In Stock Cell Lines
Homo sapiens (Human)
Kidney
Adherent
The SOX9 Knockout HEK293 Cell Line is a CRISPR/Cas9-edited knockout model derived from human embryonic kidney HEK293 cells, designed for loss-of-function studies of the SOX9 transcription factor. SOX9 is a master regulator of chondrogenesis and sex determination, activated by TGF-??/BMP and Wnt signaling and functioning through interactions with SOX5, SOX6, and other cofactors to control extracellular matrix genes such as COL2A1 and ACAN. This cell line is ideal for investigating SOX9-dependent pathways in cancer, developmental biology, and osteoarthritis, and for screening therapeutic modulators of SOX9 activity. With its epithelial background and ease of transfection, the SOX9 Knockout HEK293 Cell Line supports a range of assays including RT-qPCR, ChIP, luciferase reporter, and co-immunoprecipitation experiments, providing a robust platform for dissecting SOX9 biology in health and disease.
GNAI2 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG18070
LDHC Knockout SK-Hep-1 Polyclonal Cells
Cat. No. ARG15387
CRADD Knockout Hela Polyclonal Cells
Cat. No. ARG7943
AIP Knockout HAP1 Polyclonal Cells
Cat. No. ARG37013
PFKP Knockout HEK293T Polyclonal Cells
Cat. No. ARG4528
CHST14 Knockout AGS Polyclonal Cells
Cat. No. ARG2320
The SOX9 Knockout HEK293 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the widely used HEK293 human embryonic kidney epithelial line, designed to disrupt expression of the SOX9 gene. This loss-of-function model provides a genetically defined system for investigating SOX9-dependent biological processes, enabling precise dissection of its transcriptional networks and signaling interactions in a robust cellular context.
HEK293 cells are a transformed cell line with adenovirus 5 DNA integration, exhibiting epithelial morphology and rapid growth. They are a standard host for recombinant protein production, viral packaging, and transfection experiments due to their high transfectability and ease of culture. This background makes the SOX9 knockout line an accessible tool for a broad range of molecular and cellular analyses.
SOX9 encodes a master transcription factor of the SRY-related HMG-box family, crucial for chondrogenesis, sex determination, and stem cell pluripotency. It is activated by TGF-?? and BMP ligands through SMAD2/3/4 signaling, and by Wnt ligands via ??-catenin/TCF/LEF complexes, with additional inputs from FGFs, PTHrP, and Hedgehog pathway GLI effectors. SOX9 directly binds promoters of target genes such as COL2A1 and ACAN and cooperates with SOX5 and SOX6 to activate cartilage-specific enhancers. Interacting partners include RUNX2, SMAD3, ??-catenin, PGC-1??, and CREB-binding protein, integrating signals from MAPK/ERK (ERK1/2) and cAMP/PKA pathways. Downstream, it regulates extracellular matrix components like COL10A1, HAPLN1, and MATN1, while crosstalk with Notch (NOTCH1/NICD) further modulates cell fate.
In the HEK293 epithelial background, this knockout provides a simplified system to study SOX9 function without the complexity of chondrogenic lineage. It enables dissection of how SOX9 integrates multiple signaling cascades in a non-chondrogenic context, mimicking loss-of-function phenotypes relevant to campomelic dysplasia and 46,XY sex reversal. Moreover, the model offers a platform to explore SOX9’s roles in colorectal cancer progression, cancer stemness, and osteoarthritis pathobiology, where its dysregulation contributes to disease.
Researchers can employ this cell line in diverse assays: RT-qPCR and RNA-seq reveal transcriptome-wide changes in SOX9 targets; ChIP-qPCR maps DNA-binding sites without endogenous interference; luciferase reporters (e.g., COL2A1-driven) quantify SOX9 activity upon reintroduction; co-immunoprecipitation readily detects interactions with SOX5, SOX6, or SMAD3; immunofluorescence assesses subcellular localization; and drug screening can target upstream modulators of TGF-??/BMP or Wnt pathways for osteoarthritis therapies. For further information and technical support, please contact Ascent Research.
