In Stock Cell Lines
Homo sapiens (Human)
Blood (peripheral blood)
Suspension
The HTR2B Knockout HL-60 Cell Line is a CRISPR/Cas9-edited knockout model that disrupts the serotonin 2B receptor gene in human promyelocytic leukemia cells. This loss-of-function tool enables dissection of HTR2B-mediated Gq/11-PLC-??-calcium signaling and MAPK/ERK cascades in a leukemia-relevant context. Key downstream targets include PLC-??, ERK1/2, and the transcription factors FOS and JUN. Applications encompass calcium flux assays using Fluo-4, phospho-ERK ELISA, MTT proliferation assays, and transwell migration studies. These enable investigation of serotonin receptor roles in acute myeloid leukemia pathology and related conditions such as valvular heart disease, pulmonary hypertension, and fibrotic disorders.
LRRC8C Knockout K562 Polyclonal Cells
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PATL1 Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG15381
BLOC1S5 Knockout 786-O Polyclonal Cells
Cat. No. ARG25091
BRI3BP Knockout A549 Polyclonal Cells
Cat. No. ARG31962
PGRMC2 Knockout Raji Polyclonal Cells
Cat. No. ARG1204
Human Ocular Choroid Fibroblasts
Cat. No. ARP0122
The HTR2B Knockout HL-60 Cell Line is a CRISPR/Cas9-edited knockout model that disrupts the HTR2B gene, encoding the 5-HT2B serotonin receptor. Derived from the human promyelocytic leukemia cell line HL-60, this stable loss-of-function tool enables detailed investigation of serotonin receptor-mediated signaling in leukemia biology. This knockout cell line provides a critical platform for exploring serotonin-dependent processes in leukemic cells, including proliferation and differentiation.
HL-60 cells are a well-characterized human promyelocytic leukemia line, originally derived from a patient with acute promyelocytic leukemia. They are extensively employed to study the molecular mechanisms governing myeloid differentiation, cell cycle regulation, and apoptosis. Their ability to differentiate into macrophage- or neutrophil-like cells upon chemical induction makes them a versatile model for hematopoietic research.
HTR2B is a G protein-coupled receptor that, upon serotonin (5-HT) binding, activates G??q/11. This stimulates phospholipase C-?? (PLC-??), generating IP3 and DAG, which mobilize intracellular Ca2+ and activate protein kinase C (PKC). Downstream, the MAPK/ERK cascade is engaged, with ERK1/2 phosphorylating transcription factors FOS and JUN. ??-arrestin also interacts with the receptor to modulate signaling. The core pathway includes HTR2B, GNAQ, PLCB1, PRKCA, and MAPK1.
In HL-60 cells, serotonin/HTR2B signaling influences proliferation and survival, though precise roles remain undefined. Knockout of HTR2B eliminates serotonin-induced calcium transients and MAPK activation, providing a clean background to study receptor-specific effects. This model is pertinent for investigating acute myeloid leukemia pathology and links to HTR2B-associated disorders such as valvular heart disease, pulmonary hypertension, and fibrosis.
Researchers can leverage the HTR2B Knockout HL-60 Cell Line to perform quantitative calcium mobilization assays using Fluo-4 fluorescence, directly assessing receptor-mediated intracellular Ca2+ dynamics. Phospho-ERK ELISA or western blotting enables precise measurement of MAPK/ERK pathway activation, while MTT colorimetric assays quantify changes in cellular proliferation and viability. Flow cytometry facilitates multi-parametric analysis of differentiation markers and cell cycle distribution. Additionally, transwell migration assays can evaluate the receptor??s role in motility, and co-culture setups can dissect serotonin-dependent immune cell interactions. For technical support or licensing inquiries, please contact Ascent Research.
