| 2002 |
CPT1B (M-CPT I) encodes the muscle-type carnitine palmitoyltransferase I isoform responsible for the rate-limiting step in beta-oxidation of long-chain fatty acids in heart and skeletal muscle. When three previously described splice variants were expressed in Pichia pastoris, none had CPT I enzymatic activity, indicating that splice variation of M-CPT I does not modulate malonyl-CoA inhibition of fatty acid oxidation as previously proposed. |
Heterologous expression in Pichia pastoris, enzymatic activity assay, genomic/cDNA structural analysis |
The Journal of biological chemistry |
High |
12015320
|
| 2018 |
Malonyl-CoA-dependent inhibition of CPT1B plays a crucial role in regulating cardiac fatty acid oxidation rate. A knock-in mouse expressing CPT1B E3A mutant (reduced malonyl-CoA sensitivity) showed 1.9-fold higher FAO in isolated perfused hearts, along with increased malonylcarnitine, decreased CPT1B protein, and coordinated downregulation of FAO gene mRNA expression as compensatory responses. |
Knock-in mouse model, isolated perfused heart FAO measurements, metabolomics, proteomics, transcriptomics |
Cardiovascular research |
High |
29635338
|
| 2021 |
PHD2/3 (prolyl hydroxylase domain proteins) bind to CPT1B and promote hydroxylation of CPT1B at proline 295 (P295). This P295 hydroxylation is required for CPT1B interaction with VDAC1 and for long-chain fatty acid beta-oxidation in cardiomyocytes. A CPT1B-P295A mutant constitutively binds VDAC1 and rescues LCFA metabolism in PHD2/3-deficient cardiomyocytes, establishing an oxygen-sensitive regulatory axis for cardiac metabolism. |
Co-immunoprecipitation, mutagenesis (P295A knock-in), cardiomyocyte loss-of-function (PHD2/3 knockout mice), rescue experiments, FAO assays |
Cell reports |
High |
34610308
|
| 2025 |
TEX44 interacts physically with CPT1B to form a mitochondrial glue that anchors adjacent mitochondria and facilitates assembly of the sperm-specific mitochondrial sheath. Purified TEX44 protein modulates CPT1B enzymatic activity in vitro, limiting conversion of long-chain fatty acids (palmitic acid, myristic acid) to acyl-carnitines and thereby reducing ROS production. Loss of TEX44 leads to unregulated FAO, excessive ROS, and oxidative damage to sperm DNA and flagellar structure. Germ cell-specific Cpt1b knockout mice recapitulate TEX44-deficiency phenotypes including mitochondrial sheath defects and reduced sperm motility. |
Co-immunoprecipitation, purified protein in vitro enzymatic activity assay, Tex44 knockout mice, germ cell-specific Cpt1b knockout mice, whole-exome sequencing of patients |
Nature communications |
High |
40849303
|
| 2026 |
CPT1B is crotonylated at lysine 321 (K321cr) during endotoxic shock, and this modification impairs CPT1B enzymatic activity. The crotonyl-transferase P300 promotes K321 crotonylation while CBP normally protects CPT1B from this modification; LPS induces dissociation of CBP from CPT1B and recruitment of P300. K321R mutation prevents crotonylation, alleviates lipid droplet deposition and mitochondrial dysfunction (restored ATP and mitochondrial membrane potential), and protects against endotoxic shock-induced cardiomyopathy in vivo. |
Crotonylproteomic mass spectrometry, site-directed mutagenesis (K321R), LC-MS/MS identification of writer enzymes (P300/CBP), AAV9 cardiac-specific overexpression in rats, co-immunoprecipitation, enzymatic activity assays |
Experimental & molecular medicine |
High |
42209697
|
| 2014 |
Exercise training increases binding of MEF2A transcription factor to the Cpt1b promoter in mouse skeletal muscle, while decreasing binding of the repressor HDAC5. MEF2A overexpression in C2C12 myoblasts increases Cpt1b mRNA and promoter transcriptional activity, effects suppressed by HDAC5. Exercise induces MEF2A hyperacetylation, increases HDAC5 phosphorylation at Ser259/Ser498, and causes nuclear export of HDAC5, collectively driving CPT1B transcription. |
Chromatin immunoprecipitation (ChIP), reporter gene assay (Cpt1b promoter luciferase), MEF2A and HDAC5 overexpression in C2C12 cells, real-time PCR, Western blot, nuclear/cytoplasmic fractionation |
Acta physiologica (Oxford, England) |
Medium |
25213552
|
| 2019 |
EZH2 binds to the CPT1b promoter via H3K27me3 to repress CPT1b transcription during cardiac hypertrophy. The long noncoding RNA uc.323 protects against hypertrophy partly by interacting with EZH2, preventing CPT1b repression; overexpression of CPT1b blocks uc.323-mediated cardiomyocyte hypertrophy. |
