FLJ23436 antibody - N-terminal region (ARP33582_T100)
- Known as:
- FLJ23436 (anti-) - N-terminal region (ARP33582_T100)
- Catalog number:
- arp33582_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FLJ23436 antibody - N-terminal region (ARP33582_T100)
Related genes to: FLJ23436 antibody - N-terminal region (ARP33582_T100)
- 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: FLJ23436 antibody - N-terminal region (ARP33582_T100)
Related articles to: FLJ23436 antibody - N-terminal region (ARP33582_T100)
- 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 - We recently identified Zinc-finger protein 768 (ZNF768) as a novel transcription factor controlling cell fate decision downstream of Rat sarcoma virus (RAS). We showed that ZNF768 depletion impairs cell cycle progression and triggers cellular senescence, while its overexpression allows cells to bypass oncogene-induced senescence. Elevated ZNF768 levels is common in tumors, suggesting that ZNF768 may help to escape cellular senescence, sustain proliferation and promote malignant transformation. Here, we discuss these recent findings and highlight key questions emerging from our work. - Source: PubMed
Publication date: 2021/12/08
Villot RomainPoirier AudreyDevillers RomainKolnoguz AlionaElowe SabineManem Venkata S KJoubert PhilippeMallette Frédérick ALaplante Mathieu - Lung adenocarcinoma (LUAD) is the most common type of lung cancer and a leading cause of cancer-related deaths worldwide. Despite important recent advances, the prognosis for LUAD patients is still unfavourable, with a 5 year-survival rate close to 15%. Improving the characterization of lung tumors is important to develop alternative options for the diagnosis and the treatment of this disease. Zinc-finger protein 768 (ZNF768) is a transcription factor that was recently shown to promote proliferation and repress senescence downstream of growth factor signaling. Although ZNF768 protein levels were found to be elevated in LUAD compared to normal lung tissue, it is currently unknown whether ZNF768 expression associates with clinicopathological features in LUAD. Here, using tissue microarrays of clinical LUAD surgical specimens collected from 364 patients, we observed that high levels of ZNF768 is a common characteristic of LUAD. We show that ZNF768 protein levels correlate with high proliferative features in LUAD, including the mitotic score and Ki-67 expression. Supporting a role for ZNF768 in promoting proliferation, we report that ZNF768 depletion severely impairs proliferation in several lung cancer cell lines in vitro. A marked decrease in the expression of key proliferative genes was observed in cancer cell lines depleted from ZNF768. Altogether, our findings support a role for ZNF768 in promoting proliferation of LUAD. - Source: PubMed
Publication date: 2021/08/17
Poirier AudreyGagné AndréanneLaflamme PhilippeMarcoux MeaganOrain MichèlePlante SophieJoubert DavidJoubert PhilippeLaplante Mathieu