Ask about this productRelated genes to: EHD4 antibody
- Gene:
- EHD4 NIH gene
- Name:
- EH domain containing 4
- Previous symbol:
- PAST4
- Synonyms:
- -
- Chromosome:
- 15q15.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-03-22
- Date modifiied:
- 2016-10-05
Related products to: EHD4 antibody
Related articles to: EHD4 antibody
- The functional landscape of immune checkpoints (ICs) operating on CD4⁺FoxP3⁺ regulatory T cells (Tregs) remain incompletely defined. Although canonical IC pathways are well characterized, the full spectrum of IC molecules governing Treg-mediated immune regulation across physiological and pathological contexts has not been fully explored. We performed a comprehensive, multi-dataset transcriptomic screening of Treg membrane proteins to identify candidate immune checkpoints. This approach yielded 151 putative novel ICs, including 45 Treg-specific molecules and 106 FoxP3⁺-upregulated candidates. Cross-referencing these candidates with ten well-established IC-deficient models refined the list to 85 high-confidence ICs. A subsequent high-stringency, integrating expression specificity, functional relevance, and cross-dataset consistency, was applied to identify seven the most robust candidates. Ligand-receptor interaction mapping was then performed to define associated IC ligands and characterize their cellular expression patterns. This integrative analysis identified seven previously unrecognized immune checkpoints: CEP55, CD38, EHD4, CD200R1, PRC1, RAPH1, and CD86 expressed across Tregs and multiple T cell subsets. Ligand interaction mapping further revealed 46 corresponding IC ligands, predominantly expressed on antigen-presenting cells and tumor cells. Together, these IC-ligand interactions form extensive regulatory networks that modulate immune signaling and inflammatory responses. Our study delineates a comprehensive immune checkpoint-ligand network encompassing seven novel ICs and 46 associated ligands, providing mechanistic insight into Treg- and T cell-mediated immune regulation. This expanded IC landscape broadens the current repertoire of immune modulatory pathways and highlights new therapeutic opportunities across cancer, autoimmune disorders, infectious diseases, transplantation immunology, inflammatory conditions, and cardiovascular diseases. - Source: PubMed
Publication date: 2026/01/14
Han BaoshengXu KemanSaaoud FatmaHou YanjuanShao YingLu YifanJiang XiaohuaZhao HuaqingWang HongYang Xiaofeng - Disruption to barriers of the central nervous system (CNS) has been shown in both prime and drive pathologies observed across numerous neurological and ophthalmological conditions. These barriers are composed of well evolved endothelial tight junctions, and the key junctional component, claudin-5 (CLDN-5), is responsible for maintaining homeostasis of brain and retinal tissues. Indeed, decreased CLDN-5 expression has now been observed across many neurological and retinal diseases. Additionally, methods aimed at stabilising and upregulating CLDN-5 expression may have profound efficacy in treating a vast array of these conditions. However, very few targeted and specific methods can enhance CLDN-5 expression levels, and none of these have detailed its localisation and stability on the cell surface. In an effort to discover unknown and specific regulators of CLDN-5 expression, we performed a genome-wide cell-sorting-based phenotypic screen using CRISPR/Cas9. Sorting cells based on the phenotype of 'barrier tightness' revealed two candidate genes, EH domain-containing protein 4 (EHD4) and Arf-GAP with SH3 domain, ANK repeat, and PH domain-containing protein 2 (ASAP2), which, when suppressed, led to significant upregulation of CLDN-5 protein on the cell surface. EHD4 appeared to regulate the transcriptional activity of CLDN5, whereas ASAP2 controlled junctional localisation of CLDN-5. Identification of these candidate genes suggests that pharmacological inhibitors of EHD4 or ASAP2 may represent profound approaches to regulating CLDN-5 in neural endothelial cells. - Source: PubMed
Publication date: 2025/12/08
Hashimoto YosukePorkoláb GergőHudson NatalieO'Callaghan JeffreyHanley NicoleDelaney ConorDeli Mária AWestenskow PeterCampbell Matthew - Eps15 homology domain (EHD) proteins, including EHD1 to EHD4, play vital roles in tumor progression. In this study, we aimed to investigate which specific EHD proteins, if any, are implicated in tumor immune evasion and immunotherapy response. - Source: PubMed
Publication date: 2025/07/24
Tian FanglinHuang JianFan WeinaLi XinZhan YuningZhu KexinWang XiangyuHong XinWang XinRen JinXing YingCai Li - Endometriosis is a clinical condition characterized by the presence of endometrial glands outside the uterine cavity. While its incidence remains mostly uncertain, endometriosis impacts around 180 million women worldwide. Despite the presentation of several epidemiological and clinical explanations, the precise mechanism underlying the disease remains ambiguous. In recent years, researchers have examined the hereditary dimension of the disease. Genetic research has aimed to discover the gene or genes responsible for the disease through association or linkage studies involving candidate genes or DNA mapping techniques. - Source: PubMed
Kucukakcali ZeynepAkbulut SamiColak Cemil - : In this research, we sought to enhance our comprehension of liver cancer's genetic architecture by employing Mendelian randomization (MR) techniques to establish causative relationships between particular genetic variations and liver cancer susceptibility. : We integrated data from the public databases with MR analysis to identify differentially expressed genes (DEGs) associated with Hepatocellular Carcinoma (HCC). We conducted functional enrichment analyses to determine the biological processes and signaling cascades associated with the identified DEGs. We also used the CIBERSORT deconvolution method to evaluate immune cell composition in HCC tissues, followed by correlation studies examining relationships between our key genes of interest and various immune cell populations. Additionally, we validated our findings using a rat model of HCC and clinical HCC samples. : We obtained two key genes, and , which co-regulated M0 macrophages, suggesting their role in macrophage polarization and tumor progression. In addition, is associated with resting and activated mast cells, suggesting its involvement in regulating the tumor microenvironment. Detection of rat and clinical samples further confirmed the upregulation of these genes in HCC, supporting their potential as therapeutic targets. : Our findings emphasize the significant involvement of and in HCC, specifically regarding their influence on tumor-associated macrophage polarization and broader immune microenvironment modulation. These findings offer new insights into the molecular mechanisms driving HCC and suggest that targeting these genes may provide novel strategies for personalized treatment. - Source: PubMed
Publication date: 2025/05/27
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