CD53
- Known as:
- CD53
- Catalog number:
- 10-227-C025
- Product Quantity:
- 0.025 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD53
Ask about this productRelated genes to: CD53
- Gene:
- CD53 NIH gene
- Name:
- CD53 molecule
- Previous symbol:
- MOX44
- Synonyms:
- TSPAN25
- Chromosome:
- 1p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-16
- Date modifiied:
- 2016-10-05
Related products to: CD53
Related articles to: CD53
- Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer, often diagnosed at advanced stages with poor prognosis. CD53, a tetraspanin involved in immune regulation, has an unclear role in LUAD. - Source: PubMed
Publication date: 2026/06/11
Chen JunTan WeimingWei YichenHan ZexianZhu JichongWei Kanglai - Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease characterised by loss of immune tolerance and chronic inflammation, but its molecular pathogenesis remains incompletely understood. In this work we examine whether immune regulatory transcripts and pathways are recurrently detectable across heterogeneous publicly available SLE transcriptomic datasets, and we explore one of the recurrent pathways with a kinetic systems-biology model. We analyzed one microarray dataset (E-GEOD-46923, profiled on Affymetrix HG-U133A and HG-U133B), two bulk RNA-seq datasets (E-MTAB-7145, E-MTAB-11919), and two single-cell RNA-seq datasets (GSE135779, GSE163121) using a unified differential-expression criterion (|log2 fold change|≥ 1, Benjamini-Hochberg adjusted p-value < 0.05). KEGG pathway enrichment was performed with a per-dataset background gene universe. A mass-action kinetic model of Th1/Th2 differentiation was constructed in MATLAB SimBiology, and global sensitivity analysis was performed using the variance-based Sobol method. Across the heterogeneous datasets, CD53, IFITM1, and RPL11 were recurrently identified as differentially expressed transcripts, and the Th1/Th2 cell differentiation pathway, together with related cytokine-cytokine receptor and JAK-STAT pathways, emerged as a recurrent immune-regulatory signal. Systems-biology simulation under SLE-derived initial conditions predicted atypical IL-2 and GATA3 expression dynamics, which is consistent with, but does not by itself prove, the cytokine-signalling dysregulation reported in SLE. Sobol sensitivity analysis identified IL-4 and the modelled co-stimulatory and Notch ligand species (CDN1-6 and Jagged1/2) as the largest non-additive regulators of IL-2 in the model. Overall, this work integrates transcriptomic recurrence analysis with kinetic modelling to generate testable hypotheses regarding immune regulatory dysfunction in SLE. - Source: PubMed
Publication date: 2026/06/15
Saleem KashifParacha Rehan ZafarKhalid LintaManzoor AyeshaNisar MaryumMurad DidarDin Nazar MuhammadAmir Afreenish - BackgroundAxillary lymph node metastasis (ALNM) serves as a critical prognostic determinant in breast cancer, yet the molecular drivers governing lymphatic dissemination remain poorly characterized. Integrating single-cell transcriptomic profiling with Mendelian-randomization (MR)-based genetic prioritization may help reveal cell type-specific mechanisms underlying metastatic progression.MethodsWe analyzed the GSE195861 single-cell RNA sequencing dataset encompassing six invasive ductal carcinoma (IDC) samples and paired ALNM specimens. t-distributed Stochastic Neighbor Embedding-based clustering and SingleR annotation delineated cellular heterogeneity, while differential expression analysis identified metastasis-associated genes in epithelial compartments. MR analysis employing five robust methods (inverse variance-weighted, weighted median, MR-Egger, simple/weighted mode) integrated genome-wide association study data (GCST90018799) to establish causal gene-breast cancer associations. CellChat reconstructed ligand-receptor networks across nine annotated cell types.ResultsUnsupervised clustering resolved 27 cell clusters into nine lineages, revealing ALNM-specific expansion of monocytes, pre-B cells, and CD34+ hematopoietic stem cells (HSCs). Epithelial cells exhibited 2421 differentially expressed genes (DEGs) between IDC and ALNM, including 12 genes whose genetically predicted expression showed significant associations with breast cancer risk in MR analysis (P < 0.05). CD53 (odds ratio (OR) = 1.110, 95% confidence interval (CI) = 1.019-1.209, P = 0.017) and TCDD-inducible poly-ADP-ribose polymerase (TIPARP) (OR = 1.153, 95% CI = 1.032-1.288, P = 0.012) were prioritized as candidate genes, as their genetically predicted expression was associated with increased breast cancer risk in weighted median MR. Cell-cell communication analysis implicated macrophage-derived midkine-nucleolin signaling and B-cell-orchestrated macrophage migration inhibitory factor-(CD74 + CXCR4) axis in metastatic crosstalk. Functional enrichment linked DEGs to extracellular matrix remodeling and MAPK/PI3K-Akt activation.ConclusionThis multi-omics integration prioritizes CD53 and TIPARP as ALNM-associated candidate genes with genetically supported associations with breast cancer risk, with macrophage-epithelial and B-cell-HSC interactions serving as potential therapeutic targets. Our findings provide a roadmap for developing metastasis-interceptive strategies through precision targeting of the ALNM-associated tumor microenvironment. - Source: PubMed
Publication date: 2026/05/12
Qu LimengLi JinyangDing ShirongLong QianYi Wenjun - Hematopoietic stem and progenitor cells (HSPCs) are localized within specialized niches of the bone marrow (BM). However, during hematological disorders or infections, the functionality of these cells in the BM is compromised, leading to extramedullary hematopoiesis (EMH). Chronic inflammation drives EMH, yet its impact on HSPCs outside the BM is poorly understood. Using a mouse model of chronic autoinflammatory disease, we demonstrated the presence of extramedullary HSPCs in blood, spleen, and inflamed tails and paws. Single-cell transcriptomics revealed a unique expression profile in extramedullary HSCs, with significant up-regulation of , MHCII-associated, and immunosuppressive genes. We further demonstrated that extramedullary CD53 HSPCs act as antigen-presenting cells, promoting the development of regulatory T cells (T cells) to control chronic inflammation at extramedullary sites. Conversely, T cells exert a protective role on extramedullary HSPCs. Together, our findings revealed a mutually supportive relationship between a unique subset of HSPCs and T cells in inflamed tissues during chronic inflammation. - Source: PubMed
Publication date: 2026/05/06
Kuzmina MariaGrusanovic SrdjanBrezina JiriThelen FlavianVanickova KarolinaMilosevic MirkoBas Irina RibeiroPavliuchenko NataliiaRuzickova SarkaRohlena JakubFilipp DominikRohlenova KaterinaNombela-Arrieta CesarBrdicka TomasAlberich-Jorda Meritxell - Cholesterol plays critical roles in prostate cancer (PCa) proliferation, immune evasion, and androgen signaling. PCSK9 regulates cholesterol metabolism. Its role in PCa remains unclear. - Source: PubMed
Publication date: 2026/04/06
Gu YanWei FengxiangDong YingLin XiaozengSu YingyingWood GeoffreySeidah Nabil GBonert MichaelWerstuck GeoffAziz TariqMajor PierreTang Damu