ArticleProceedings of the National Academy of Sciences of the United States of America2005
Mutant mice lacking acetyl-CoA carboxylase 1 are embryonically lethal.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.
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Who cites it
109 citing papers in PubMed, 258 citations in OpenAlex.
- Making sense of cardiomyopathy caused by deletion of acetyl-CoA carboxylase 1 and 2.The Journal of clinical investigation · 2026Article
- Triglyceride-lowering therapies for hepatic steatosis: mechanisms, efficacy, and clinical perspectives.Frontiers in pharmacology · 2026Review
- Acetyl-CoA carboxylase maintains energetic balance for functional oogenesis.Nature communications · 2025Article
- Deep metabolic profiling of immune cells by spectral flow cytometry-A comprehensive validation approach.iScience · 2025Article
- Metabolic reprogramming of interleukin-17-producing γδ T cells promotes ACC1-mediated de novo lipogenesis under psoriatic conditions.Nature metabolism · 2025Article
- The role of fatty acid metabolism on B cells and B cell-related autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Increasing cisplatin exposure promotes small-cell lung cancer transformation after a shift from glucose metabolism to fatty acid metabolism.Journal of cancer research and clinical oncology · 2025Article
- Insulin Resistance, Hyperinsulinemia and Atherosclerosis: Insights into Pathophysiological Aspects and Future Therapeutic Prospects.Current cardiology reviews · 2025Review
- Metabolic Reprogramming and Adaption in Breast Cancer Progression and Metastasis.Advances in experimental medicine and biology · 2025Review
- Identification of fatty acids synthesis and metabolism-related gene signature and prediction of prognostic model in hepatocellular carcinoma.Cancer cell international · 2024Article
- Selective Elimination of Genetic Variants of Human Embryonic Stem Cells from High Vulnerability to Ferroptosis.Biomaterials research · 2024Article
- In-depth analysis ofLiver research (Beijing, China) · 2023Review
- Amelioration of ethanol-induced oxidative stress and alcoholic liver disease byActa pharmaceutica Sinica. B · 2023Article
- NFYA promotes malignant behavior of triple-negative breast cancer in mice through the regulation of lipid metabolism.Communications biology · 2023Article
- Physiological and pathological roles of lipogenesis.Nature metabolism · 2023Review
- Integrated Control of Fatty Acid Metabolism in Heart Failure.Metabolites · 2023Review
- Acetyl-CoA metabolism in cancer.Nature reviews. Cancer · 2023Review
- Circadian clock and lipid metabolism disorders: a potential therapeutic strategy for cancer.Frontiers in endocrinology · 2023Review
- Recent insights into the molecular mechanisms of simultaneous fatty acid oxidation and synthesis in brown adipocytes.Frontiers in endocrinology · 2023Review
- Obesity promotes lipid accumulation in mouse cartilage-A potential role of acetyl-CoA carboxylase (ACC) mediated chondrocyte de novo lipogenesis.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2022Article
49 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Acetyl-CoA carboxylases (ACC1 and ACC2) catalyze the carboxylation of acetyl-CoA to form malonyl-CoA, an intermediate metabolite that plays a pivotal role in the regulation of fatty acid metabolism. We previously reported that ACC2 null mice are viable, and that ACC2 plays an important role in the regulation of fatty acid oxidation through the inhibition of carnitine palmitoyltransferase I, a mitochondrial component of the fatty-acyl shuttle system. Herein, we used gene targeting to knock out the ACC1 gene. The heterozygous mutant mice (Acc1(+/-)) had normal fertility and lifespans and maintained a similar body weight to that of their wild-type cohorts. The mRNA level of ACC1 in the tissues of Acc1(+/-) mice was half that of the wild type; however, the protein level of ACC1 and the total malonyl-CoA level were similar. In addition, there was no difference in the acetate incorporation into fatty acids nor in the fatty acid oxidation between the hepatocytes of Acc1(+/-) mice and those of the wild type. In contrast to Acc2(-/-) mice, Acc1(-/-) mice were not detected after mating. Timed pregnancies of heterozygotes revealed that Acc(-/-) embryos are already undeveloped at embryonic day (E)7.5, they die by E8.5, and are completely resorbed at E11.5. Our previous results of the ACC2 knockout mice and current studies of ACC1 knockout mice further confirm our hypotheses that malonyl-CoA exists in two independent pools, and that ACC1 and ACC2 have distinct roles in fatty acid metabolism.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.