Cat. No. ARG43750
The BDH1 Knockout AC16 Cell Line is a CRISPR/Cas9-edited knockout derived from AC16 human ventricular cardiomyocytes, disrupting the BDH1 mitochondrial ketone body enzyme. BDH1, regulated by PPARA and PPARGC1A, functions in ketolysis with interacting partners OXCT1 and ACAT1. This model enables study of cardiac ketone metabolism defects, metabolic stress, and heart failure remodeling. Ideal for ketone metabolism studies, cardiomyopathy modeling, and drug screening, with applications including Seahorse flux analysis, enzyme assays, and cell viability tests.
| Host Cell | AC16 |
| Derived From Site | Ventricle |
| Gene Name | BDH1 |
| Gene Identifier | NCBI Gene ID 622 |
| Morphology | Cardiomyocyte |
| Growth Mode | Adherent |
| Storage | Liquid nitrogen (LN2) |
| Temperature | 37°C |
| Atmosphere | 5% CO₂ |
| Sterility testing | The bacterial, yeast, and fungi are not detected in these cells by daily monitor. |
| Mycoplasma testing | Negative for mycoplasma through PCR analysis |
Intended Use: This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.
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This product is provided "AS IS". For Research Use Only. Not for human or animal therapeutic use.
The BDH1 Knockout AC16 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from human AC16 ventricular cardiomyocytes, designed to disrupt BDH1. BDH1 encodes a mitochondrial enzyme that catalyzes oxidation of D-3-hydroxybutyrate to acetoacetate in ketone body metabolism. This cell line provides a defined loss-of-function model to study cardiac ketolysis and metabolic adaptation. CRISPR/Cas9-mediated gene disruption results in functional ablation of BDH1, enabling precise investigation of its role in cardiomyocyte energy homeostasis.
The AC16 host cell line is an immortalized human ventricular cardiomyocyte model retaining contractile and metabolic features of primary cardiac muscle. These cells are highly oxidative, utilizing fatty acids, glucose, and ketone bodies for ATP production, making them suited for metabolic studies. Their ventricular origin is relevant for adult cardiac pathologies including heart failure and cardiomyopathy. The consistent AC16 background provides a scalable platform to investigate metabolic signaling and stress responses in a human cardiomyocyte context.
BDH1 functions at the rate-limiting step of ketolysis, converting D-3-hydroxybutyrate to acetoacetate, which is further metabolized by OXCT1 and ACAT1 to acetyl-CoA for the TCA cycle and ATP generation. This pathway is regulated by PPARA and PPARGC1A (PGC-1??), activated by fasting, ketogenic stimuli, and glucagon, while insulin suppresses it. BDH1 interacts with mitochondrial ketone body enzymes OXCT1 and ACAT1, forming a functional unit. Acetyl-CoA produced fuels oxidative phosphorylation and contributes to histone acetylation, linking metabolism to epigenetic regulation. Key pathway components include HMGCS2 and HMGCL, integrating ketogenesis and ketolysis in cardiac energy metabolism.
In AC16 cardiomyocytes, BDH1 knockout impairs ketone body utilization, forcing reliance on alternative substrates and inducing metabolic stress. This models the metabolic remodeling in heart failure, where ketone body oxidation becomes critical as fatty acid oxidation declines. Loss of BDH1 may reduce ATP synthesis, cause metabolite imbalance, and alter redox state, mirroring ketone body metabolic disorders and cardiomyopathy. This cell line enables dissection of how defective ketolysis promotes contractile dysfunction and pathological signaling in the heart.
This knockout cell line is ideally suited for cardiac ketone metabolism studies, metabolic cardiomyopathy modeling, and heart failure metabolic remodeling research. Applicable assays include Seahorse metabolic flux analysis for ketone-driven respiration, enzyme activity assays, Western blotting, and RT-qPCR. It supports drug screening for metabolic modulators, evaluation of ketogenic diet effects, and cell viability assays under metabolic stress. For inquiries or further details, contact Ascent Research.
