SBZF3 antibody - N-terminal region (ARP35968_T100)
- Known as:
- SBZF3 (anti-) - N-terminal region (ARP35968_T100)
- Catalog number:
- arp35968_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SBZF3 antibody - N-terminal region (ARP35968_T100)
Related genes to: SBZF3 antibody - N-terminal region (ARP35968_T100)
- Gene:
- ZNF695 NIH gene
- Name:
- zinc finger protein 695
- Previous symbol:
- -
- Synonyms:
- SBZF3
- Chromosome:
- 1q44
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-23
- Date modifiied:
- 2015-01-12
Related products to: SBZF3 antibody - N-terminal region (ARP35968_T100)
Related articles to: SBZF3 antibody - N-terminal region (ARP35968_T100)
- Understanding lung cancer evolution can identify tools for intercepting its growth. Here, in a landscape analysis of 1,024 lung adenocarcinomas (LUADs) with deep whole-genome sequencing integrated with multiomic data, we identified 542 LUADs with a diverse clonal architecture. In this group, we observed divergent evolutionary trajectories based on tobacco smoking exposure, ancestry and sex. LUAD from smokers showed an abundance of tobacco-related C:G>A:T driver mutations in KRAS and short subclonal diversification. LUAD in people who have never smoked (hereafter, never-smokers) showed early occurrence of copy-number alterations and EGFR mutations associated with SBS5 and SBS40a mutational signatures. Tumours containing EGFR mutations exhibited long latency, particularly in female individuals of European-ancestry. Tumours from Asian never-smokers showed a short clonal evolution. Importantly, we found that the mutational signature ID2 is a marker of a previously unrecognized mechanism for LUAD evolution. Tumours with ID2 showed short latency and high long interspersed nuclear element-1 (LINE-1, hereafter L1) retrotransposon activity linked to L1 promoter demethylation. These tumours exhibited an aggressive phenotype with genomic instability, elevated hypoxia scores, low neoantigen burden, metastasis propensity and poor overall survival. Reactivated L1-retrotransposition-induced mutagenesis probably contributes to the mutational signature ID2, including through the regulation of the transcriptional factor ZNF695, a member of the KZFP family. The complex nature of LUAD evolution creates both challenges and opportunities for screening and treatment plans. - Source: PubMed
Publication date: 2025/12/10
Zhang TongwuZhao WeiWirth ChristopherDíaz-Gay MarcosYin JinhuCecati MoniaMarchegiani FrancescaHoang Phuc HLeduc CharlesBaine Marina KTravis William DSholl Lynette MJoubert PhilippeSang JianMcElderry John PAntony MichelleKlein AlyssaKhandekar AzharHartman CalebRosenbaum JenniferColón-Matos Frank JMiraftab MonaSaha MonjoyLee Olivia WJones Kristine MCaporaso Neil EWong Maria PikLeung Kin ChungHsiung Chao AgnesChen Chih-YiEdell Eric SSantamaría Jacobo MartínezSchabath Matthew BYendamuri Sai SManczuk MartaLissowska JolantaŚwiątkowska BeataMukeria AnushShangina OxanaZaridze DavidHolcatova IvanaMates DanaMilosavljevic SasaSavic MilanBossé YohanRothberg Bonnie E GouldChristiani David CGaborieau ValerieBrennan PaulLiu GeoffreyHofman PaulHomer RobertYang Soo-RyumPesatori Angela CConsonni DarioYang LixingZhu BinShi JianxinBrown KevinRothman NathanielChanock Stephen JAlexandrov Ludmil BChoi JiyeonCardelli MaurizioLan QingNowak Martin AWedge David CLandi Maria Teresa - Breast cancer (BC) is a major global health concern, ranking among the most common neoplasms and representing one of the leading causes of cancer-related deaths worldwide. Early recognition and classification of BC subtypes are crucial for improving patient outcomes. Therefore, identifying novel biomarkers with diagnostic and prognostic significance is of great importance. The Wnt signaling pathway plays a significant role in BC by influencing various cell cycle regulation processes and stem cell renewal. This study aims to identify novel Wnt-associated biomarker panels for BC patients, composed of multiple molecular factors. A series of bioinformatical analyses have been employed, including weighted gene co-expression network analysis, differential expression analysis, Kaplan-Meier survival analysis, logistic regression model evaluation, and receiver operating characteristic construction. Thus, this study revealed potential diagnostic and prognostic signatures based on comprehensive analyses of BC patient data sourced from The Cancer Genome Atlas database. Consequently, four gene signatures were constructed: two differentiate ER+ from ER-BC: and for overall survival (OS); and for disease free survival (DFS), while the other two effectively distinguish tumor from normal samples: for OS; and for DFS. - Source: PubMed
