein 768
- Previous symbol:
- -
- Synonyms:
- FLJ23436
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-08-14
- Date modifiied:
- 2017-11-28
Related products to: ZNF768 Blocking Peptide
Related articles to: ZNF768 Blocking Peptide
- Adaptive therapeutic tolerance frequently limits first-line lenvatinib efficacy in hepatocellular carcinoma (HCC). This study explored the C2H2-type zinc finger (ZNF) protein family (the largest class of transcription factors) and hypothesized that specific members of the ZNF protein family are hijacked by cancer cells to orchestrate pro-survival defenses against lenvatinib-induced ferroptosis. - Source: PubMed
Publication date: 2026/05/11
Hua JialeiZhao ShuyaBai ChangsenCui RanliangWang YichaoLiu YangLi YueguoDong Dong - Diabetic foot ulcers (DFUs) are among the most severe and debilitating diabetic complications, often leading to extremely high morbidity and mortality. Recently, increasing evidence has highlighted the role of necroptosis, a distinct type of programmed cell death distinct from apoptosis, in the progression and severity of DFUs. Understanding necroptosis-associated genes in DFUs could open new therapeutic avenues aimed at modulating this form of cell death, potentially improving outcomes for patients suffering from this serious diabetic complication. - Source: PubMed
Publication date: 2025/04/20
Yuan MeijieSun JianZhao ZhuoHu XiaomingFan WeijingShi HongshuoLiu Guobin - Zinc-finger protein 768 (ZNF768) is an emerging transcription factor regulating cell proliferation and senescence. Although the role of ZNF768 in regulating cell fate decision has been demonstrated in vitro, its importance in controlling physiological and pathophysiological processes in vivo is still unclear. Here, we report the generation of a transgenic mouse model allowing the conditional overexpression of ZNF768. This was achieved by inserting an inverted Znf768 coding sequence surrounded by heterologous Cre recognition sites in the Gt(ROSA)26Sor mouse locus (FLExZnf768). To study the impact linked to systemic overexpression of ZNF768, mice carrying the FLExZnf768 allele were crossed with CMV-Cre mice to produce a whole-body ZNF768 transgenic mouse (WB-ZNF768-Tg). As expected, WB-ZNF768-Tg mice showed higher ZNF768 levels in various tissues. These mice were born at the expected Mendelian ratio and did not display apparent phenotypes. Because ZNF768 levels are often overexpressed in cancer, we assessed tumor development in WB-ZNF768-Tg mice. However, ZNF768 overexpression was not sufficient to promote 3-methylcholantrene-induced fibrosarcoma and KRAS-induced lung adenocarcinoma in mice. Overall, we report the generation of a conditional mouse for ZNF768 overexpression and reveal that forcing ZNF768 expression is not sufficient to alter tumour development in mice. - Source: PubMed
Publication date: 2025/06/05
Poirier AudreyTribouillard LauraKordahi ManalGélinas YvesRoy JoannyBeaulieu Marie-JoséeOrain MichèleBlanchet Marie-RenéeJoubert PhilippeLaplante Mathieu - Cell proliferation is a fundamental process required for organismal development, growth, and maintenance. Failure to control this process leads to several diseases, including cancer. Zinc finger protein 768 (ZNF768) is an emerging transcription factor that plays key roles in driving proliferation. In addition to controlling a gene network supporting cell division, ZNF768 physically interacts and inhibits the activity of the tumor suppressor p53. Although the importance of ZNF768 in promoting cell proliferation has been well demonstrated in vitro, the physiological and pathological roles of ZNF768 in vivo are still unknown. Here, we report the generation and characterization of a ZNF768 null mouse model. ZNF768 null mice are viable but show a growth defect early in life. Mouse embryonic fibroblasts (MEFs) isolated from ZNF768 null embryos exhibit higher p53 levels, premature senescence, and higher sensitivity to genotoxic stress. In line with these findings, ZNF768 null mice showed increased radiosensitivity. This effect was associated not only with higher expression of a subset of p53 target genes, but also with alterations in genes regulating transmembrane receptor signaling, cell adhesion, and growth. Because ZNF768 levels are elevated in tumors, we tested the impact of ZNF768 loss on cancer development in mice. Here, we show that ZNF768 deletion was sufficient to repress lung tumor development in a KRAS-induced cancer mouse model. Overall, our findings establish ZNF768 as an important protein controlling cell proliferation that could potentially be targeted to reduce tumorigenesis. - Source: PubMed
Publication date: 2025/03/25
Poirier AudreyUtecht TimonVillot RomainGélinas YvesMouchiroud MathildeKordahi ManalKolnohuz AlonaPasteur ColineRoy JoannyBeaulieu Marie-JoséeOrain MichèleSamson NolwennBlanchet Marie-RenéeJoubert PhilippeLaplante Mathieu - Immune checkpoint inhibitors (ICIs) have become one important therapeutic strategy for advanced non-small-cell lung cancer (NSCLC). It remains imperative to identify reliable and convenient biomarkers to predict both the efficacy and toxicity of immunotherapy, and tumor-associated autoantibodies (TAAbs) are recognized as one of the promising candidates for this. - Source: PubMed
Publication date: 2023/01/02
Zhao JingWu YangYue YuanChen MinjiangXu YanLiu XiangningLiu XiaoyanGao XiaoxingWang HanpingSi XiaoyanZhong WeiZhang XiaotongZhang LiWang Mengzhao