The HNRNPAB Knockout HAP1 Polyclonal Cells product offers a CRISPR/Cas9-edited polyclonal knockout cell population targeting HNRNPAB in the near-haploid human HAP1 cell line. This heterogeneous population, generated by CRISPR/Cas9-mediated gene disruption, contains cells with diverse loss-of-function alleles, enabling pooled knockout studies without single-cell cloning. It is ideal for functional genomics screens where a mixed knockout population suffices.
The HAP1 cell line is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) line of a male blast crisis patient. Its near-haploid karyotype simplifies genetic analyses, as most genes are present in a single copy, reducing compensatory effects and facilitating genotype-phenotype correlations. HAP1 cells retain CML signaling pathways, providing a disease-relevant milieu for studying RNA-binding protein functions in cancer.
HNRNPAB is an RNA-binding protein that regulates alternative splicing, mRNA transport, stability, and translation. It interacts with spliceosomal components (U1 snRNP, U2AF), other hnRNPs (HNRNPA1, HNRNPC), RNA polymerase II, and splicing factors such as SRSF1 and TDP-43. Upstream regulators include MAP kinase signaling, SR protein kinases, MYC, and arginine methylation. Downstream, HNRNPAB controls splicing of targets like BCL-X and VEGF, and mRNAs encoding cell cycle regulators, thereby integrating signaling cues to modulate gene expression.
Disruption of HNRNPAB in the HAP1 CML background likely impairs splicing and metabolism of proliferation- and stress-related transcripts. Given HNRNPAB overexpression in breast, lung, and colorectal tumors, this model enables dissection of RNA processing aberrations in cancer. The near-haploid genome simplifies target identification and validation, and the leukemic origin provides insight into splicing dysregulation in hematological malignancies.
This polyclonal knockout population is suited for splicing analysis via RNA-seq and RT-qPCR, protein interaction studies by RIP and co-IP, and functional assays including splicing reporter and proliferation assays. It supports research into alternative splicing, cancer biology, functional genomics, drug target validation, and neurological disease modeling. For further details, contact Ascent Research.