Publication date: 2025/10/08
Waszczykowska KlaudiaKołat DamianKałuzińska-Kołat ŻanetaPłuciennik Elżbieta - Colorectal cancer (CRC) is the third most common malignant tumor and the second leading cause of cancer‑related deaths worldwide. Identifying driver genes in CRC development may provide clinical benefits for patients. Zinc finger protein 695 (ZNF695) is a nuclear protein with transcriptional regulatory activity, which has been implicated in tumor progression; however, the role of ZNF695 in CRC is unclear. The clinical relevance of ZNF695 and NIMA‑related kinase 2 (NEK2) in patients with CRC was analyzed based on The Cancer Genome Atlas database. Knockdown was performed by transfecting the cells with small interfering RNAs, whereas overexpression was induced by infecting the cells with a lentivirus. In addition, cell Counting Kit‑8, colony formation, cell cycle and apoptosis assays were carried out to assess the role of ZNF695 and NEK2 in CRC. Chromatin immunoprecipitation‑quantitative PCR (qPCR) and dual luciferase reporter assays were used to examine the transcriptional regulation of ZNF695 on the NEK2 gene. Reverse transcription‑qPCR and western blotting were applied to assess mRNA and protein abundance, respectively. The present study aimed to investigate the clinical relevance, contribution and downstream effects of ZNF695 in CRC. The results revealed that ZNF695 was upregulated in CRC tissues compared with that in non‑cancer tissues. CRC cells also expressed higher ZNF695 expression than normal cells. , knockdown of ZNF695 suppressed the proliferation of HCT‑8 cells; conversely, overexpression of ZNF695 promoted the malignancy of HT‑29 cells. Moreover, ZNF695 accelerated cell cycle progression and inhibited apoptosis in CRC cells. Mechanistically, it was revealed that ZNF695 upregulated the expression of NEK2 at both the mRNA and protein levels. Luciferase reporter assay demonstrated that ZNF695 enhanced the transcriptional activity of the NEK2 promoter. Furthermore, knockdown of NEK2 reversed the oncogenic function of ZNF695. Additionally, ZNF695 activated the PI3K/Akt/mTOR signaling pathway in CRC cells. Inhibition of this pathway with rapamycin resulted in higher cytotoxicity to CRC cells with ZNF695 overexpression, suggesting that elevated ZNF695 levels may increase the sensitivity of CRC cells to rapamycin. In summary, the current study identified ZNF695 as a tumor‑promoting protein in CRC through activation of the NEK2 and PI3K/Akt/mTOR signaling pathways. Targeting the NEK2 and PI3K/Akt/mTOR signaling pathways may therefore be a promising strategy for the treatment of patients with CRC and high ZNF695 expression. - Source: PubMed
Publication date: 2025/07/19
Li XiaoweiLi XubinWang JingXue MeiZhang MengqiaoShuai JunfangZhang JieDing DanyangWang YeHou ShiyangChi XiaoqianSun HaiyingGao QiangKang Chunbo - Boys' pubertal overweight associates with future offspring's asthma and low lung function. To identify how paternal overweight is associated with offspring's DNA methylation (DNAm), we conducted an epigenome-wide association study of father's body silhouette (FBS) at three timepoints (age 8, voice break and 30) and change in FBS between these times, with offspring DNAm, in the RHINESSA cohort (N = 339). We identified 2005 differentially methylated cytosine-phosphate-guanine (dmCpG) sites (FDR < 0.05), including dmCpGs associated with offspring asthma (119), lung function (178) and BMI (291). Voice break FBS