CCHCR1 Knockout hTERT-RPE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the CCHCR1 gene has been disrupted. This product offers a heterogeneous loss-of-function model suitable for bulk functional analyses, enabling researchers to interrogate CCHCR1-dependent mechanisms without clonal selection artifacts. The polyclonal format captures a range of editing events, providing a robust system for studying gene function in a population context.
The host cell line, hTERT-RPE1, is a non-transformed, hTERT-immortalized human retinal pigment epithelial cell line. These cells maintain key features of primary RPE, including polarized epithelial morphology, primary cilia formation, phagocytic activity, and roles in nutrient transport and blood-retina barrier integrity. Widely employed in RPE biology, epithelial polarity, and ciliogenesis research, hTERT-RPE1 cells provide a physiologically relevant background for CCHCR1 knockout studies.
CCHCR1 encodes a coiled-coil alpha-helical rod protein that localizes to centrosomes and cilia, where it regulates cell cycle progression, cytoskeletal organization, and transcription. Mechanistically, CCHCR1 is activated by upstream regulators such as TNF-?? and IL-17, and it interacts with pericentrin, NF-??B subunits, and IFT88. Downstream of these signals, CCHCR1 modulates expression of cyclins, CDKs, and NF-??B target genes. Through these interactions, CCHCR1 mediates signaling downstream of TNFR and IL17R, influencing the NF-??B pathway and cell cycle control. Disruption of CCHCR1 alters centrosomal function, leading to aberrant proliferation and cytokine responses, as summarized: CCHCR1 localizes to centrosomes and cilia, modulating cell cycle progression and NF-??B signaling; its knockout disrupts centrosomal function and contributes to psoriasis pathogenesis.
In hTERT-RPE1 cells, CCHCR1 knockout holds particular significance for centrosome and cilia biology, given the cell line??s ciliogenic capacity and epithelial architecture. This model permits examination of ciliary assembly, basal body integrity, and the interplay between centrosomal proteins and inflammatory signaling. The RPE context further allows dissection of how CCHCR1 loss impacts epithelial homeostasis and responses to cytokines, with direct relevance to psoriasis and related inflammatory disorders.
This polyclonal knockout cell population supports diverse research applications in psoriasis, centrosome biology, ciliopathy studies, epithelial cell cycle regulation, and inflammatory signaling. Representative assays include Western blotting, immunofluorescence for centrosome/cilia markers (e.g., pericentrin, acetylated tubulin), RT-qPCR, cell cycle flow cytometry, migration/invasion assays, and drug sensitivity studies with NF-??B inhibitors. RNA-seq analysis can further define transcriptional changes upon CCHCR1 disruption. For additional information, please contact Ascent Research.
