The GPATCH4 Knockout HEK293T Polyclonal Cells provide a CRISPR/Cas9-generated pool of HEK293T cells with targeted disruption of the GPATCH4 gene. This polyclonal knockout population enables loss-of-function studies without the biases of clonal isolation, serving as a versatile tool for RNA biology research. GPATCH4 encodes a putative RNA-binding protein harboring a G-patch domain, a motif commonly found in RNA processing factors. This ready-to-use product is suited for functional genomics, transcriptomics, and disease modeling applications.
The HEK293T host cell line is a human embryonic kidney derivative stably expressing the SV40 large T antigen, a feature that promotes high-copy episomal replication of transfected plasmids and yields exceptional transfection efficiencies. This line is a standard workhorse for protein overexpression, viral packaging, and gene silencing applications, offering a robust and well-characterized background for knockout studies.
At the molecular level, GPATCH4 is predicted to interact with spliceosomal and nucleolar machinery, including PRPF splicing factors, U2 and U5 snRNPs, snoRNPs, and RNA helicases, thereby contributing to pre-mRNA splicing and ribosome biogenesis. Its expression is regulated by the MYC transcription factor, growth factor signaling, and stress cues, tying GPATCH4 activity to cell proliferation and homeostasis. Disruption of this gene likely impairs alternative splicing and rRNA maturation, altering global gene expression.
Within the HEK293T system, the GPATCH4 knockout model enables dissection of RNA processing defects relevant to cancer and neurological disorders, where splicing dysregulation is increasingly recognized. The polyclonal nature of the knockout captures population-level responses, facilitating the identification of robust phenotypes. Moreover, this model can serve as a platform for screening small molecules or genetic modifiers that rescue splicing defects.
Researchers can apply this product in RNA-seq experiments to profile transcriptome-wide splicing changes, RT-qPCR validations of isoform shifts, co-immunoprecipitation assays to probe protein?Cprotein interactions with spliceosomal factors such as PRPF proteins and snRNPs, and immunofluorescence for nucleolar integrity assessment. These approaches support functional mapping of GPATCH4 in RNA metabolism and its potential involvement in cancer and neurological disease pathways. For further product details or customization, contact Ascent Research.