associated with dmCpGs in loci including KCNJ10, FERMT1, NCK2 and WWP1. Change in FBS across sexual maturation associated with DNAm at loci including NOP10, TRRAP, EFHD1, MRPL17 and NORD59A;ATP5B and showed strong correlation in reduced gene expression in loci NAP1L5, ATP5B, ZNF695, ZNF600, VTRNA2-1, SOAT2 and AGPAT2. We identified 24 imprinted genes including: VTRNA2-1, BLCAP, WT1, NAP1L5 and PTPRN2. Identified pathways relate to lipid and glucose metabolism and adipogenesis. Father's overweight at puberty and during reproductive maturation was strongly associated with offspring DNA, suggesting a key role for epigenetic mechanisms in intergenerational transfer from father to offspring in humans. The results support an important vulnerability window in male puberty for future offspring health. - Source: PubMed
Publication date: 2025/05/24
Kitaba Negusse TadesseØstergaard Toril MørkveLønnebotn MarianneAccordini SimoneReal Francisco GómezMalinovschi AndreiOudin AnnaBenediktsdottir BryndisGonzález Francisco Javier CallejasGómez Leopoldo PalaciosHolm MathiasJõgi Nils OskarDharmage Shyamali CSkulstad Svein MagneSchlünssen ViviSvanes CecilieHolloway John W - Understanding lung cancer evolution can identify tools for intercepting its growth. In a landscape analysis of 1024 lung adenocarcinomas (LUAD) with deep whole-genome sequencing integrated with multiomic data, we identified 542 LUAD that displayed diverse clonal architecture. In this group, we observed an interplay between mobile elements, endogenous and exogenous mutational processes, distinct driver genes, and epidemiological features. Our results revealed divergent evolutionary trajectories based on tobacco smoking exposure, ancestry, and sex. LUAD from smokers showed an abundance of tobacco-related C:G>A:T driver mutations in plus short subclonal diversification. LUAD in never smokers showed early occurrence of copy number alterations and mutations associated with SBS5 and SBS40a mutational signatures. Tumors harboring mutations exhibited long latency, particularly in females of European-ancestry (EU_N). In EU_N, mutations preceded the occurrence of other driver genes, including and . Tumors from Asian never smokers showed a short clonal evolution and presented with heterogeneous repetitive patterns for the inferred mutational order. Importantly, we found that the mutational signature ID2 is a marker of a previously unrecognized mechanism for LUAD evolution. Tumors with ID2 showed short latency and high L1 retrotransposon activity linked to L1 promoter demethylation. These tumors exhibited an aggressive phenotype, characterized by increased genomic instability, elevated hypoxia scores, low burden of neoantigens, propensity to develop metastasis, and poor overall survival. Reactivated L1 retrotransposition-induced mutagenesis can contribute to the origin of the mutational signature ID2, including through the regulation of the transcriptional factor , a member of the KZFP family. The complex nature of LUAD evolution creates both challenges and opportunities for screening and treatment plans. - Source: PubMed
Publication date: 2025/03/16
Zhang TongwuZhao WeiWirth ChristopherDíaz-Gay MarcosYin JinhuCecati MoniaMarchegiani FrancescaHoang Phuc HLeduc CharlesBaine Marina KTravis William DSholl Lynette MJoubert PhilippeSang JianMcElderry John PKlein AlyssaKhandekar AzharHartman CalebRosenbaum JenniferColón-Matos Frank JMiraftab MonaSaha MonjoyLee Olivia WJones Kristine MCaporaso Neil EWong Maria PikLeung Kin ChungAgnes Hsiung ChaoChen Chih-YiEdell Eric SMartínez Santamaría JacoboSchabath Matthew BYendamuri Sai SManczuk MartaLissowska JolantaŚwiątkowska BeataMukeria AnushShangina OxanaZaridze DavidHolcatova IvanaMates DanaMilosavljevic SasaSavic MilanBossé YohanGould Rothberg Bonnie EChristiani David CGaborieau ValerieBrennan PaulLiu GeoffreyHofman PaulHomer RobertYang Soo-RyumPesatori Angela CConsonni DarioYang LixingZhu BinShi JianxinBrown KevinRothman NathanielChanock Stephen JAlexandrov Ludmil BChoi JiyeonCardelli MaurizioLan QingNowak Martin AWedge David CLandi Maria Teresa