In Stock Cell Lines
The Sema4d Knockout AML12 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from non-transformed mouse AML12 hepatocytes, with targeted disruption of Sema4d. It abolishes Semaphorin-4D function, which normally signals through Plexin B1 to activate RhoA/ROCK and PI3K/Akt pathways, regulating hepatocyte migration, proliferation, survival, and fibrogenic responses. This model enables detailed study of liver fibrosis mechanisms, hepatocellular carcinoma, wound healing, and drug-induced hepatotoxicity, using techniques such as Western blotting, migration assays, phospho-Akt/ERK analysis, and co-immunoprecipitation, offering a robust system for hepatic signal transduction research.
MEIS1 Knockout jurkat Polyclonal Cells
Cat. No. ARG13220
AKAIN1 Knockout HAP1 Polyclonal Cells
Cat. No. ARG21763
ACAA2 Knockout A549 Polyclonal Cells
Cat. No. ARG27210
JPH1 Knockout AGS Polyclonal Cells
Cat. No. ARG27089
PHACTR4 Knockout Hela Polyclonal Cells
Cat. No. ARG7538
MORC2 Knockout 786-O Polyclonal Cells
Cat. No. ARG5264
The Sema4d Knockout AML12 Cell Line is a CRISPR/Cas9-mediated gene-disrupted cell line derived from the AML12 mouse hepatocyte line, eliminating functional expression of Sema4d. This loss-of-function model allows dissection of Semaphorin-4D (CD100) roles in hepatic biology.
AML12 cells are non-transformed mouse hepatocytes from transgenic mice expressing human TGF-alpha. They retain metabolic, secretory, and detoxification functions, offering a physiologically relevant system for studying liver parenchymal cell processes, including fibrogenesis and injury responses, without oncogenic transformation.
Sema4d encodes Semaphorin-4D (CD100), a transmembrane ligand that primarily engages Plexin B1 (PLXNB1) on hepatocytes. This interaction triggers RhoA/ROCK and PI3K/Akt signaling cascades, which coordinate cell migration, proliferation, and survival. Additionally, Sema4D crosstalks with MAPK/ERK and TGF-?? pathways, integrating inputs from upstream regulators like TGF-??, inflammatory cytokines, hypoxia, and growth factors. Downstream targets include RhoA, ROCK, Akt, ERK, and PI3K, while interacting factors such as CD72 and MET receptor tyrosine kinase further diversify its signaling repertoire. Through these networks, Sema4D regulates cytoskeletal dynamics and transcriptional programs essential for hepatocyte behavior.
In the liver, Sema4D signaling through Plexin B1-RhoA/ROCK promotes hepatic stellate cell activation and fibrogenesis. Knocking out Sema4d in AML12 cells provides a clean system to investigate how loss of this semaphorin disrupts fibrotic cascades and hepatocyte survival, modeling aspects of fibrosis, cirrhosis, and hepatocarcinogenesis.
The Sema4d Knockout AML12 Cell Line is a versatile tool for studying liver fibrosis mechanisms, hepatocellular carcinoma progression, hepatocyte migration and wound healing, and drug-induced hepatotoxicity. Researchers can perform a range of biochemical and functional assays, including Western blotting and RT-qPCR for gene expression analysis, phospho-Akt/ERK signaling analysis, migration/invasion assays, immunofluorescence, apoptosis assays, and co-immunoprecipitation for protein interaction mapping. Flow cytometry enables phenotypic profiling, while genetic and pharmacological interventions can be combined to explore semaphorin pathways. This model accelerates target validation and drug screening. For further technical information, please contact Ascent Research.
