Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
| Cat.No. | Product Name | Price |
|---|---|---|
| CSC-DC005641 | Panoply™ Human FCGR3A Knockdown Stable Cell Line | Inquiry |
| CSC-DC005642 | Panoply™ Human FCGR3B Knockdown Stable Cell Line | Inquiry |
| CSC-SC005641 | Panoply™ Human FCGR3A Over-expressing Stable Cell Line | Inquiry |
| CSC-SC005642 | Panoply™ Human FCGR3B Over-expressing Stable Cell Line | Inquiry |
| CSC-RO0145 | Human FCGR3B Stable Cell Line-CHO-K1 | Inquiry |
| CLOE-1033 | Human FCGR3B HEK293 Cell Lysate | Inquiry |
| CLOE-1034 | Human FCGR3B CHO Cell Lysate | Inquiry |
| CLOE-1445 | Human FCGR3A HEK293 Cell Lysate | Inquiry |
| CLOE-1449 | Human FCGR3A CHO Cell Lysate | Inquiry |
| CLOE-1450 | Human FCGR3A(His) HEK293 Cell Lysate | Inquiry |
| CLOE-1451 | Human FCGR3A HEK293 Cell Lysate | Inquiry |
| CLOE-1452 | Human FCGR3A(His) CHO Cell Lysate | Inquiry |
| CLOE-1454 | Human FCGR3A HEK293 Cell Lysate | Inquiry |
| CSC-RO01412 | Human FCGR3A Stable Cell Line - A375 | Inquiry |
| CSC-RO02481 | Human FCGR3A Stable Cell Line - CHO-K1 | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| AD06150Z | Human FCGR3A adenoviral particles | Inquiry |
| AD06151Z | Human FCGR3B adenoviral particles | Inquiry |
| LV12740L | human FCGR3A (NM_000569) lentivirus particles | Inquiry |
| LV12741L | human FCGR3A (NM_001127596) lentivirus particles | Inquiry |
| LV12742L | human FCGR3A (NM_001127592) lentivirus particles | Inquiry |
| LV12743L | human FCGR3A (NM_001127593) lentivirus particles | Inquiry |
| LV12744L | human FCGR3B (NM_000570) lentivirus particles | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| SHH054569 | shRNA set against Human FCGR3A(NM_000569.6) | Inquiry |
| SHH293753 | shRNA set against Human FCGR3B (NM_000570.4) | Inquiry |
| SHH054551 | shRNA set against Rat Fcgr3a(NM_207603.1) | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| CDFH006734 | Human FCGR3A cDNA Clone(NM_001127593.1) | Inquiry |
| MiUTR3H-01156 | FCGR3A miRNA 3'UTR clone | Inquiry |
| MiUTR3H-01155 | FCGR3A miRNA 3'UTR clone | Inquiry |
| MiUTR3H-01154 | FCGR3A miRNA 3'UTR clone | Inquiry |
| MiUTR1R-01860 | FCGR3A miRNA 3'UTR clone | Inquiry |
| MiUTR1H-03595 | FCGR3A miRNA 3'UTR clone | Inquiry |
| CDFR015352 | Rat Fcgr3a cDNA Clone(NM_207603.1) | Inquiry |
| CDFH006737 | Human FCGR3A cDNA Clone(NM_001127596.1) | Inquiry |
| CDFH006736 | Human FCGR3A cDNA Clone(NM_001127592.1) | Inquiry |
| CDFH006735 | Human FCGR3A cDNA Clone(NM_001127595.1) | Inquiry |
| MiUTR3H-01157 | FCGR3A miRNA 3'UTR clone | Inquiry |
| MiUTR3H-11401 | FCGR3B miRNA 3'UTR clone | Inquiry |
| CDCS405756 | Human FCGR3A ORF Clone (BC017865) | Inquiry |
| CDFH006733 | Human FCGR3A cDNA Clone(NM_000569.6) | Inquiry |
| CDCS405757 | Human FCGR3B ORF Clone (BC128562) | Inquiry |
| CDCS405755 | Human FCGR3A ORF Clone (BC036723) | Inquiry |
| CDCS405754 | Human FCGR3A ORF Clone (BC033678) | Inquiry |
| CDCR348745 | Human FCGR3A ORF Clone(NM_001127595.1) | Inquiry |
| CDCL183210 | Rat CD16a ORF clone(NM_207603.1) | Inquiry |
| CDCL183209 | Human CD16a ORF clone(NM_000569.6) | Inquiry |
| CDCL107625 | Human FCGR3A ORF clone (NM_001127596.1) | Inquiry |
| CDCL107623 | Mouse FCGR3A ORF clone (NM_001127592.1) | Inquiry |
| CDCL107619 | Human FCGR3A ORF clone (NM_001127593.1) | Inquiry |
CD16A, encoded by the FCGR3A gene, is a key member of the immunoglobulin G (IgG) Fc receptor family and is located on human chromosome 1q23.3. This region constitutes a highly homologous and complex gene cluster containing multiple Fcγ receptor genes. Among them, FCGR3A and FCGR3B share high sequence similarity but differ significantly in expression patterns, membrane anchoring mechanisms, and functional properties.
