Molecule Information
General Information of the Molecule (ID: Mol04100)
| Name |
Carnitine palmitoyltransferase 1B (CPT1B)
,Homo sapiens
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| Synonyms |
Carnitine O-palmitoyltransferase I, muscle isoform; Carnitine palmitoyltransferase 1B; Carnitine palmitoyltransferase I-like protein
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| Molecule Type |
Protein
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| Gene Name |
CPT1B
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| Gene ID | |||||
| Location |
chr22:50568861-50578465[-]
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| Sequence |
MAEAHQAVAFQFTVTPDGVDFRLSREALKHVYLSGINSWKKRLIRIKNGILRGVYPGSPT
SWLVVIMATVGSSFCNVDISLGLVSCIQRCLPQGCGPYQTPQTRALLSMAIFSTGVWVTG IFFFRQTLKLLLCYHGWMFEMHGKTSNLTRIWAMCIRLLSSRHPMLYSFQTSLPKLPVPR VSATIQRYLESVRPLLDDEEYYRMELLAKEFQDKTAPRLQKYLVLKSWWASNYVSDWWEE YIYLRGRSPLMVNSNYYVMDLVLIKNTDVQAARLGNIIHAMIMYRRKLDREEIKPVMALG IVPMCSYQMERMFNTTRIPGKDTDVLQHLSDSRHVAVYHKGRFFKLWLYEGARLLKPQDL EMQFQRILDDPSPPQPGEEKLAALTAGGRVEWAQARQAFFSSGKNKAALEAIERAAFFVA LDEESYSYDPEDEASLSLYGKALLHGNCYNRWFDKSFTLISFKNGQLGLNAEHAWADAPI IGHLWEFVLGTDSFHLGYTETGHCLGKPNPALAPPTRLQWDIPKQCQAVIESSYQVAKAL ADDVELYCFQFLPFGKGLIKKCRTSPDAFVQIALQLAHFRDRGKFCLTYEASMTRMFREG RTETVRSCTSESTAFVQAMMEGSHTKADLRDLFQKAAKKHQNMYRLAMTGAGIDRHLFCL YLVSKYLGVSSPFLAEVLSEPWRLSTSQIPQSQIRMFDPEQHPNHLGAGGGFGPVADDGY GVSYMIAGENTIFFHISSKFSSSETNAQRFGNHIRKALLDIADLFQVPKAYS Click to Show/Hide
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| Function |
Catalyzes the transfer of the acyl group of long-chain fatty acid-CoA conjugates onto carnitine, an essential step for the mitochondrial uptake of long-chain fatty acids and their subsequent beta-oxidation in the mitochondrion. .
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| Uniprot ID | |||||
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Type(s) of Resistant Mechanism of This Molecule
MRAP: Metabolic Reprogramming via Altered Pathways
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
Gemcitabine
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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Metabolic Reprogramming via Altered Pathways (MRAP)
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| Disease Class: Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Resistant Disease | Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | |||
| Resistant Drug | Gemcitabine | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Identified from the Human Clinical Data | |||
| Cell Pathway Regulation | Hepatocellular carcinoma | Activation | hsa05225 | |
| Fluid shear stress and atherosclerosis | Activation | hsa05418 | ||
| In Vivo Model | Patients with PDAC | Homo Sapiens | ||
| Experiment for Molecule Alteration |
Western blotting and quantitative reverse transcription polymerase chain reaction | |||
| Experiment for Drug Resistance |
Overall survival assay (OS) | |||
| Mechanism Description | In our study, we observed that the CPT1B expression level was higher in pancreatic ductal adenocarcinoma tissues than in normal tissues and correlated with a low rate of survival. Moreover, silencing of CPT1B significantly suppressed the proliferative ability and metastasis of Pancreatic Cancercells. Furthermore, we discovered that CPT1B interacts with Kelch-like ECH-associated protein 1, and CPT1B knockdown led to decreased NRF2 expression and ferroptosis induction. In addition, CPT1B expression increased after gemcitabine treatment, and it was highly expressed in gemcitabine-resistant pancreatic ductal adenocarcinoma cells. Finally, we discovered that ferroptosis induced by CPT1B knockdown enhanced the gemcitabine toxicity in pancreatic ductal adenocarcinoma. | |||
| Disease Class: Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Resistant Disease | Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | |||
| Resistant Drug | Gemcitabine | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| Cell Pathway Regulation | Hepatocellular carcinoma | Activation | hsa05225 | |
| Fluid shear stress and atherosclerosis | Activation | hsa05418 | ||
| In Vitro Model | MiaPaCa-2 cells | Blood | Homo sapiens (Human) | CVCL_0428 |
| Experiment for Molecule Alteration |
Western blotting and quantitative reverse transcription polymerase chain reaction | |||
| Experiment for Drug Resistance |
CCK8 assay | |||
| Mechanism Description | In our study, we observed that the CPT1B expression level was higher in pancreatic ductal adenocarcinoma tissues than in normal tissues and correlated with a low rate of survival. Moreover, silencing of CPT1B significantly suppressed the proliferative ability and metastasis of Pancreatic Cancercells. Furthermore, we discovered that CPT1B interacts with Kelch-like ECH-associated protein 1, and CPT1B knockdown led to decreased NRF2 expression and ferroptosis induction. In addition, CPT1B expression increased after gemcitabine treatment, and it was highly expressed in gemcitabine-resistant pancreatic ductal adenocarcinoma cells. Finally, we discovered that ferroptosis induced by CPT2B knockdown enhanced the gemcitabine toxicity in pancreatic ductal adenocarcinoma. | |||
| Disease Class: Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Resistant Disease | Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | |||
| Resistant Drug | Gemcitabine | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| Cell Pathway Regulation | Hepatocellular carcinoma | Activation | hsa05225 | |
| Fluid shear stress and atherosclerosis | Activation | hsa05418 | ||
