CD52
- Known as:
- CD52
- Catalog number:
- 11-368-C025
- Product Quantity:
- 0.025 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD52
Related genes to: CD52
- Gene:
- CD52 NIH gene
- Name:
- CD52 molecule
- Previous symbol:
- CDW52
- Synonyms:
- HE5, EDDM5
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-12
- Date modifiied:
- 2017-03-15
Related products to: CD52
Anti-CD52 (Campath-1H), Human IgG1 AntibodyAnti-CD52 (Campath-1H), Human IgG1 Antibodyanti-CD52 (mouse) antibody, rabbit serumanti-CD52 (mouse) antibody, rabbit serumAnti-CD52 AntibodyAnti-CD52 antibodyAnti-Human CD52, UnlabeledAnti-Human CD52-FITC conjugateAnti-Human CD52-PE conjugateAnti-Human CD52-PE-Cy5-conjugateAntibodies: Mouse Monoclonal to CD52 _ CAMPATH-1, Species Reactivity: Human, Clone: HI186, Isotype: IgG2bAntibodies: Mouse Monoclonal to CD52 _ CAMPATH-1, Species Reactivity: Human, Clone: HI186, Isotype: IgG2bAntibodies: Mouse Monoclonal to CD52 _ CAMPATH-1, Species Reactivity: Human, Clone: HI186, Isotype: IgG2bAntibodies: Mouse Monoclonal to CD52 _ CAMPATH-1, Species Reactivity: Human, Clone: HI186, Isotype: IgG2bAntibodies: Mouse Monoclonal to CD52 _ CAMPATH-1, Species Reactivity: Human, Clone: HI186, Isotype: IgG2b Related articles to: CD52
- Alemtuzumab, a monoclonal antibody targeting CD52, is associated with a high incidence of secondary autoimmune disease, most commonly thyroid dysfunction. Alemtuzumab-induced Graves' disease (AIGD) typically follows a relapsing course and may exhibit atypical or severe phenotypes during immune reconstitution (IR). - Source: PubMed
Publication date: 2026/08/05
O'Brolchain AongusReda Elham - Treatment options for clear cell renal cell carcinoma (ccRCC) refractory to immune checkpoint inhibitors (ICIs) and targeted therapy are needed. ALLO-316 is an allogeneic chimeric antigen receptor (CAR) T-cell product that targets CD70-expressing ccRCC and resists immune rejection by targeting and eliminating patients' CD70 alloreactive T cells. - Source: PubMed
Publication date: 2026/07/14
Srour Samer AChahoud JadDrakaki AlexandraCurti Brendan DGibney Geoffrey TTang LilyJiang YizhouCharmsaz SaraRobbins Paul BMcLeroy JeffSeveryn Christopher JLe Gall John BRoberts Zachary JTannir Nizar MPal SumantaKotecha Ritesh R - Pancreatic ductal adenocarcinoma (PDAC) remains a highly aggressive malignancy driven by rapid metastasis and a profoundly immunosuppressive microenvironment. While the surface glycoprotein CD52 is a known immunoregulator, its precise role in solid tumors remains controversial, partly due to its broad expression across diverse cell populations and its compartment-specific functions within the tumor microenvironment. In this study, we utilized integrated single-cell RNA sequencing (scRNA-seq), functional assays, and compartment-specific clinical validation to elucidate the tumor-intrinsic functions of CD52 in PDAC. We identified a highly plastic, restricted subpopulation of CD52-high malignant epithelial cells that actively drives metastasis initiation by enhancing cellular invasive capacity. Concurrently, we demonstrated that tumor-derived CD52 orchestrated a multi-layered immunosuppressive network that attenuates CD8 + T cell cytotoxicity, facilitating early immune evasion. Furthermore, by systematically separating expression sources, our clinical validation established that tumor-derived CD52 is a prognostic indicator of poor patient survival. These findings characterize CD52 as a critical, tumor-intrinsic driver of PDAC progression, highlighting its value as a prognostic biomarker and a therapy target in combination with immune checkpoint blockade to overcome innate therapeutic resistance in PDAC. - Source: PubMed
Publication date: 2026/06/27
Zhang ZeyuTao JinxinFu YifanDong YiWang YuanyangZhang MenggangYe LiyuanQiu JiangdongLiu YuezeChen HaoXiao JianchunHuang HuaCao ZheYang GangZhang Taiping - Suppressive myeloid cells play a central role in cancer escape from anti-tumor immunity and exert multiple pro-tumoral activities, including the promotion of cancer cell survival, invasion, and metastasis. Recent evidence suggests that certain subsets may also influence tumor heterogeneity and cellular plasticity. However, their role in cancer stem cell promotion and plasticity and the underlying molecular mechanisms have yet to be deciphered. Here we demonstrate that human immunosuppressive myeloid cells, generated in vitro or isolated from patients with breast cancer, induce cancer stem-like cells exhibiting mesenchymal features. This cancer-stemness-inducing function was restricted to a CD52-expressing myeloid subset. Single cell transcriptomic- and surface proteome-based interactome analyses identify membrane-bound TGF-β1 as a potential mediator of this effect. Functional inhibition of the TGF-β1 pathway blocks stem-like feature induction by suppressive myeloid cells. These results provide insights into the cancer stemness-promoting capacity of suppressive myeloid cells and its associated molecular mechanisms in breast cancer. - Source: PubMed
Publication date: 2026/06/18
Boyer ThomasBlaye CélineChalopin DomitilleMadéry MathildeBoucher JonathanMoisand AlexandraTheodoly-Lannes AudreyGiraud JuliePeyraud FlorentSeeneevassen LornellaKlein ClémentMebroukine SamyAuriol SophieChaibi AssiaZouine AtikaIzotte JulienCharrot Léa MoraAlizadeh DaryaIggo RichardMacGrogan GaetanLamarthée BaptisteBonnotte BernardBonneil EricRoux Philippe PVaron ChristineDomblides CharlotteLarmonier Nicolas - Hemophagocytic lymphohistiocytosis (HLH) is a rare and potentially fatal disorder characterized by immune hyper-activation and subsequent tissue and organ infiltration by proinflammatory cytokines. Primary HLH is caused by underlying genetic mutations in key genes responsible for cellular cytotoxicity, whereas secondary HLH is driven by infection, malignancy, and autoimmune disease as the underlying trigger for immune activation. Chemotherapy-based treatments for pediatric HLH have improved survival and outcomes for patients, however, there is a significant unmet need in the development of targeted therapies to limit drug toxicity and further improve overall survival. - Source: PubMed
Publication date: 2026/06/23
Cahill HilaryWynn Robert FSenthil Srividhya