The FCGR3A gene encodes CD16A, a transmembrane glycoprotein comprising an extracellular domain that binds the IgG Fc portion, a single transmembrane segment, and an intracellular domain. The intracellular domain itself lacks signaling motifs and requires association with homodimeric or heterodimeric adaptor proteins containing immunoreceptor tyrosine-based activation motifs (ITAMs) to initiate downstream signaling. CD16A expression is primarily restricted to natural killer (NK) cells, macrophages, and a small subset of T cells, indicating its central role in specific immune responses. In contrast, FCGR3B encodes CD16B, which is glycosylphosphatidylinositol (GPI)-anchored on neutrophils, and this anchoring difference profoundly influences signaling and functional regulation.
CD16A serves as a bridge between humoral and cellular immunity, mediating antibody-dependent cellular cytotoxicity (ADCC) to eliminate pathogen-infected or transformed target cells. CD16A exhibits low affinity for monomeric IgG, preventing nonspecific activation of immune cells in the absence of antigen. However, when infection or tumorigenesis leads to dense antigen–IgG complexes on target cells, CD16A efficiently binds these Fc clusters, triggering receptor clustering and potent activation signaling.
Figure 1. CD16a⁺ NK cells and nonclassical monocytes correlate with kidney allograft rejection severity. (Perkins GB, et al., 2024)
On NK cells, CD16A associates non-covalently with adaptor proteins such as CD3ζ and FCER1γ chains. Upon receptor crosslinking, Src-family kinases phosphorylate ITAMs on adaptor proteins, recruiting and activating Syk kinase, which in turn signals through PI3K and PLCγ pathways, elevating intracellular Ca²⁺, reorganizing the cytoskeleton, and driving degranulation of perforin and granzymes, along with secretion of cytokines like interferon-γ, leading to efficient target cell lysis.
Beyond ADCC, CD16A profoundly influences NK cell development, homeostasis, and functional shaping. Its signaling is crucial for survival of NK progenitors, apoptosis inhibition, and induction of memory-like adaptive NK cells, which exhibit enhanced and rapid responses upon re-encountering antigens. In myeloid cells such as macrophages, CD16A activation similarly triggers inflammatory cytokine release and ADCC effects, although signaling may vary depending on adaptor composition. Notably, CD16A also mediates antibody-dependent enhancement (ADE) in viral infections such as dengue, where subneutralizing IgG-virus complexes bind CD16A on myeloid cells, facilitating viral entry and replication, exacerbating disease.
CD16A is clinically significant in two key areas: as a critical effector in therapeutic monoclonal antibody (mAb) therapy and as a genetic determinant of treatment efficacy and disease susceptibility. Most IgG1-based anti-cancer mAbs act, in part, by engaging CD16A on effector cells, recruiting NK cells and macrophages for target elimination. Therefore, CD16A expression and function directly impact therapeutic outcomes.
A functional single-nucleotide polymorphism (SNP) at residue 158 of FCGR3A results in either valine (V) or phenylalanine (F). The V allele exhibits significantly higher affinity for IgG1 and IgG3 Fc regions compared to the F allele, translating into enhanced ADCC. Clinical studies confirm that patients with the FCGR3A-158VV genotype display higher response rates and longer progression-free survival following treatment with rituximab or trastuzumab. This genetic insight has driven next-generation antibody engineering, such as afucosylated antibodies with enhanced CD16A binding, showing superior tumor clearance in preclinical and clinical settings.
In autoimmune diseases, FCGR3A polymorphisms are associated with susceptibility to conditions like systemic lupus erythematosus, likely through effects on immune complex clearance and modulation of immune cell activation thresholds. In infectious diseases, CD16A-mediated ADE represents a safety concern in dengue vaccines and antibody therapies.
Future CD16A-targeted immunotherapies may extend beyond leveraging endogenous NK cells, including bispecific antibodies targeting CD16A or CAR-NK cells expressing CD16A, offering more precise and potent tumor targeting.
References