CXCR4 Knockout HEK293T Cell Line

The choice depends on whether you are studying CXCR4 (C-X-C chemokine receptor 4, CD184)'s role as the principal CXCL12/SDF-1 receptor or modeling its functions in HIV entry, stem cell mobilization, and WHIM syndrome. The Knockout line is the standard tool for asking whether CXCR4 is required for these processes — CXCR4 is a Gαi-coupled seven-transmembrane GPCR activated by CXCL12/SDF-1α, with established roles in hematopoietic stem cell retention in bone marrow, T-lymphocyte trafficking, and cancer metastasis; CXCR4 is also a co-receptor for X4-tropic HIV entry. Overexpression is useful for studying CXCR4 gain-of-function effects. For HIV, stem cell, and cancer metastasis research, the EDITGENE CXCR4 Knockout in HEK293T is a workhorse mechanistic platform — HEK293T's very high transfection efficiency supports systematic structure-function studies. Rescue with wild-type, signaling-deficient, or WHIM-associated truncation mutant (e.g., R334X — WHIM syndrome causes gain-of-function CXCR4 truncations that resist β-arrestin-mediated internalization) CXCR4 enables comprehensive disease and pharmacology studies. The knockout is a critical specificity tool for ⭐ plerixafor (Mozobil, FDA-approved CXCR4 antagonist for HSC mobilization in lymphoma/myeloma transplants), mavorixafor (Xolremdi, FDA-approved 2024 for WHIM syndrome), motixafortide, and emerging CXCR4-targeted therapies.

Primary applications: • CXCL12-induced signaling: cAMP suppression (Gαi), Ca²⁺ mobilization, and ERK activation following CXCL12/SDF-1α stimulation in CXCR4-null cells. • HIV entry studies: X4-tropic HIV envelope-mediated entry analysis in CXCR4-null cells to characterize HIV co-receptor function. • Plerixafor specificity: critical genetic control for plerixafor (Mozobil, FDA-approved CXCR4 antagonist for HSC mobilization). • Mavorixafor specificity: critical genetic control for mavorixafor (Xolremdi, FDA-approved 2024 for WHIM syndrome). • WHIM syndrome modeling: rescue with WHIM-associated CXCR4 truncation mutations (R334X, others) for genotype-function studies of warts-hypogammaglobulinemia-infections-myelokathexis syndrome. EDITGENE recommends this HEK293T-based model as a critical specificity control for CXCR4-targeted drug development across HSC mobilization, WHIM syndrome, HIV entry, and cancer metastasis research.

Yes. CXCR4 rescue experiments are well-established for chemokine receptor research: • Construct design: use a codon-modified CXCR4 sequence with a small intracellular C-terminal tag (FLAG, HA). CXCR4 is a seven-transmembrane GPCR with extracellular CXCL12-binding pocket — preserve all elements; note that C-terminal tags may affect β-arrestin recruitment. • Surface localization validation: confirm plasma membrane localization before CXCL12 binding studies. • Signaling-deficient rescue: DRY motif mutations disrupt Gαi-coupling. • WHIM mutation rescue: R334X and other C-terminal truncation mutations cause WHIM syndrome by resisting β-arrestin-mediated internalization, generating gain-of-function CXCR4 — invaluable for disease modeling. • HIV co-receptor studies: HIV envelope-mediated entry assays following CXCR4 rescue. • Functional readout: rescue should restore CXCL12-induced Gαi signaling, β-arrestin recruitment, and receptor internalization. HEK293T transduces with very high efficiency and supports stable rescue line generation for systematic CXCR4 mutation analysis.