In Stock Cell Lines
Homo sapiens (Human)
Blood (peripheral blood)
Suspension
CD19 Knockout HMy2.C1R Cell Line is a CRISPR/Cas9-edited B-lymphoblastoid model lacking the CD19 co-receptor. Derived from HMy2.C1R cells that express HLA-A*0201, this knockout line enables investigation of BCR signaling without CD19-mediated amplification. CD19 interacts with CD21, CD81, and LYN to recruit PI3K and activate AKT, NF-??B, and MAP kinase pathways. Applications include dissection of B-cell activation thresholds, B-cell malignancy research, and T-cell stimulation assays where CD19 loss may alter antigen-presenting cell function. Researchers can assess CD19-dependent signaling through flow cytometry, western blotting, and functional assays of B-cell proliferation and NF-??B activity.
DAB2 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG16694
BRD3 Knockout HCT116 Polyclonal Cells
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APH1A Knockout A549 Polyclonal Cells
Cat. No. ARG38714
MGME1 Knockout AGS Polyclonal Cells
Cat. No. ARG2773
DENND1B Knockout Raji Polyclonal Cells
Cat. No. ARG917
Pkd1 Knockout GC-1spg Cell Line
Cat. No. ARG0237
The CD19 Knockout HMy2.C1R Cell Line is a CRISPR/Cas9-edited human B-lymphoblastoid cell line in which the CD19 gene has been disrupted, generating a loss-of-function model for probing B-cell biology. This knockout cell line is derived from the HMy2.C1R host, enabling researchers to analyze CD19-dependent mechanisms without altering the host cell??s engineered antigen-presenting capabilities.
The HMy2.C1R cell line is a human B-lymphoblastoid line that lacks endogenous HLA-A and -B expression and has been stably transfected with the class I MHC allele HLA-A*0201. This modification makes HMy2.C1R a versatile tool for T-cell stimulation assays, as it presents peptide epitopes restricted through HLA-A*0201 while minimizing interference from other classical MHC class I molecules. The B-cell origin of the host provides a physiologically relevant environment for studying B-cell receptor (BCR) signaling and antigen processing.
CD19 functions as a critical co-receptor for BCR signaling, enhancing signal transduction upon antigen engagement. It forms a complex with CD21 (complement receptor 2), CD81 (TAPA-1), and CD225 (Leu-13). Upon BCR activation, CD19 is phosphorylated by Src-family kinases, including LYN, which creates docking sites for PI3K (via the p85 subunit) and adaptor proteins such as Vav, GRB2, and BLNK. This recruitment amplifies downstream cascades, including PI3K-AKT, NF-??B, and MAP kinase (ERK, JNK, p38) pathways, ultimately driving B-cell survival, proliferation, and differentiation. CD19 integrates signals from the BCR and complement system, serving as a rheostat for B-cell activation thresholds.
In the HMy2.C1R context, CD19 knockout allows dissection of BCR signal transduction independently of CD19 co-receptor activity. Since HMy2.C1R is used as an antigen-presenting cell for T-cell stimulation, the absence of CD19 may alter B-cell signaling events that influence antigen presentation and cytokine responses. This model is valuable for distinguishing CD19-dependent from CD19-independent pathways downstream of the BCR, as well as for evaluating CD19 as a therapeutic target in B-cell malignancies. The knockout cell line retains the HLA-A*0201 restriction element, supporting studies that require a defined MHC-I context.
This knockout cell line is suitable for a wide range of research applications, including studies of B-cell receptor signaling, leukemia and lymphoma pathogenesis, and immunotherapy target validation. Researchers can employ flow cytometry to confirm CD19 surface loss, western blotting to assess downstream phosphorylation events (e.g., phospho-CD19, phospho-AKT), co-immunoprecipitation to probe CD19-containing complexes, and calcium flux assays to measure early BCR signaling events. NF-??B reporter assays and B-cell proliferation assays can further delineate functional consequences of CD19 loss. Additionally, the HMy2.C1R background allows for T-cell cytotoxicity and epitope presentation experiments, linking B-cell co-receptor function to adaptive immunity. For further information, please contact Ascent Research.
