PHACTR4 Knockout HEK293T Cell Line

The choice depends on whether you are studying PHACTR4 (phosphatase and actin regulator 4)'s role as a PP1 regulatory subunit with actin-binding activity or its functions in neural tube closure and cancer biology. The Knockout line is appropriate for asking whether PHACTR4 is required for predicted PP1-actin regulatory activities — PHACTR4 is a member of the phactr family (PHACTR1-4) of PP1 holoenzyme regulatory subunits that also bind actin and modulate actin cytoskeleton dynamics. Overexpression is useful for studying PHACTR4 in heterologous expression contexts. For PHACTR family research, the EDITGENE PHACTR4 Knockout in HEK293T enables study of PHACTR4-specific PP1 targeting and actin regulation. PHACTR1-3 paralog expression analysis aids interpretation. Rescue with wild-type or actin-binding/PP1-binding-deficient PHACTR4 enables structure-function studies. PHACTR4 has been characterized in neural tube closure (Phactr4 mouse mutants show neural tube defects), tumor suppressor functions, and integrin signaling regulation.

Primary applications: • PP1-actin holoenzyme assembly: co-immunoprecipitation analysis of PPP1CA and F-actin with PHACTR4 to characterize PP1-PHACTR4 holoenzyme composition. • Actin cytoskeleton biology: actin dynamics imaging and cell morphology analysis in PHACTR4-null cells. • Integrin signaling: focal adhesion analysis given PHACTR4's reported role in integrin-mediated signaling. • PHACTR family comparative studies: PHACTR1-3 expression analysis to interpret PHACTR4-specific functions. EDITGENE recommends this model for researchers investigating PHACTR family PP1-actin regulatory biology.

Yes. PHACTR4 rescue experiments require attention to dual PP1-actin biology: • Construct design: use a codon-modified PHACTR4 sequence with a small C-terminal tag (FLAG, HA). PHACTR4 has actin-binding RPEL motifs and PP1-binding RVxF motif — preserve both elements. • PP1-binding-deficient rescue: RVxF motif mutations abolish PP1 binding and enable studies of PP1-dependent versus actin-only functions. • Actin-binding-deficient rescue: RPEL motif mutations disrupt actin association. • Functional readout: rescue should restore PP1-PHACTR4 holoenzyme assembly and actin-dependent phenotypes. HEK293T transduces with very high efficiency and supports systematic rescue experiments.