Genome-edited Cells
Gastrointestinal (GI) tract
The CSDE1 Knockout GIST-T1 Cell Line is a CRISPR/Cas9-edited knockout cell line from the GIST-T1 cell line, a human gastrointestinal stromal tumor model with a KIT exon 11 deletion. It disrupts the CSDE1 RNA-binding protein, which modulates targets including c-FOS and PTEN mRNAs and interacts with UPF1 and PABP, linking it to MAPK/ERK and PI3K/AKT pathways. This knockout cell line is ideal for investigating post-transcriptional regulation in cancer, assessing proliferation and apoptosis, and performing assays such as Western blotting, RT-qPCR, RIP, and dual-luciferase reporter assays. It supports studies on GIST tumor biology, drug screening, and RNA regulatory mechanisms.
PDCD2 Knockout THP-1 Polyclonal Cells
Cat. No. ARG7411
HMMR Knockout HEK293T Polyclonal Cells
Cat. No. ARG26073
LIPT2 Knockout Hela Polyclonal Cells
Cat. No. ARG7804
MVD Knockout MES-OV Polyclonal Cells
Cat. No. ARG6037
MCTS1 Knockout 786-O Polyclonal Cells
Cat. No. ARG4675
OR1M1 Knockout HEK293T Polyclonal Cells
Cat. No. ARG3625
The CSDE1 Knockout GIST-T1 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the GIST-T1 human gastrointestinal stromal tumor (GIST) cell line. It features a loss-of-function mutation in the CSDE1 gene, generated via CRISPR/Cas9-mediated gene disruption. This model enables functional studies of the CSDE1 RNA-binding protein in a KIT-mutant, tumorigenic mesenchymal background, providing a platform to investigate post-transcriptional regulatory mechanisms in cancer.
GIST-T1 is an established cell line from a human GIST harboring an activating KIT exon 11 deletion (V560_Y578del), driving constitutive MAPK/ERK and PI3K/AKT signaling. Widely used in GIST research, these cells recapitulate the oncogenic properties of the disease and serve as a relevant host for examining the impact of CSDE1 knockout on KIT-dependent pathways.
CSDE1 (UNR) is an RNA-binding protein that interacts with PABP, UPF1, eIF4G, and PAIP1 to regulate mRNA stability and translation. It acts as a translational repressor or activator and participates in nonsense-mediated mRNA decay and IRES-mediated translation. CSDE1 is regulated by AKT phosphorylation and the MAPK/ERK pathway, with miR-125b modulating its expression. It controls key targets including c-FOS, c-JUN, PTEN, and BCL2 mRNAs, linking it to cell proliferation, apoptosis, and cell cycle progression.
In GIST-T1 cells, where KIT mutation aberrantly activates downstream signaling, CSDE1 knockout may disrupt post-transcriptional control of oncogenes and tumor suppressors. Altered expression of targets such as c-FOS and PTEN can impact MAPK/ERK and PI3K/AKT network output, influencing proliferation and survival. This model thus allows dissection of how RNA-binding protein function intersects with kinase-driven oncogenesis in GIST.
This cell line is suitable for target validation by Western blotting and RT-qPCR, protein?CRNA interaction studies via RIP, IRES activity analysis using dual-luciferase reporters, and functional assays including MTT/BrdU proliferation and annexin V apoptosis measurements. It also supports co-immunoprecipitation with UPF1 and PABP, and RNA-seq transcriptome profiling. These applications address roles of CSDE1 in GIST tumorigenesis, post-transcriptional regulation, and drug target screening. For additional information, contact Ascent Research.