| In Vitro Model | Panc1 cells | Pancreas | Homo sapiens (Human) | CVCL_0480 |
| Experiment for Molecule Alteration |
Western blotting and quantitative reverse transcription polymerase chain reaction | |||
| Experiment for Drug Resistance |
CCK8 assay | |||
| Mechanism Description | In our study, we observed that the CPT1B expression level was higher in pancreatic ductal adenocarcinoma tissues than in normal tissues and correlated with a low rate of survival. Moreover, silencing of CPT1B significantly suppressed the proliferative ability and metastasis of Pancreatic Cancercells. Furthermore, we discovered that CPT1B interacts with Kelch-like ECH-associated protein 1, and CPT1B knockdown led to decreased NRF2 expression and ferroptosis induction. In addition, CPT1B expression increased after gemcitabine treatment, and it was highly expressed in gemcitabine-resistant pancreatic ductal adenocarcinoma cells. Finally, we discovered that ferroptosis induced by CPT3B knockdown enhanced the gemcitabine toxicity in pancreatic ductal adenocarcinoma. | |||
| Disease Class: Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Resistant Disease | Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | |||
| Resistant Drug | Gemcitabine | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| Cell Pathway Regulation | Hepatocellular carcinoma | Activation | hsa05225 | |
| Fluid shear stress and atherosclerosis | Activation | hsa05418 | ||
| In Vitro Model | MiaPaCa-2 cells with CPT1B knockdown | Pancreas | Homo sapiens (Human) | CVCL_0428 |
| Experiment for Molecule Alteration |
Western blotting and quantitative reverse transcription polymerase chain reaction | |||
| Experiment for Drug Resistance |
CCK8 assay | |||
| Mechanism Description | In our study, we observed that the CPT1B expression level was higher in pancreatic ductal adenocarcinoma tissues than in normal tissues and correlated with a low rate of survival. Moreover, silencing of CPT1B significantly suppressed the proliferative ability and metastasis of Pancreatic Cancercells. Furthermore, we discovered that CPT1B interacts with Kelch-like ECH-associated protein 1, and CPT1B knockdown led to decreased NRF2 expression and ferroptosis induction. In addition, CPT1B expression increased after gemcitabine treatment, and it was highly expressed in gemcitabine-resistant pancreatic ductal adenocarcinoma cells. Finally, we discovered that ferroptosis induced by CPT4B knockdown enhanced the gemcitabine toxicity in pancreatic ductal adenocarcinoma. | |||
| Disease Class: Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Resistant Disease | Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | |||
| Resistant Drug | Gemcitabine | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| Cell Pathway Regulation | Hepatocellular carcinoma | Activation | hsa05225 | |
| Fluid shear stress and atherosclerosis | Activation | hsa05418 | ||
| In Vitro Model | PANC-1 cells with CPT1B knockdown | Pancreas | Homo sapiens (Human) | CVCL_0480 |
| Experiment for Molecule Alteration |
Western blotting and quantitative reverse transcription polymerase chain reaction | |||
| Experiment for Drug Resistance |
CCK8 assay | |||
| Mechanism Description | In our study, we observed that the CPT1B expression level was higher in pancreatic ductal adenocarcinoma tissues than in normal tissues and correlated with a low rate of survival. Moreover, silencing of CPT1B significantly suppressed the proliferative ability and metastasis of Pancreatic Cancercells. Furthermore, we discovered that CPT1B interacts with Kelch-like ECH-associated protein 1, and CPT1B knockdown led to decreased NRF2 expression and ferroptosis induction. In addition, CPT1B expression increased after gemcitabine treatment, and it was highly expressed in gemcitabine-resistant pancreatic ductal adenocarcinoma cells. Finally, we discovered that ferroptosis induced by CPT5B knockdown enhanced the gemcitabine toxicity in pancreatic ductal adenocarcinoma. | |||
| Disease Class: Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Resistant Disease | Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | |||
| Resistant Drug | Gemcitabine | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| Cell Pathway Regulation | Hepatocellular carcinoma | Activation | hsa05225 | |
| Fluid shear stress and atherosclerosis | Activation | hsa05418 | ||
| In Vivo Model | Cell-derived xenografts were created in mice using MiaPaCa-2 cells with CPT1B knockdown and scramble short hairpin RNA | Mice | ||
| Experiment for Molecule Alteration |
Western blotting and quantitative reverse transcription polymerase chain reaction | |||
| Experiment for Drug Resistance |
Tumor volume assay | |||
| Mechanism Description | In our study, we observed that the CPT1B expression level was higher in pancreatic ductal adenocarcinoma tissues than in normal tissues and correlated with a low rate of survival. Moreover, silencing of CPT1B significantly suppressed the proliferative ability and metastasis of Pancreatic Cancercells. Furthermore, we discovered that CPT1B interacts with Kelch-like ECH-associated protein 1, and CPT1B knockdown led to decreased NRF2 expression and ferroptosis induction. In addition, CPT1B expression increased after gemcitabine treatment, and it was highly expressed in gemcitabine-resistant pancreatic ductal adenocarcinoma cells. Finally, we discovered that ferroptosis induced by CPT6B knockdown enhanced the gemcitabine toxicity in pancreatic ductal adenocarcinoma. | |||
References
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