CD52
- Known as:
- CD52
- Catalog number:
- 1P-368-T025
- Product Quantity:
- 25 tests
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD52
Ask about this productRelated 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
- Delayed neutrophil recovery after peripheral blood hematopoietic stem cell transplantation (PBHSCT) remains a leading driver of post-transplant infections and is closely associated with adverse outcomes. Current graft potency assessments rely on bulk CD34+ cell counts, which fail to resolve functional heterogeneity within the CD34+ compartment and poorly predict short-term engraftment outcomes. - Source: PubMed
Publication date: 2026/09/30
Chen LiWang XiaojieWang XiaoqiHu LanyueTan ChengningYin XiaotingZhang GenlingMiao YingyingWang MaolinXiang LixinXiao YanniYang ZhenxingXiang YangChen MaoshanRan QianLi Zhongjun - Bipolar Disorder (BD) is a severe psychiatric condition with high heritability and clinical heterogeneity. Despite numerous genetic variants linked to BD through Genome- Wide Association Studies (GWAS), the molecular mechanisms and effective therapeutic targets remain unclear. This study aims to identify potential therapeutic targets for BD using a systematic approach. - Source: PubMed
Publication date: 2026/09/25
Jin Yan-TingZhang Tian-YuXiang Chang-ChengMa Cai-YiHuang Cheng-Bing - Polycystic ovary syndrome (PCOS) is a common endocrine disorder associated with a substantial health burden. - Source: PubMed
Yu JingChen SiChen YueChu TongZhou KedaWang Peijuan - Acute kidney allograft rejection is a significant cause of graft dysfunction in pediatric transplant recipients. Standard of care for moderate to severe acute T-cell-mediated rejection among pediatric transplant recipients includes lymphocyte-depleting agents such as rabbit anti-thymocyte globulin (rATG). However, intolerance to or contraindications to rATG may limit its use and necessitate alternative immunosuppressive strategies. Alemtuzumab, a humanized monoclonal antibody targeting CD52, induces profound depletion of T- and B- lymphocytes and has been used in the transplantation setting. However, data remain limited for pediatric rejection, and the precise role for alemtuzumab is not well defined. - Source: PubMed
O'Connor Kevin WBagnasco SerenaPruette CozumelGoswami ElizabethCharnaya Olga - Chimeric antigen receptor (CAR) T cell therapy for acute myeloid leukemia (AML) is constrained by antigen heterogeneity and shared expression with healthy compartments, and there are often challenges in obtaining autologous T cells from heavily pretreated patients. To address these challenges, we developed universal donor-derived, base-edited, anti-CD33 CAR T cells (BE-CAR33) that used precise multiplexed cytidine deamination to simultaneously disrupt the , , and loci to prevent graft-versus-host disease and evade immunotherapy effects. An open-label, nonrandomized, single-center phase 1 study (ISRCTN14430213) evaluated the safety, feasibility, and activity of BE-CAR33 cell therapy ahead of allogeneic stem cell transplantation (allo-SCT) for patients with AML. Eligible participants were aged less than 16 years with relapsed/refractory AML. Five patients were screened, and three were enrolled; one additional adult received BE-CAR33 through compassionate access. Participants received fludarabine, cyclophosphamide, and alemtuzumab followed by 1.2 to 1.8 × 10 BE-CAR33 cells per kilogram. Treatment-emergent adverse events included cytokine release syndrome (grade ≤2), neurotoxicity (grade 3), cytopenias (grade 4), and transient rashes. Two patients demonstrated reduced minimal residual disease and proceeded to allo-SCT. Serial flow cytometry, chimerism quantification, and vector copy number analyses tracked BE-CAR33 T cells until elimination during transplant. Differentially expressed genes included editing signatures and switched from manufacturing-related toward postexpansion effector and exhaustion profiles. Although primary end points were not met, this first-in-human study demonstrated the feasibility of an "off-the-shelf" base-edited CAR T cell approach and informs future multiantigen strategies against AML. - Source: PubMed
Publication date: 2026/08/19
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