Molecule Information
General Information of the Molecule (ID: Mol01873)
| Name |
Fructose-bisphosphatase 1 (FBP1)
,Homo sapiens
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| Synonyms |
FBP1; FBP
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| Molecule Type |
Protein
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| Gene Name |
FBP1
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| Gene ID | |||||
| Location |
chr9:94,603,133-94,640,249[-]
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| Sequence |
MADQAPFDTDVNTLTRFVMEEGRKARGTGELTQLLNSLCTAVKAISSAVRKAGIAHLYGI
AGSTNVTGDQVKKLDVLSNDLVMNMLKSSFATCVLVSEEDKHAIIVEPEKRGKYVVCFDP LDGSSNIDCLVSVGTIFGIYRKKSTDEPSEKDALQPGRNLVAAGYALYGSATMLVLAMDC GVNCFMLDPAIGEFILVDKDVKIKKKGKIYSLNEGYARDFDPAVTEYIQRKKFPPDNSAP YGARYVGSMVADVHRTLVYGGIFLYPANKKSPNGKLRLLYECNPMAYVMEKAGGMATTGK EAVLDVIPTDIHQRAPVILGSPDDVLEFLKVYEKHSAQ Click to Show/Hide
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| 3D-structure |
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| Function |
Catalyzes the hydrolysis of fructose 1,6-bisphosphate to fructose 6-phosphate in the presence of divalent cations, acting as a rate-limiting enzyme in gluconeogenesis. Plays a role in regulating glucose sensing and insulin secretion of pancreatic beta-cells. Appears to modulate glycerol gluconeogenesis in liver. Important regulator of appetite and adiposity; increased expression of the protein in liver after nutrient excess increases circulating satiety hormones and reduces appetite-stimulating neuropeptides and thus seems to provide a feedback mechanism to limit weight gain.
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| Uniprot ID | |||||
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Type(s) of Resistant Mechanism of This Molecule
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: B-cell non-Hodgkin lymphoma [ICD-11: 2A85.2] | [1] | |||
| Resistant Disease | B-cell non-Hodgkin lymphoma [ICD-11: 2A85.2] | |||
| Resistant Drug | Doxorubicin | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Identified from the Human Clinical Data | |||
| In Vitro Model | OCI-LY8 cells | Oral | Homo sapiens (Human) | CVCL_8803 |
| Daudi cells | Peripheral blood | Homo sapiens (Human) | CVCL_0008 | |
| Experiment for Molecule Alteration |
Immunoblot analysis | |||
| Experiment for Drug Resistance |
CCK-8 assay | |||
| Mechanism Description | Cell adhesion mediated drug resistance (CAM DR) remains a major obstacle to the effectiveness of chemotherapeutic treatment of lymphoma. Far upstream element binding protein 1 (FBP1) is a multifunctional protein that is highly expressed in proliferating cells of several solid neoplasms. CAM-DR is considered a major mechanism by which tumor cells escape the cytotoxic effects of therapeutic agents. | |||
| Drug Sensitivity Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: B-cell non-Hodgkin lymphoma [ICD-11: 2A85.2] | [1] | |||
| Sensitive Disease | B-cell non-Hodgkin lymphoma [ICD-11: 2A85.2] | |||
| Sensitive Drug | Doxorubicin | |||
| Molecule Alteration | Expression | Down-regulation |
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| Experimental Note | Identified from the Human Clinical Data | |||
| In Vitro Model | OCI-LY8 cells | Oral | Homo sapiens (Human) | CVCL_8803 |
| Daudi cells | Peripheral blood | Homo sapiens (Human) | CVCL_0008 | |
| Experiment for Molecule Alteration |
Immunoblot analysis | |||
| Experiment for Drug Resistance |
CCK-8 assay | |||
| Mechanism Description | Cell adhesion mediated drug resistance (CAM DR) remains a major obstacle to the effectiveness of chemotherapeutic treatment of lymphoma. Far upstream element binding protein 1 (FBP1) is a multifunctional protein that is highly expressed in proliferating cells of several solid neoplasms. CAM-DR is considered a major mechanism by which tumor cells escape the cytotoxic effects of therapeutic agents. | |||
References
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