The KRT19 Knockout DLD-1 Polyclonal Cells product provides a CRISPR/Cas9-mediated polyclonal knockout population of the KRT19 gene in the human DLD-1 colorectal adenocarcinoma cell line. As a heterogeneous pool of edited cells, this format preserves the spectrum of Cas9-induced mutations and avoids the selective bias of clonal derivation. The resulting loss-of-function model enables interrogation of keratin 19 biology in an epithelial cancer context without presupposing complete gene inactivation across the population.
The host DLD-1 cell line was established from a colorectal adenocarcinoma of a male patient at Dukes?? stage C. These epithelial cells harbor mutations in APC, KRAS, and TP53, reflecting the genetic landscape of advanced colorectal cancer. DLD-1 cells are extensively used to study cell adhesion, migration, invasion, and drug response. This well-characterized adenocarcinoma background offers a clinically relevant platform for dissecting KRT19 function.
KRT19 encodes a type I intermediate filament protein that heterodimerizes with keratin 8 (KRT8) to form cytoskeletal networks in simple epithelia. Its expression is controlled by upstream regulators such as TP63, TCF/LEF factors, NOTCH1, and EGF signaling, and it functions within a network comprising downstream targets KRT8, desmoplakin, and plectin. KRT19 engages with junctional complexes via interactions with desmoplakin, plectin, 14-3-3 proteins, and plakoglobin, and it connects to the E-cadherin/??-catenin adhesion system. Disruption of KRT19 is expected to impair intermediate filament organization, thereby influencing cell mechanics, adhesion, and signal transduction.
In DLD-1 cells, KRT19 knockout addresses the role of keratins in colorectal cancer progression, where KRT19 is commonly expressed. The polyclonal population allows study of heterogeneous phenotypic responses, which is relevant to tumor cell diversity. Loss of KRT19 may compromise mechanical resilience, adhesion, and migratory/invasive behavior, while also modulating responses to chemotherapeutic stress. This model is particularly suited for investigating EMT, as KRT19 sits at a node connecting cytoskeletal integrity to cell-cell contact signals.
Research applications include epithelial cell biology, metastasis, EMT, biomarker validation, and drug resistance studies. The cells are compatible with western blotting, immunofluorescence, transwell migration/invasion assays, cell adhesion experiments, drug sensitivity profiling, and RNA-seq. This polyclonal knockout resource offers a versatile platform for functional genomics and cancer cell biology. For further information, contact Ascent Research.
