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.
LYRM1 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG17169
MARCKS Knockout jurkat Polyclonal Cells
Cat. No. ARG12788
HPCAL1 Knockout HEK293T Polyclonal Cells
Cat. No. ARG26080
BATF3 Knockout KYSE150 Polyclonal Cells
Cat. No. ARG36218
KIAA1217 Knockout HAP1 Polyclonal Cells
Cat. No. ARG27680
DHX57 Knockout MES-OV Polyclonal Cells
Cat. No. ARG6100
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.