Chromatin immunoprecipitation (ChIP), microarray mRNA expression analysis, gain/loss-of-function in cardiomyocytes, CPT1b overexpression rescue experiments, aortic banding mouse model |
Hypertension (Dallas, Tex. : 1979) |
Medium |
31735087
|
| 2015 |
In response to lipid exposure, CPT1B gene transcription in skeletal muscle is regulated by epigenetic modifications including CpG methylation, H3/H4 histone acetylation, and transcription factor occupancy (PPARδ and HNF4α) at the CPT1B promoter. Methylation of specific CpG sites blocks binding of the transcription factor USF (upstream stimulatory factor), suggesting a causal mechanism for the blunted CPT1B induction seen in severely obese individuals. |
Primary human skeletal muscle cultures, bisulfite sequencing (CpG methylation), ChIP (histone acetylation, transcription factor occupancy), RT-PCR, transcription factor binding assays |
American journal of physiology. Endocrinology and metabolism |
Medium |
26058865
|
| 2020 |
Androgen receptor (AR) regulates CPT1B transcriptional activity via specific binding sites in the CPT1B promoter, as confirmed by dual luciferase reporter assay and ChIP assay in prostate cancer cells. AR inhibition affects CPT1B expression; CPT1B overexpression in enzalutamide-resistant C4-2R cells increases AKT expression and phosphorylation, promoting drug resistance. |
Dual luciferase reporter assay, chromatin immunoprecipitation (ChIP), JASPAR binding site analysis, stable knockdown/overexpression cell lines, CCK-8 assay |
The Prostate |
Medium |
32648618
|
| 2024 |
ZNF263 transcription factor binds to the CPT1B promoter to activate its transcription, thereby enhancing fatty acid beta-oxidation and promoting cisplatin resistance in lung adenocarcinoma cells. This was confirmed by dual-luciferase reporter assay and ChIP assay. |
Dual-luciferase reporter assay, chromatin immunoprecipitation (ChIP), qRT-PCR, Western blot, FAO rate measurement, IC50 assay (CCK-8) |
The pharmacogenomics journal |
Medium |
39500874
|
| 2023 |
MITF transcription factor binds the CPT1B promoter and inhibits its transcription in lung adenocarcinoma cells, reducing fatty acid beta-oxidation and suppressing cancer stem cell stemness. Confirmed by dual-luciferase reporter assay and ChIP assay. |
Dual-luciferase reporter assay, ChIP assay, qRT-PCR, Western blot, sphere-forming assay, FAO measurement |
Pharmacology |
Medium |
38016436
|
| 2025 |
STAT3 directly interacts with CPT1B in pancreatic cancer stem cells, as demonstrated by chromatin immunoprecipitation assay. Manipulation of STAT3 expression (overexpression or siRNA knockdown) alters CPT1B mRNA and protein levels. Quercetin inhibits CPT1B expression via the STAT3 signaling pathway, affecting lipid metabolism. |
Chromatin immunoprecipitation (ChIP), STAT3 siRNA knockdown and overexpression, qRT-PCR, Western blot, CCK-8, sphere formation assay |
Biochemical and biophysical research communications |
Low |
40412371
|
| 2019 |
In LRP6 cardiac-specific knockout mice, CPT1B protein is sharply decreased coincident with Drp1 activation, and Drp1 inhibitor restores CPT1B expression. In cardiomyocytes in vitro, c-Myc (but not CTCF) was identified as a transcriptional regulator of CPT1B expression and lipid accumulation. |
Cardiac-specific LRP6 knockout mice, Drp1 inhibitor treatment, GC-FID/MS fatty acid analysis, ChIP-like transcription factor binding assay, c-Myc overexpression in cardiomyocytes |
Cell and tissue research |
Low |
31811407
|
| 2013 |
CB1 (cannabinoid receptor 1) is upstream of CPT1B in porcine intramuscular adipocytes: CB1 agonist (Δ9-THC) decreased CPT1B mRNA and increased lipid accumulation, while CB1 antagonist (SR141716) increased CPT1B mRNA and decreased lipid accumulation. CPT1 antagonist etomoxir did not affect CB1 expression, confirming CB1 is upstream of CPT1B. PPARα expression was co-regulated with CPT1B. |
Pharmacological agonist/antagonist treatment of porcine intramuscular adipocytes, mRNA expression analysis, lipid accumulation assay |
Animal genetics |
Low |
23914904
|
| 2022 |
SMAD3, a transcription factor downstream of myostatin (Mstn) signaling, directly binds to the Cpt1b promoter as shown by chromatin immunoprecipitation. Mstn knockdown upregulates Cpt1b expression and CPT1 enzyme activity in skeletal muscle, promoting fatty acid beta-oxidation. |
Chromatin immunoprecipitation (ChIP) for SMAD3 binding to Cpt1b promoter, RNA interference (Mstn knockdown mice), CPT1 enzyme activity assay, fatty acid composition analysis |
