The HABP4 Knockout HEK293T Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the HABP4 gene in the HEK293T host cell line. This heterogeneous cellular model provides a versatile loss-of-function tool for studying HABP4 biology, as the polyclonal composition encompasses diverse gene-editing outcomes and reduces the influence of clonal bias, making it ideal for robust functional analyses at the population level.
The HEK293T cell line is a widely used human embryonic kidney epithelial line transformed with SV40 large T-antigen, known for high transfection efficiency, rapid growth, and extensive application in protein expression and viral production. Its epithelial origin and well-characterized signaling networks??including active TP53 and PKC pathways??make it an appropriate host for investigating nuclear regulatory proteins like HABP4. The presence of SV40 T-antigen provides a unique context for exploring interplay with p53-dependent processes.
HABP4 encodes a nuclear hyaluronan-binding protein that acts as a transcriptional co-regulator engaged in cell cycle control, apoptosis, and DNA repair. It functions within the p53 signaling cascade: phosphorylated by PRKCA, HABP4 forms complexes with CHD3 and SART3 to modulate TP53-mediated transcription of target genes including CDKN1A (p21) and BAX. Additionally, HABP4 interacts with PRKDC, linking it to DNA damage response pathways. Through these interactions, HABP4 integrates PKC signaling and hyaluronan cues to regulate TP53-dependent transcription, influencing cell cycle arrest and apoptotic execution.
Knockout of HABP4 in HEK293T cells enables dissection of its co-regulatory function within an epithelial context that endogenously expresses relevant pathway components such as TP53, PRKCA, CHD3, and SART3. This polyclonal knockout model allows systematic evaluation of how HABP4 disruption alters cell cycle distribution, apoptotic sensitivity, and transcriptional responses downstream of TP53. Moreover, the partial inactivation of p53 by SV40 T-antigen offers a distinctive setting to study HABP4??s role under conditions that mimic certain tumor contexts, enhancing the relevance for cancer research.
Applications include cancer biology, particularly glioma research, as well as studies of DNA damage signaling, transcriptional regulation, and cell cycle dynamics. Researchers can employ standard techniques such as Western blotting, RT-qPCR for CDKN1A and BAX transcripts, immunofluorescence, flow cytometry for cell cycle and apoptosis assays, and reporter gene assays to probe HABP4-dependent molecular events. This product enables detailed mechanistic investigation of the HABP4-PRKCA-TP53 signaling axis. For inquiries, contact Ascent Research.
