The HAX1 Knockout HEK293T Polyclonal Cells product provides a heterogeneous pool of HEK293T cells engineered via CRISPR/Cas9-mediated disruption of the HAX1 gene, creating a polyclonal loss-of-function model. This format avoids clonal artifacts and represents the full spectrum of genetic edits across the population, making it suitable for robust functional studies. The cells are supplied as a polyclonal population ready for expansion and downstream analysis, with each vial containing viable, gene-edited cells that can be directly incorporated into apoptosis, migration, and signaling experiments.
HEK293T cells originate from human embryonic kidney tissue and are stably transformed with adenovirus type 5 E1A/E1B genes and the SV40 large T antigen. This immortalization imparts high proliferative capacity, ease of transfection, and efficient episomal plasmid replication, establishing HEK293T as a premier cell line for protein expression, viral packaging, and biochemical assays. Their epithelial morphology and genetic tractability make them particularly useful for studying signal transduction and cell survival mechanisms in a well-characterized background.
HAX1 is an anti-apoptotic protein that preserves mitochondrial membrane potential and inhibits caspase activation, thereby promoting cell survival. It is regulated by cytokines such as IL-3 and GM-CSF, and by Akt kinase within the PI3K/Akt pathway. HAX1 interacts with HCLS1 and cortactin to coordinate cell migration and endocytosis, and it influences downstream effectors including Bcl-2 family proteins and caspases. Through its association with the PI3K/Akt/NF-kappaB axis, HAX1 integrates growth factor signals to sustain mitochondrial integrity and block apoptotic initiation, functioning as a critical node in survival regulation.
Disruption of HAX1 in HEK293T cells impairs anti-apoptotic defenses, rendering the cells more susceptible to mitochondrial depolarization and death stimuli. This knockout model enables precise dissection of HAX1??s contributions to Akt-dependent survival, integrin-mediated adhesion, and NF-kappaB-driven transcription. Given HEK293T??s widespread use in signaling research, the polyclonal knockout population offers a physiologically relevant context to explore HAX1-related pathologies such as severe congenital neutropenia (Kostmann disease) and cancers including breast cancer and leukemia, where HAX1 dysregulation alters cell fate.
Typical applications include apoptosis analyses via Annexin V flow cytometry, mitochondrial membrane potential measurement with JC-1 dye, and cell viability assays under stress conditions. Co-immunoprecipitation and western blotting evaluate interactions with HCLS1, cortactin, or polycystin-2, while transwell migration and invasion assays assess cytoskeletal functions. These cells also support RT-qPCR and signaling studies of PI3K/Akt/NF-kappaB pathway dynamics. This versatile tool facilitates fundamental research into apoptotic regulation and translational investigation of congenital neutropenia and cancer cell survival. For further information or custom requests, please contact Ascent Research.
