In Stock Cell Lines
The MIR31 Knockout IPEC-J2 Cell Line is a CRISPR/Cas9-edited porcine intestinal epithelial model with targeted disruption of the MIR31 gene, encoding miR-31. Derived from non-transformed IPEC-J2 cells, it abolishes miR-31-mediated silencing of targets such as LATS2 and PPP2R2A, derepressing tumor-suppressive and anti-inflammatory pathways downstream of NF-??B and Wnt/??-catenin. This cell line is designed for investigations of intestinal barrier integrity, inflammatory bowel disease, host-microbe interactions, and colorectal cancer. Researchers can apply RT-qPCR, Western blotting, luciferase assays, TEER measurement, and permeability studies to explore miR-31-dependent mechanisms in the gut epithelium.
PDE6D Knockout A2780 Polyclonal Cells
Cat. No. ARG18728
LRRC8D Knockout HT29 Polyclonal Cells
Cat. No. ARG14072
HSPA4L Knockout 786-O Polyclonal Cells
Cat. No. ARG25297
HPCAL1 Knockout huh-7 Polyclonal Cells
Cat. No. ARG28327
MAP4K3 Knockout HCT116 Polyclonal Cells
Cat. No. ARG7304
CLTA Knockout 786-O Polyclonal Cells
Cat. No. ARG5350
The MIR31 Knockout IPEC-J2 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from porcine intestinal epithelial IPEC-J2 cells, engineered to disrupt the MIR31 gene encoding microRNA-31 (miR-31). This model abolishes miR-31-mediated post-transcriptional silencing, enabling study of de-repressed target mRNAs and downstream effects on proliferation, apoptosis, and inflammatory signaling. Applicable to cancer biology, inflammatory bowel disease, and epithelial barrier research.
The parental IPEC-J2 line is a non-transformed, differentiated porcine jejunal epithelial cell line maintaining polarized monolayer formation, tight junctions, and enterocyte-specific functions. It serves as an authentic in vitro model for swine intestinal barrier integrity, nutrient transport, and immune responses. Its retention of epithelial characteristics ensures physiological relevance for gene-edited derivatives used in host-microbe interaction and mucosal immunology studies.
miR-31 post-transcriptionally represses target mRNAs by binding 3??UTRs, with validated targets including tumor suppressors LATS2 and PPP2R2A, adaptor DOCK1, hydroxylase FIH-1, and Wnt antagonist DKK1. Its expression is induced by NF-??B, STAT3, IL-6, and hypoxia, and it functions within the RISC via AGO2 and TNRC6A. Consequently, miR-31 influences NF-??B (IKK??/??, I??B??, p65), Wnt/??-catenin (??-catenin, TCF4), MAPK/ERK, PI3K/Akt, and JAK-STAT pathways, thereby regulating proliferation, apoptosis, and inflammatory responses.
In IPEC-J2 cells, MIR31 knockout derepresses target mRNAs, potentially strengthening barrier integrity and attenuating inflammation. Relief of LATS2 and PPP2R2A repression promotes cell cycle arrest, while reduced DKK1 silencing enhances Wnt-driven epithelial renewal. Loss of miR-31??s inhibition on NF-??B components may modulate innate immune responses. This cell line enables dissection of miR-31??s role in tight junction regulation, cytokine signaling, and epithelial homeostasis under pathological challenges.
This cell line supports intestinal barrier studies via TEER and junctional immunofluorescence, inflammatory signaling analyses by Western blotting, ELISA, and flow cytometry, and host-microbe interaction assays. It is suitable for cancer biology (colorectal, gastric), drug transport/permeability assays, and combined with dual-luciferase reporter assays and RNA-seq for transcriptome-wide insights. For additional information, technical support, or custom inquiries, please contact Ascent Research.
