ELK4 Antibody - C-terminal region (P100985_P050)
- Known as:
- ELK4 Antibody - C-terminal region (P100985_P050)
- Catalog number:
- p100985_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ELK4 Antibody - C-terminal region (P100985_P050)
Related genes to: ELK4 Antibody - C-terminal region (P100985_P050)
- Gene:
- ELK4 NIH gene
- Name:
- ETS transcription factor ELK4
- Previous symbol:
- -
- Synonyms:
- SAP1
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-23
- Date modifiied:
- 2019-01-21
Related products to: ELK4 Antibody - C-terminal region (P100985_P050)
Related articles to: ELK4 Antibody - C-terminal region (P100985_P050)
- A major technical challenge in single-cell transcriptomics is the absence of an integrative analytic pipeline that can simultaneously leverage gene regulatory network (GRN) architecture, AI-assisted gene panel discovery, and functional relevance analyses to generate coherent biological insights. Existing approaches often treat these components independently, focusing on clusters, marker genes, or predictive features without integrating them into a mechanistically grounded framework. Consequently, comprehensive screening that links regulatory association, gene signature screening, and functional interpretation within single-cell datasets remains limited, underscoring the need for an integrated strategy. - Source: PubMed
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Borra SantoshiYan DaWelner Robert SYue Zongliang - The genetic mechanisms underlying type 1 diabetes (T1D) remain incompletely understood, limiting the development of targeted therapies. - Source: PubMed
Publication date: 2026/01/21
Liu YimingCao YuJiang Yaohui - The regulatory mechanisms governing vasculogenic mimicry (VM) in oral squamous cell carcinoma (OSCC) remain largely undefined. This study aimed to identify critical factors and elucidate the epigenetic mechanisms underlying VM in OSCC. - Source: PubMed
Publication date: 2025/12/30
Qiu YongleLi KunshanWang WenjingZhang WenjuanLiu JilunBai YangXu FeiGuo Jie - Individual differences in immune responses to African swine fever virus (ASFV), whether induced by vaccination or natural infection, may be linked to genetic variation in the genes involved in antigen presentation. - Source: PubMed
Publication date: 2025/12/11
Zhang FanghongNiu SiqiFrancisco Alegria AgostinhoAnzol Beneque AlbertoYao MinLiu GuopinWang JianwuHuang Tinghua - As a dominant component within the tumor microenvironment, macrophages exert essential roles in nearly all aspects of triple-negative breast cancer (TNBC). This work explored macrophage-associated signature genes for prognostication and treatment for TNBC. Single-cell (GSE180286) and bulk transcriptome profiles (TCGA-TNBC, GSE96058 and GSE45255) were analyzed by multiple computational approaches. The expression of signature genes was verified in tumor tissues and paracancerous normal tissues from patients with TNBC (n=5), HER2 breast cancer (n=5), and HR breast cancer (n=5) through immunofluorescence and Western blot. Additionally, gene expression was examined in breast cancer cells (MDA-MB-231, and MCF-7) and mammary epithelial cells (MCF10A) using RT-qPCR and Western blot. Following RNA interference or overexpression, CCK-8, wound scratch and Transwell assays were performed. To assess model robustness, 1000 iterations of Bootstrap resampling were performed to calculate optimism-corrected performance metrics; calibration curves were generated via the rms package. Decision Curve Analysis (DCA) was conducted to evaluate the clinical decision-making value. A single-cell map of the microenvironment in non-TNBC and TNBC was depicted. At both the single-cell and bulk levels, macrophages exhibited a higher abundance in TNBC versus non-TNBC. A macrophage-based gene signature (CTSD, CTSL, ELK4, HSPA8, XRCC4) was developed, with a high-risk score predicting poorer outcomes. This signature demonstrated reliable performance in external validation, particularly for one-year survival (AUC > 0.9). Bootstrap analysis corrected the original AUC from 0.706 to 0.739 (optimism=-0.033, difference <5%), and AUC values from 1000 resamplings concentrated in 0.70-0.75 (standard deviation=0.018). External validation confirmed the signature's ability to reliably predict patient prognosis, especially one-year survival. High-risk patients showed greater responsiveness to immunotherapy. The aberrant expression of CTSD, CTSL, ELK4, HSPA8, and XRCC4 in TNBC and non-TNBC was validated both and . Knockdown of XRCC4 attenuated malignant behaviors of MDA-MB-231, MCF-7, and MCF10A cells, whereas overexpression of CTSD, CTSL, and HSPA8 produced the opposite effect. Altogether, a novel macrophage-based gene signature was proposed for estimating survival outcomes and treatment responses in TNBC. The aberrant expression of these signature genes contributes to tumor malignant progression. Our findings offer valuable insights for future clinical research involving macrophages in TNBC. - Source: PubMed
Publication date: 2026/01/01
Huang YuanYu YuanZhu YufeiLu QianhuiZhang ZiwenWang XiaojiaWang XiaoweiZheng Yabing