In Stock Cell Lines
Homo sapiens (Human)
Skin
Adherent
The GPR4 Knockout SK-MEL-28 Cell Line is a CRISPR/Cas9-edited knockout cell line with disruption of the GPR4 gene in the human melanoma cell line SK-MEL-28. GPR4 is a proton-sensing GPCR that couples to Gs and G12/13 proteins, driving cAMP/PKA and RhoA/ROCK signaling, leading to ERK1/2 activation and inflammatory cytokine production. This knockout model is ideal for studying pH-dependent adaptation in melanoma and GPCR signaling in the acidic tumor microenvironment. Typical applications include cancer biology, pH sensing, melanoma research, and drug target validation, with assays such as phospho-ERK1/2 western blotting, cAMP measurement, migration/invasion studies, apoptosis assays, and RNA-seq for inflammatory gene expression profiling.
CA9 Knockout A2780 Polyclonal Cells
Cat. No. ARG35240
BMP2 Knockout A2780 Polyclonal Cells
Cat. No. ARG35238
ANLN Knockout Hela Polyclonal Cells
Cat. No. ARG37657
CCDC85C Knockout MES-OV Polyclonal Cells
Cat. No. ARG43087
CALHM2 Knockout KYSE30 Polyclonal Cells
Cat. No. ARG41854
CAB39 Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG41704
The GPR4 Knockout SK-MEL-28 Cell Line is a CRISPR/Cas9-edited knockout cell line that enables targeted disruption of the GPR4 gene in the SK-MEL-28 human cutaneous melanoma cell line. This loss-of-function knockout model provides a defined genetic background for investigating the role of proton-sensing G protein-coupled receptor (GPCR) signaling in melanoma biology, eliminating endogenous GPR4 expression to allow precise functional characterization of pH-sensing mechanisms.
The SK-MEL-28 host cell line, derived from a male patient with malignant melanoma, is an adherent human cell line widely utilized in melanoma research. It retains characteristic features of metastatic melanoma, including dysregulated proliferation, migration, and invasive capacity, making it an appropriate platform for dissecting the molecular mechanisms that drive tumor progression and for performing comparative studies alongside other melanoma models.
GPR4 functions as a proton-sensing GPCR activated by extracellular acidic pH, coupling to multiple G proteins including Gs, Gi/o, Gq/11, and G12/13. Gs-mediated activation of adenylyl cyclase increases intracellular cAMP and PKA activity, while G12/13 stimulates RhoA/ROCK signaling; both converge on ERK1/2 phosphorylation and transcriptional upregulation of inflammatory cytokines IL-6 and IL-8. Interacting factors such as ??-arrestins modulate receptor trafficking. Representative pathway components??G??s, adenylyl cyclase, PKA, ERK1/2, RhoA, and ROCK??form a signaling network that translates acidic microenvironments into cellular responses.
In the context of SK-MEL-28 melanoma cells, GPR4 serves as a critical mediator for adaptation to the acidic tumor microenvironment, a hallmark of solid tumors. Disruption of GPR4 abrogates pH-dependent cAMP production, ERK1/2 phosphorylation, and inflammatory cytokine expression, offering a robust model to assess how proton sensing contributes to melanoma cell proliferation, migration, and inflammatory phenotypes. This knockout cell line enables dissection of pH-regulated signaling pathways distinct from other acid-sensing mechanisms.
This GPR4 knockout cell line supports diverse research applications, including cancer biology, tumor microenvironment pH sensing, GPCR signaling interrogation, melanoma research, and drug target validation. Representative experimental assays include western blotting for phospho-ERK1/2, cAMP accumulation measurements, cell migration and invasion assays, pH-dependent signaling analyses, immunofluorescence for GPR4 localization, apoptosis assessment, and RNA sequencing for inflammatory gene expression profiling. These techniques facilitate detailed mechanistic studies and preclinical evaluation of pH-sensitive pathways. For further information, please contact Ascent Research.
