In Stock Cell Lines
Homo sapiens (Human)
Kidney
Adherent
The C2orf76 Knockout HEK293T Cell Line is a CRISPR/Cas9-edited knockout cell line targeting the human C2orf76 gene, which encodes cartilage intermediate layer protein 2 (CILP2). This model enables functional investigation of CILP2 in TGF-?? signaling, extracellular matrix regulation, and osteoarthritis research using the versatile HEK293T host. CILP2 interacts with TGF-??, TGFBR1, and SMAD3, and modulates expression of ECM components such as COL2A1 and ACAN. The knockout line is suited for reporter gene assays, protein interaction studies, and signal transduction analysis, providing a clean loss-of-function background for mechanistic studies.
CAMK4 Knockout HAP1 Polyclonal Cells
Cat. No. ARG34863
B3GALT6 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG31307
KAT6B Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG30887
ECI2 Knockout MES-OV Polyclonal Cells
Cat. No. ARG40413
HIEC-6
Cat. No. ARP0995
Rabbit Oral Mucosal Fibroblasts
Cat. No. ARP0899
The C2orf76 Knockout HEK293T Cell Line is a CRISPR/Cas9-edited knockout cell line carrying a targeted disruption of the C2orf76 gene, which encodes the cartilage intermediate layer protein 2 (CILP2). This loss-of-function model enables researchers to directly interrogate the cellular roles of CILP2, particularly its involvement in transforming growth factor beta (TGF-??) signaling and extracellular matrix (ECM) regulation. The cell line provides a defined system for functional assays without the confounding presence of endogenous CILP2, facilitating mechanistic studies in signal transduction and matrix biology.
The host cell line, HEK293T, is a highly tractable human embryonic kidney epithelial derivative extensively used for recombinant protein expression, viral production, and signaling experiments. HEK293T cells were originally derived from HEK293 cells via stable integration of the SV40 large T antigen, which promotes episomal amplification of plasmids containing the SV40 origin of replication and supports high transfection efficiency. Their well-characterized molecular landscape includes expression of key TGF-?? pathway components such as TGFBR1, SMAD2, SMAD3, and SMAD4, making them an ideal platform for dissecting CILP2-mediated regulatory mechanisms.
C2orf76 encodes CILP2, a cartilage extracellular matrix protein that interacts with TGF-?? and its type I receptor TGFBR1, potentially inhibiting canonical TGF-?? signaling. This interaction may attenuate SMAD2/3 phosphorylation and downstream transcription of anabolic genes like COL2A1 and ACAN. Upstream regulators include TGFB1, BMPs, and mechanical stress, placing CILP2 at a regulatory node in cartilage homeostasis. Additional partners such as SMAD3 and collagen type II suggest a scaffold-like role in the pericellular matrix.
In the HEK293T background, knockout of C2orf76 removes a potential inhibitor of TGF-?? signaling, allowing researchers to assess the protein??s impact on pathway activity without chondrocyte-specific confounding factors. Although HEK293T cells are not cartilaginous, they retain the core TGF-?? signaling machinery and can be engineered to express cartilage-related genes. This model thus offers a simplified, manipulable system to delineate CILP2??s effects on SMAD-dependent transcription, receptor complex formation, and downstream target gene regulation. It is particularly advantageous for complementation studies where wild-type or mutant CILP2 is reintroduced.
Key applications include SMAD-responsive luciferase reporter assays to monitor TGF-?? pathway activity, co-immunoprecipitation to probe CILP2 complexes with TGFBR1 and SMAD3, and phospho-SMAD2/3 detection by Western blot or ELISA. The cell line also supports osteoarthritis research through ECM gene expression analysis and drug screening for TGF-?? modulators. For further details, contact Ascent Research.
