The BSDC1 Knockout HAP1 Polyclonal Cells product provides a polyclonal population of CRISPR/Cas9-edited HAP1 cells with targeted disruption of the BSDC1 gene. This polyclonal knockout model offers a genetically heterogeneous loss-of-function pool, avoiding clonal biases and enabling robust functional studies. CRISPR/Cas9-mediated gene disruption abrogates BSDC1 expression, facilitating investigation of this uncharacterized BSD domain-containing protein.
HAP1 is a near-haploid human chronic myeloid leukemia (CML) cell line derived from the KBM-7 line, widely adopted as a model system for functional genomics. Its haploid nature facilitates the generation and phenotypic readout of gene knockouts by ensuring that a single disruption event leads to complete loss of function. HAP1 cells retain myelomonocytic characteristics, making them suitable for studies in hematopoietic cell biology and cancer-relevant signaling pathways.
BSDC1 encodes a BSD (BTF2-like transcription factors, Synapse-associated, DOS2-like) domain protein, a motif typically involved in metal ion coordination or nucleic acid binding. BSD domain proteins often participate in transcriptional regulation, though the precise role of BSDC1 remains unknown. Based on domain homology, BSDC1 may interact with DNA or metal cofactors to modulate transcription, but no validated upstream regulators, downstream targets, or binding partners have been reported, highlighting the need for unbiased functional studies.
In the near-haploid HAP1 background, BSDC1 disruption can unmask phenotypes obscured by diploid redundancy. This model supports systematic investigation of BSDC1’s functions in proliferation, apoptosis, and transcriptional control. The polyclonal population encompasses a range of mutations, providing a comprehensive loss-of-function resource for drug sensitivity profiling and genetic interaction screens.
Typical applications include RNA-seq for transcriptional profiling to identify gene expression changes upon BSDC1 loss, and protein-binding assays (e.g., pull-downs, mass spectrometry) to discover interacting partners. Phenotypic assays measuring proliferation and apoptosis reveal functional consequences, while Western blotting and RT-qPCR confirm knockout at protein and mRNA levels. This product empowers researchers to define the molecular role of BSDC1 in metal-dependent transcriptional regulation. For further information, please contact Ascent Research.