Sheng wu gong cheng xue bao = Chinese journal of biotechnology |
Medium |
36002433
|
| 2021 |
In proximal tubular epithelial cells, ANXA1 silencing suppresses phosphorylation of AMPK at Thr172 via FPR2/ALX signaling, leading to decreased PPARα and CPT1B expression and increased lipid accumulation. This places CPT1B downstream of the ANXA1/FPR2/AMPK/PPARα axis in renal lipid metabolism. |
siRNA knockdown of ANXA1 in human PTECs, phospho-AMPK Western blot, CPT1B expression measurement, lipid accumulation assay, diabetic mouse model with ANXA1 deletion |
Diabetes |
Low |
34103347
|
| 2024 |
CPT1B interacts with KEAP1 (Kelch-like ECH-associated protein 1), and CPT1B knockdown leads to decreased NRF2 expression and induction of ferroptosis in pancreatic cancer cells, establishing a CPT1B-KEAP1-NRF2 regulatory connection that maintains redox homeostasis. |
Co-immunoprecipitation (CPT1B-KEAP1 interaction), CPT1B siRNA knockdown, NRF2 expression measurement, ROS/lipid peroxidation/glutathione assays, flow cytometry for ferroptosis markers, xenograft model |
Surgery |
Medium |
38302326
|
| 2026 |
BHLHE40 recruits HDAC1 to the CPT1B promoter (confirmed by CUT&Tag) to transcriptionally repress CPT1B expression, impairing NRF2 signaling and driving ferroptosis in E. coli-infected endometrial cells. Overexpression of CPT1B reactivates NRF2 and its downstream targets to inhibit ferroptosis. |
CUT&Tag, RNA-sequencing, CPT1B overexpression rescue, NRF2 inhibitor epistasis, siRNA knockdown of BHLHE40, lipid peroxidation/glutathione/Fe2+ assays |
Free radical biology & medicine |
Medium |
42128070
|
| 2025 |
AAV-mediated cardiac overexpression of CPT1B in neonatal rat cardiomyocytes attenuates phenylephrine-induced hypertrophy and decreases mitochondrial ROS generation. In mice subjected to transverse aortic constriction (TAC), cardiac CPT1B overexpression attenuates cardiomyocyte hypertrophy, cardiac fibrosis, and systolic dysfunction in vivo. |
AAV gene transfer to neonatal rat cardiomyocytes and mouse hearts, phenylephrine-induced hypertrophy model, TAC pressure overload model, mitochondrial ROS measurement, echocardiography, histology |
Basic research in cardiology |
Medium |
40646338
|
| 2024 |
cpt1b regulates cardiomyocyte proliferation during zebrafish development through modulation of glutamine synthetase. Knockout of cpt1b impairs cardiomyocyte proliferation, while cardiomyocyte-specific overexpression promotes it. Pharmacological studies and RNA sequencing identified glutamine synthetase as a key downstream effector. |
cpt1b knockout zebrafish, cardiomyocyte-specific cpt1b overexpression, RNA sequencing, pharmacological glutamine synthetase inhibition |
Journal of cardiovascular development and disease |
Medium |
39590187
|
| 2020 |
miR-138-5p directly targets CPT1B mRNA: miR-138-5p mimic reduces CPT1B expression and luciferase activity from a wild-type CPT1B 3'UTR reporter, while miR-138-5p inhibitor increases CPT1B expression. When CPT1B is mutated at the predicted binding site, miR-138-5p can no longer regulate luciferase activity, confirming direct targeting. |
Dual-luciferase reporter assay with wild-type and mutant CPT1B 3'UTR, miR-138-5p mimic/inhibitor transfection, RT-PCR |
Biomedicine & pharmacotherapy |
Medium |
32325349
|
| 2016 |
Cardiac-specific CPT1B silencing (via intramyocardial lentiviral injection) in obese mice on a high-fat diet protected against HFD-induced cardiac remodeling by decreasing heart weight/tibial length ratio, improving left ventricular ejection fraction and fractional shortening, reducing intramyocardial ROS production, and aggravating myocardial lipid accumulation, indicating CPT1B-driven FAO is a source of ROS in the obese heart. |
Lentiviral cardiac-specific CPT1B knockdown in mice, HFD obesity model, echocardiography, histology, biochemical parameters, ROS measurement |
Obesity (Silver Spring, Md.) |
Medium |
27804274
|
| 2025 |
PPARG activation by the compound DHDK upregulates CPT1B expression, enhancing fatty acid beta-oxidation (FAO) in cardiomyocytes. This protective effect is abolished by inhibition of either PPARG or CPT1B, placing CPT1B downstream of PPARG in the cardioprotective PPARG-CPT1B-FAO axis. |
Molecular docking, lipidomics, qPCR, Western blot, CCK-8, flow cytometry, pharmacological inhibition of PPARG and CPT1B, in vivo rat model |
Pharmaceuticals (Basel, Switzerland) |
Low |
41305001
|