HDAC4 Knockout HAP1 Cell Line

The choice depends on whether you are studying HDAC4's role as a class IIa HDAC or its functions in MEF2 co-repression and cardiac/skeletal muscle biology. The Knockout line is the standard tool for asking whether HDAC4 is required for these processes — HDAC4 is a class IIa HDAC that, like HDAC7, shuttles between nucleus and cytoplasm based on CaMK/PKD-mediated phosphorylation and 14-3-3 binding; HDAC4 represses MEF2-driven transcription in muscle, neurons, and other contexts. Overexpression is useful for studying HDAC4 gain-of-function effects. Important consideration: class IIa HDAC paralog (HDAC5, HDAC7, HDAC9) expression analysis aids interpretation. This product complements the parallel HDAC7 Knockout in HAP1 (also available) for class IIa HDAC family functional dissection. HDAC4 haploinsufficiency causes brachydactyly-mental retardation syndrome (BDMR). Rescue with wild-type or 14-3-3-binding-resistant HDAC4 enables structure-function studies.

Primary applications: • MEF2 co-repression: MEF2-driven transcription analysis in HDAC4-null cells. • Nuclear-cytoplasmic shuttling: phospho-HDAC4 (S246/S467/S632) and 14-3-3 binding analysis given the regulatory phospho-export mechanism. • BDMR modeling: rescue with patient-derived HDAC4 mutations for genotype-function studies of brachydactyly-mental retardation syndrome. • Class IIa HDAC family dissection: parallel analysis with HDAC7 Knockout in HAP1 (also available) for paralog-specific studies. EDITGENE recommends this model for researchers investigating HDAC4 biology, class IIa HDAC functional specialization, and BDMR disease mechanisms.

Yes. HDAC4 rescue experiments require attention to class IIa architecture: • Construct design: use a codon-modified HDAC4 sequence with a small C-terminal tag (FLAG, HA). HDAC4 has the canonical class IIa architecture (N-terminal regulatory, central catalytic, C-terminal) — preserve all elements. • 14-3-3-binding-resistant rescue: S246A/S467A/S632A triple phospho-site mutations abolish 14-3-3-mediated cytoplasmic retention. • Catalytically-dead rescue: HDAC catalytic domain mutations abolish intrinsic deacetylase activity. • Functional readout: rescue should restore MEF2 co-repression activity. 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.