The CC2D1A Knockout A-549 Polyclonal Cells product offers a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A-549 lung adenocarcinoma cell line. This model features disruption of the CC2D1A gene, which encodes a transcriptional repressor implicated in NF-??B and Notch signaling pathways. The polyclonal format provides a heterogeneous knockout population suitable for studying loss-of-function effects without clonal selection artifacts. Researchers can utilize this system to dissect CC2D1A??s roles in transcriptional regulation, inflammatory responses, and cancer-relevant signaling networks within an established epithelial context.
The A-549 cell line is a widely used model originating from the lung adenocarcinoma tissue of a 58-year-old Caucasian male. These adherent epithelial cells exhibit characteristics of human alveolar type II pneumocytes and are commonly employed in studies of drug metabolism, respiratory infection, and oncogenic signaling. The A-549 background maintains key features such as expression of surfactant proteins and metabolic enzymes, facilitating physiologically relevant investigations. The integration of CC2D1A knockout into this well-characterized lung cancer cell line enables interrogation of the gene??s impact on NF-??B and Notch pathways in a disease-relevant setting, particularly regarding lung adenocarcinoma biology and inflammatory microenvironments.
CC2D1A functions as a transcriptional repressor through direct interaction with the p65 (RELA) subunit of NF-??B, inhibiting its nuclear translocation and subsequent transcriptional activation of pro-inflammatory targets such as IL-6, TNF, and BCL2. It also associates with NOTCH1 to modulate Notch signaling, influencing downstream effectors like HES1 and MYC. Additionally, CC2D1A recruits a co-repressor complex containing PIAS1 and HDAC1 to the promoter of HTR1A, repressing serotonin 5-HT1A receptor expression. Upstream regulators include TNF-??, IL-1??, and Notch ligands JAG1 and DLL1. Through these interactions, CC2D1A integrates signals from inflammatory and developmental pathways, positioning it as a node at the intersection of NF-??B, Notch, and serotonin receptor signaling cascades.
In the A-549 context, CC2D1A knockout offers a valuable platform to investigate the gene??s regulatory influence on NF-??B-driven processes relevant to lung cancer and inflammation. Given that A-549 cells exhibit basal NF-??B activity and respond to TNF-?? stimulation, this model is particularly suited for studying how CC2D1A loss affects pro-inflammatory cytokine production, apoptosis, and cell survival. Furthermore, the interaction with NOTCH1 and potential impact on epithelial?Cmesenchymal transition and cancer stemness can be explored. While primarily used for cancer and immunology research, the well-conserved signaling modules also make this model useful for dissecting molecular mechanisms that may have implications in neurodevelopmental disorders, where CC2D1A mutations are linked to intellectual disability and autism.
This polyclonal knockout product is ideal for a range of experimental applications, including western blot analysis of NF-??B targets and CC2D1A, NF-??B luciferase reporter assays, qRT-PCR for HTR1A and cytokines, and immunofluorescence to monitor p65 subcellular localization. Co-immunoprecipitation experiments can assess interactions with RELA and NOTCH1, while Notch reporter assays probe transcriptional outputs. Functional studies may include apoptosis, proliferation, migration, and invasion assays, as well as cytokine ELISAs to quantify inflammatory mediators. Overall, this model supports investigations into NF-??B regulation, Notch mechanism, serotonin receptor biology, and lung cancer signaling. For further technical details or inquiries, please contact Ascent Research.
