PPP1R21 Knockout HAP1 Cell Line

PPP1R21 Knockout HAP1 Cell Line
Cat.No.:

EDC08312

Species:

Human

Cell Name:

HAP1

Gene:

PPP1R21

Gene ID:

129285

Size:

1×10⁶cells

PPP1R21 Knockout HAP1 Cell Line is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performotion Cas9 Protein and Hassle-Free Cell Selection.
Cat.No. EDC08312
Product Name PPP1R21 Knockout HAP1 Cell Line
Species Human
Cell Line HAP1
Cellosaurus ID CVCL_0F62
Gene ID
Cell Line Synonyms Highly Aggressively Proliferating Immortalized
Gene PPP1R21
Summary
Enables RNA binding activity. Located in early endosome. [provided by Alliance of Genome Resources, Jul 2025]
Digestion Time 1 min 30 s
Morphology Adherent
Passage Ratio 1:15-1:10
Complete Culture Medium IMDM + 10% FBS
Freezing Medium 90% FBS + 10% DMSO
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.

FAQ

The choice depends on whether you are studying PPP1R21 (also called KLRAQ1) — a less-characterized PP1 regulatory subunit with emerging roles in cilia biology and intellectual disability — or its specific functions in PP1 substrate targeting. The Knockout line is appropriate for asking whether PPP1R21 is required for predicted PP1-dependent substrate dephosphorylation — PPP1R21 has been reported to function in vesicle trafficking and to be associated with intellectual disability in patient genome studies. Overexpression is useful for studying PPP1R21 in heterologous contexts. For PP1 family research, the EDITGENE PPP1R21 Knockout in HAP1 enables characterization of this regulatory subunit's substrate scope and tissue-relevant functions. PPP1R21 has been associated with neurodevelopmental disorder phenotypes in human genetics studies. Rescue with wild-type PPP1R21 enables initial functional characterization.
Primary applications: • Substrate discovery: untargeted phosphoproteomics to identify PPP1R21-dependent dephosphorylation events. • Cilia and intellectual disability biology: phenotypic profiling for cilia-related and trafficking-related phenotypes given PPP1R21's reported associations. • Vesicle trafficking studies: endosomal and Golgi trafficking analysis in PPP1R21-null cells. • Neurodevelopmental disease modeling: rescue with patient-derived PPP1R21 variants for genotype-function studies where applicable. EDITGENE recommends this model for researchers investigating PPP1R21 biology and its emerging links to neurodevelopmental disease.
Yes. PPP1R21 rescue experiments require attention to its emerging biology: • Construct design: use a codon-modified PPP1R21 sequence with a small C-terminal tag (FLAG, HA). Preserve KLRAQ-containing region and any PP1-binding motifs. • Discovery-oriented rescue: parallel wild-type rescue distinguishes PPP1R21-dependent phenotypes from off-target effects given its emerging characterization status. • Disease variant rescue: where patient-derived PPP1R21 variants are available, rescue enables genotype-function correlation studies of neurodevelopmental phenotypes. • Functional readout: rescue should restore phenotypes identified during knockout characterization (vesicle trafficking, candidate substrate dephosphorylation). HAP1-specific considerations: • Diploidization: HAP1 cells gradually diploidize during extended culture — confirm ploidy by flow cytometry at the time of phenotypic assay. • Integration site sensitivity: position effects on transgene expression are more pronounced in near-haploid backgrounds; generating multiple independent rescue clones is strongly recommended. • Transduction efficiency: HAP1 transduces with lentivirus at moderate efficiency — increase MOI compared to standard immortalized lines.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.

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