In Stock Cell Lines
Homo sapiens (Human)
Blood (peripheral blood)
Suspension
The FSHR Knockout THP-1 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from human THP-1 monocytic leukemia cells. It provides a loss-of-function model for follicle-stimulating hormone receptor (FSHR), a G protein-coupled receptor that activates cAMP/PKA and PI3K/AKT pathways upon FSH binding, regulating downstream effectors such as CREB and CYP19A1. This knockout model enables investigation of FSH signaling in monocyte/macrophage activation, cytokine production, and phagocytosis, facilitating studies on reproductive-immune crosstalk. Key applications include western blotting, cAMP accumulation assays, and cytokine ELISA. It is a valuable tool for immunology, endocrinology, and extragonadal tumor research.
NOTCH3 Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG16207
PCMTD1 Knockout Hela Polyclonal Cells
Cat. No. ARG7965
ASF1A Knockout HT29 Polyclonal Cells
Cat. No. ARG33059
DMXL1 Knockout 786-O Polyclonal Cells
Cat. No. ARG39006
H2AJ Knockout HEK293T Polyclonal Cells
Cat. No. ARG38231
EEF2K Knockout HEK293 Polyclonal Cells
Cat. No. ARG40583
The FSHR Knockout THP-1 Cell Line is a CRISPR/Cas9-edited knockout cell line engineered to disrupt the FSHR gene in the THP-1 human acute monocytic leukemia cell line. This product delivers a robust loss-of-function model for studying follicle-stimulating hormone receptor biology in a monocytic context. CRISPR/Cas9-mediated gene disruption ablates functional FSHR expression, enabling precise dissection of receptor-dependent signaling events without the variability of transient silencing methods.
THP-1 is a well-characterized human acute monocytic leukemia cell line used extensively as a model for monocyte and macrophage differentiation, activation, and immune function. Phorbol ester treatment induces macrophage-like differentiation, facilitating studies of phagocytosis, cytokine production (e.g., TNF-??, IL-6), and intracellular signaling.
FSHR encodes a G protein-coupled receptor for follicle-stimulating hormone (FSH). Ligand binding activates the Gs alpha subunit, which stimulates adenylate cyclase to produce cAMP. Elevated cAMP activates protein kinase A (PKA), leading to phosphorylation of the transcription factor CREB at Ser133. CREB drives expression of steroidogenic enzymes such as aromatase (CYP19A1) and STAR. FSHR also engages PI3K/AKT and MAPK/ERK pathways, resulting in phosphorylation of Akt at Ser473 and ERK1/2. Receptor regulation involves interacting factors such as beta-arrestins, APPL1, and 14-3-3 proteins. Together, these signaling networks control cellular proliferation, differentiation, and steroidogenic responses.
Introducing an FSHR knockout in the THP-1 monocytic lineage allows dissection of FSH-dependent signaling in immune cells. Emerging evidence suggests extragonadal FSHR expression and potential roles in monocyte/macrophage activation, cytokine release, and phagocytosis. This knockout model is well suited for exploring crosstalk between reproductive hormones and innate immunity and may help clarify FSHR contributions to inflammatory diseases or extragonadal tumorigenesis.
Typical applications include cAMP accumulation assays, western blotting for phospho-CREB (Ser133), phospho-Akt (Ser473), and phospho-ERK1/2, ELISA for cytokine secretion, phagocytosis assays, and flow cytometry for surface markers. The cell line supports drug target validation, mechanistic studies, and screening of FSHR modulators in an immune-relevant background. For further product details, please contact Ascent Research.
