Recombinant Human CD300A Protein
- Known as:
- Recombinant Human CD300A Protein
- Catalog number:
- cd-805
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human CD300A Protein
Related genes to: Recombinant Human CD300A Protein
- Gene:
- CD300A NIH gene
- Name:
- CD300a molecule
- Previous symbol:
- -
- Synonyms:
- Irp60, CMRF35H, CMRF-35-H9, IRC1, IRC2, IGSF12
- Chromosome:
- 17q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-08
- Date modifiied:
- 2016-10-05
Related products to: Recombinant Human CD300A Protein
Related articles to: Recombinant Human CD300A Protein
- Introduction Breast cancer (BC) is a common cancer type in women and a major cause of death. CD300a is an inhibitory receptor expressed on immune cells, particularly mast cells (MCs). CD300a ligands expression was found on several cancer cells. We hypothesized that CD300a has a role in suppression of anti-tumor immunity in BC. Methods To test our hypothesis, we induced the 4T1 BC model in WT and CD300a-KO mice and evaluated, by toluidine blue staining, the activation level of tumor associated MCs. 4T1 cells were co-cultured with WT or CD300a-KO mouse bone marrow derived MCs (BMMCs) and 4T1 cell viability was analyzed using trypan blue. Human MDA-231 BC cells were co-cultured with cord blood derived MCs (hCBMCs) and soluble hCD300a-Fc was added. FACS analysis for MDA-231 cell viability and WB for CD300a signal transduction in CBMCs were performed. Results In vivo, smaller 4T1-cell tumors with more activated MCs were found in CD300a-KO mice. In vitro, 4T1 cell growth was reduced in co-culture with WT BMMCs and further reduced with CD300a-KO BMMCs. Similarly, growth of MDA-231 BC cells in co-culture with CBMCs was reduced following treatment with CD300a-Fc which feasibly interfered with CD300a pro-tumorigenic interactions. CD300a signal transduction pathway was activated in CBMCs co-cultured with MDA-231 cells and this activation was inhibited following treatment with CD300a-Fc. Conclusion Our results would imply that in BC, tumor cells activate CD300a on MCs and probably on other immune cells to downregulate their anti-tumorigenic activity and therefore suggest CD300a as a potential immune-suppressor in BC. - Source: PubMed
Publication date: 2026/03/23
Ben-Zimra MichaNiazov ShiranRahimli Alekberli FidanLevi-Schaffer Francesca - Zika virus (ZIKV) causes severe neurological disease, including microcephaly and Guillain-Barré syndrome, through complex interactions with host cell proteins. This review synthesizes the 2015-2025 published literature on ZIKV-host protein interactions and their therapeutic targeting. ZIKV enters cells via multiple receptor pathways: adhesion receptors (DC-SIGN, Hsp70), high-affinity entry receptors (ITGB4, GRP78, NCAM1), internalization receptors (integrin αvβ5, sialic acid), and endosomal receptors (AXL, TIM-1, CD300a). Viral structural proteins direct virion assembly, while nonstructural proteins NS1-NS5 suppress immune responses, remodel cellular membranes, and dysregulate gene expression. NS5 uniquely suppresses neurodevelopmental genes and disrupts ciliary function through nuclear localization, directly driving microcephaly pathogenesis. Therapeutic strategies include receptor antagonists, protease inhibitors, and polymerase inhibitors. However, receptor redundancy, viral protein multifunctionality, and pregnancy safety constraints limit clinical translation. This review identifies ZIKV-host protein interactions as therapeutic targets and highlights barriers to drug development. - Source: PubMed
Publication date: 2026/02/04
Han XiaodongDu JiansenLi WenhuiYang ShuqianSun HuamuziWang GuihuaCong Haolong - Neuronal apoptosis suppression and efficient apoptotic cell clearance are crucial for preventing secondary spinal cord injury (SCI). The immunoreceptor CD300a is a phosphatidylserine receptor expressed on myeloid cells that modulates secondary neuronal damage by regulating efferocytosis. CD300a blockade has previously enhanced efferocytosis and improved neurological deficits in an ischemic stroke mouse model. However, the mechanisms and roles of CD300a in acute SCI remain unclear. Therefore, we evaluated the effects of CD300a regulation on acute SCI. First, an SCI model was created in CD300a-deficient mice and compared with that in wild-type mice. Second, we compared the effects of treating wild-type mice with anti-CD300a or control antibodies. The effects were evaluated over 6 weeks by analyzing behavioral outcomes using the Basso Mouse Scale and injured spinal cord tissue. Damage-associated molecular patterns (DAMPs) were evaluated in the acute phase, and oligodendrocyte apoptosis was assessed in the subacute phase of SCI to assess the effects of CD300a on inflammation and secondary injury. CD300a-deficient mice exhibited improved motor function, a reduced lesion area, and an increased residual myelin area. Immunohistochemical staining revealed reduced scarring and more surviving neurons. CD300a-deficient mice exhibited decreased extracellular DAMPs and oligodendrocyte apoptosis in the acute and subacute phases, respectively. The antibody-treated group also exhibited improved motor function, reduced lesion area, and increased residual myelin. These findings suggest that CD300a regulation mitigates SCI by suppressing DAMP release and apoptosis, thereby contributing to reduced tissue damage and functional recovery. These findings highlight CD300a regulation as a potentially effective treatment for acute SCI. - Source: PubMed
Publication date: 2026/02/17
Okuwaki ShunTakahashi HiroshiNakahashi-Oda ChigusaSakashita KotaroNakagawa TakaneOgata YosukeSunami TakahiroShimizu TomoakiGamada HisanoriNoguchi HiroshiMiura KouseiFunayama ToruYamazaki MasashiShibuya AkiraKoda Masao - The role of efferocytosis in chronic rhinosinusitis (CRS), particularly CRS with nasal polyps (CRSwNP), remains poorly understood. - Source: PubMed
Publication date: 2026/02/02
Liang ShuangYan BingShen ShenLi YingZhang LuoWang Chengshuo - Rheumatoid arthritis (RA) is a common autoimmune disease causing significant bone lesions. This study aims to explore RA through efferocytosis, identify hub genes, and construct a risk prediction model for clinical management and targeted therapy. - Source: PubMed
Publication date: 2026/01/30
Fei HaoMei YouhanHe JiafengLi YixuanXu RuiLiu WeiYu Ziliang