Ask about this productRelated genes to: ZNF587 Blocking Peptide
- Gene:
- ZNF587 NIH gene
- Name:
- zinc finger protein 587
- Previous symbol:
- -
- Synonyms:
- ZF6, FLJ14710, UBF-fl, FLJ20813
- Chromosome:
- 19q13.43
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-19
- Date modifiied:
- 2016-11-09
Related products to: ZNF587 Blocking Peptide
Related articles to: ZNF587 Blocking Peptide
- Lung adenocarcinoma (LUAD) is a leading cause of cancer mortality, necessitating the identification of robust biomarkers and a deeper understanding of its molecular underpinnings. This study is aimed at screening for potential LUAD biomarkers and characterizing their biological functions. Using an integrative computational framework, we combined multitranscriptomic data analysis with three machine learning algorithms (LASSO, SVM-RFE, and random forest) to identify a consensus seven-gene signature (TTC13, TAF1D, ZNF587, PRPF3, LINC01355, TARBP1, and CCNL2). A classifier based on this signature achieved exceptional diagnostic accuracy (AUC = 0.972), with TAF1D identified as the most influential predictor via SHAP analysis. TAF1D was significantly upregulated in tumors, correlated with an immunosuppressive microenvironment, and promoted cancer cell proliferation by regulating cell cycle and immune-related pathways. Critically, TAF1D exhibited significant spatial heterogeneity in expression across different samples and tissue regions, suggesting it may exert region-specific biological functions within the tumor. In conclusion, our work defines a validated gene signature for LUAD, nominating TAF1D as a key oncogenic driver and promising candidate for diagnostic and therapeutic development. - Source: PubMed
Publication date: 2026/04/11
Ding LanXu QingmeiLiu DongdongWu JingyuCai XufanXu FeiqiMa ShuhanWang HaitaoShi Yanyan - Genes involved in the regulation of chromatin structure are frequently disrupted in cancer, contributing to an aberrant transcriptome and phenotypic plasticity. Yet, therapeutics targeting mutant forms of chromatin-modifying enzymes have yielded only modest clinical utility, underscoring the difficulty of targeting the epigenomic underpinnings of aberrant gene regulatory networks. Here, we sought to identify novel epigenetic vulnerabilities in diffuse large B-cell lymphoma (DLBCL). Through phenotypic screens and biochemical analysis, we demonstrated that inhibition of the H3K9 demethylases KDM4A and KDM4C elicits potent, subtype-agnostic cytotoxicity by antagonizing transcriptional networks associated with B-cell identity and epigenetically rewiring heterochromatin. KDM4 demethylases associated with the KRAB zinc finger ZNF587, and their enzymatic inhibition led to DNA replication stress and DNA damage-einduced cGAS-STING activation. Broad surveys of transcriptional data from patients also revealed KDM4 family dysregulation in several other cancer types. To explore this potential therapeutic avenue, we performed high-throughput small molecule screens with H3K9me3 nucleosome substrates and identified novel KDM4 demethylase inhibitors. AI-guided protein-ligand binding predictions suggested diverse modes of action for various small molecule hits. Our findings underscore the relevance of targeting fundamental transcriptional and epigenetic mechanisms for anti-cancer therapy. - Source: PubMed
Publication date: 2025/02/05
Najia Mohamad AliJha Deepak KZhang ChengLaurent BenoitKubaczka CarolineMarkel AriannaLi ChristopherMorris VivianTompkins AllisonHensch LucaQin YueChapuy BjoernHuang Yu-ChungMorse MichaelMarunde Matthew RVaidya AnupGillespie Zachary BHoward Sarah ANorth Trista EDominguez DanielKeogh Michael-ChristopherSchlaeger Thorsten MShi YangLi HuShipp Margaret MBlainey Paul CDaley George Q - Heterochromatin loss and genetic instability enhance cancer progression by favoring clonal diversity, yet uncontrolled replicative stress leads to mitotic catastrophe and inflammatory responses that promote immune rejection. KRAB domain-containing zinc finger proteins (KZFP) contribute to heterochromatin maintenance at transposable elements (TE). Here, we identified an association of upregulation of a cluster of primate-specific KZFPs with poor prognosis, increased copy-number alterations, and changes in the tumor microenvironment in diffuse large B-cell lymphoma (DLBCL). Depleting two of these KZFPs targeting evolutionarily recent TEs, ZNF587 and ZNF417, impaired the proliferation of cells derived from DLBCL and several other tumor types. ZNF587 and ZNF417 depletion led to heterochromatin redistribution, replicative stress, and cGAS-STING-mediated induction of an interferon/inflammatory response, which enhanced susceptibility to macrophage-mediated phagocytosis and increased surface expression of HLA-I, together with presentation of a neoimmunopeptidome. Thus, cancer cells can exploit KZFPs to dampen TE-originating surveillance mechanisms, which likely facilitates clonal expansion, diversification, and immune evasion. - Source: PubMed
Martins FilipeRosspopoff OlgaCarlevaro-Fita JoanaForey RomainOffner SandraPlanet EvaristPulver CyrilPak HuiSongHuber FlorianMichaux JustineBassani-Sternberg MichalTurelli PriscillaTrono Didier - The Warburg effect is a characteristic tumor cell behavior regarded as one of the cancer hallmarks and promotes tumor progression by promoting glucose uptake and lactate production. Long non-coding RNAs (lncRNAs) had been reported to emerge as a vital function in cancer development. The present research is designed to investigate the underlying molecular mechanism of lncRNA TMEM147 antisense RNA 1 (TMEM147-AS1) on aerobic glycolysis in prostatic carcinoma. - Source: PubMed
Publication date: 2022/10/17
Wu TaoHan NiweiZhao ChangyongHuang XiangSu PengLi Xiaoguang - Eukaryotic genomes harbor sequences derived from the chromosomal integration of ancient viruses, such as endogenous retroviruses (ERVs), which comprise 8% of the human genome. Like exogenous retroviruses, ERVs retain many common functional elements, including the corresponding DNA sequences of transfer RNA (tRNA) primer binding sites (PBSs), which are utilized for reverse transcription initiation by exogenous retroviruses. Here, through a medium-scale analysis of PBS loci positioned within ERVs, coupled with chromatin immunoprecipitation sequencing (ChIP-seq) of Kruppel-associated box zinc finger proteins (KRAB-ZFPs), we identified multiple ZFPs that specifically bind to different PBS loci. Among these, we focused on PBS-Lys, which is utilized by HIV-1, and identified its specific binding proteins to be mouse ZFP961 and human ZNF417/ZNF587. We found that these proteins not only repress ERV transcription but also inhibit retrovirus integration and transcription. Disruption of these ZFPs rendered cells more susceptible to HIV-1 infection. Thus, our research provides a methodology for identifying potential host factors that target retroviruses by ERVs. - Source: PubMed
Publication date: 2022/03/08
Yang BoFang LuGao QianqianXu CeXu JunqinChen Zhen-XiaWang YixuanYang Peng