The H4C1 Knockout DLD-1 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population targeting the H4C1 gene in the DLD-1 human colorectal adenocarcinoma cell line. This gene disruption model employs transient Cas9 and guide RNA introduction to create a heterogeneous pool of edited alleles, resulting in a functional loss-of-function model for histone H4. The polyclonal format preserves the diversity of genetic alterations without single-cell cloning, enabling researchers to assess population-level effects of H4C1 deficiency on chromatin biology and cancer-associated processes.
DLD-1 is a widely characterized human colorectal adenocarcinoma cell line with an epithelial morphology. It harbors oncogenic mutations in KRAS (G13D) and TP53, reflecting common genetic lesions in colorectal cancer. This cell line is extensively utilized as an in vitro model for studying colorectal cancer cell proliferation, apoptosis, and drug sensitivity. The established culture conditions and well-documented molecular profile of DLD-1 provide a robust setting for investigating the functional roles of chromatin-related genes in tumorigenesis.
The H4C1 gene encodes histone H4, a core histone protein that constitutes the nucleosome along with H2A, H2B, and H3. During S phase, H4C1 transcription is activated by E2F transcription factors in cooperation with NPAT and HINFP, downstream of cyclin E/CDK2 signaling. Histone H4 is essential for nucleosome assembly and chromatin fiber stability. It interacts with histone chaperones ASF1 and CAF-1 during DNA replication and repair, and is targeted by chromatin remodeling complexes like SWI/SNF and histone-modifying enzymes that regulate chromatin accessibility and epigenetic gene expression.
Disruption of H4C1 in DLD-1 cells is expected to impair nucleosome assembly, leading to global chromatin decompaction and altered epigenetic landscapes. Given the critical role of histone H4 in chromatin integrity, the knockout model may exhibit defects in DNA replication, DNA repair, and cell cycle progression. In the context of a colorectal adenocarcinoma background with mutant KRAS and TP53, H4C1 loss can synergistically perturb oncogenic transcriptional programs and tumor cell phenotypes, offering a valuable tool to dissect how epigenetic mechanisms intersect with established cancer driver mutations to influence proliferation, survival, and drug responses.
This polyclonal knockout cell population is suited for epigenetic regulation studies, chromatin biology, and colorectal cancer research. Assays such as western blotting, RT-qPCR, ChIP, and ATAC-seq can characterize histone levels and chromatin state. RNA-seq enables transcriptomic profiling. Functional assays??including flow cytometry for cell cycle, MTT or BrdU proliferation, Annexin V apoptosis, and colony formation??support drug screening for epigenetic therapies. For further information, please contact Ascent Research.
