Cat. No. ARG43724
The Api5 Knockout MC38 Cell Line is a CRISPR/Cas9-edited murine colon adenocarcinoma cell line with disruption of the apoptosis inhibitor Api5. This model enables investigation of apoptosis resistance, colorectal cancer progression, and drug response in a syngeneic C57BL/6 background. Api5 suppresses caspase-3 and caspase-9 activation via Akt and NF-??B signaling, interacting with FGF2, Acinus, and CBP/p300. The knockout allows functional studies using Western blotting, flow cytometry, and cell viability assays, supporting research in cancer biology, drug resistance, and immune evasion.
| Host Cell | MC38 |
| Gene Name | API5 |
| Gene Identifier | NCBI Gene ID 11800 |
| Storage | Liquid nitrogen (LN2) |
| Temperature | 37°C |
| Atmosphere | 5% CO₂ |
| Sterility testing | The bacterial, yeast, and fungi are not detected in these cells by daily monitor. |
| Mycoplasma testing | Negative for mycoplasma through PCR analysis |
Intended Use: This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.
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This product is provided "AS IS". For Research Use Only. Not for human or animal therapeutic use.
The Api5 Knockout MC38 Cell Line is a CRISPR/Cas9-edited murine colon epithelial cell line carrying a targeted disruption of the Api5 gene. This loss-of-function model enables researchers to interrogate the functional role of Api5 in apoptosis regulation within a colorectal cancer background. The cell line is provided as a ready-to-use knockout cell line, facilitating direct integration into apoptosis and cancer signaling studies.
The MC38 parental cell line is a well-established C57BL/6-derived murine colon adenocarcinoma line extensively employed as a syngeneic model of colorectal cancer. These cells exhibit typical epithelial morphology and are immunocompetent in C57BL/6 recipients, making them particularly valuable for tumor immunology and immune evasion research. The MC38 model has been instrumental in evaluating immunotherapies and dissecting mechanisms of tumor progression.
Api5 (Apoptosis inhibitor 5) functions as a critical suppressor of apoptosis by blocking caspase activation downstream of survival signaling cascades. Mechanistically, Api5 is activated by upstream factors including EGF, FGF2, and serum growth factors through Akt and NF-??B pathways. It interacts with FGF2, Acinus, and the transcriptional coactivators CBP/p300 to suppress caspase-9 and caspase-3 activation. Additionally, Api5 modulates cell cycle progression by regulating Cyclin D1 expression and intersects with Bcl-2 family proteins. Thus, Api5 orchestrates a network that links growth factor signaling to apoptotic and cell cycle machineries.
Disruption of Api5 in the MC38 adenocarcinoma background provides a powerful system to dissect apoptosis resistance mechanisms inherent to colorectal cancer. The knockout is expected to abrogate Api5-mediated inhibition of caspases, thereby sensitizing cells to apoptotic stimuli and compromising pro-survival signals transduced through Akt and NF-??B. This model enables investigation of how Api5 loss affects tumor cell viability, clonogenic survival, and response to chemotherapeutic agents. Moreover, it allows exploration of interactions between apoptotic pathways and the tumor microenvironment in a syngeneic setting.
Researchers can employ this knockout cell line in diverse experimental paradigms, including Western blotting for cleaved caspase-3 and caspase-9, flow cytometry?Cbased Annexin V/PI apoptosis assays, cell viability measurements, colony formation analyses, and caspase activity assays. It serves as an ideal tool for studying apoptosis resistance, colorectal cancer progression, drug resistance mechanisms, and immune evasion. By pairing with the parental MC38 line, users can dissect Api5-dependent signaling networks and evaluate therapeutic strategies targeting survival pathways. For additional information and technical support, please contact Ascent Research.
