Molecule Information
General Information of the Molecule (ID: Mol00087)
Name |
Heme oxygenase 1 (HMOX1)
,Homo sapiens
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Synonyms |
HO-1; HO; HO1
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Molecule Type |
Protein
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Gene Name |
HMOX1
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Gene ID | |||||
Location |
chr22:35380361-35394214[+]
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Sequence |
MERPQPDSMPQDLSEALKEATKEVHTQAENAEFMRNFQKGQVTRDGFKLVMASLYHIYVA
LEEEIERNKESPVFAPVYFPEELHRKAALEQDLAFWYGPRWQEVIPYTPAMQRYVKRLHE VGRTEPELLVAHAYTRYLGDLSGGQVLKKIAQKALDLPSSGEGLAFFTFPNIASATKFKQ LYRSRMNSLEMTPAVRQRVIEEAKTAFLLNIQLFEELQELLTHDTKDQSPSRAPGLRQRA SNKVQDSAPVETPRGKPPLNTRSQAPLLRWVLTLSFLVATVAVGLYAM Click to Show/Hide
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Function |
Heme oxygenase cleaves the heme ring at the alpha methene bridge to form biliverdin. Biliverdin is subsequently converted to bilirubin by biliverdin reductase. Under physiological conditions, the activity of heme oxygenase is highest in the spleen, where senescent erythrocytes are sequestrated and destroyed. Exhibits cytoprotective effects since excess of free heme sensitizes cells to undergo apoptosis.
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Uniprot ID | |||||
Ensembl ID | |||||
HGNC ID | |||||
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Type(s) of Resistant Mechanism of This Molecule
UAPP: Unusual Activation of Pro-survival Pathway
Drug Resistance Data Categorized by Drug
Approved Drug(s)
2 drug(s) in total
Arsenic trioxide
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Unusual Activation of Pro-survival Pathway (UAPP) | ||||
Disease Class: Lung cancer | [1] | |||
Resistant Disease | Lung cancer [ICD-11: 2C25.5] | |||
Resistant Drug | Arsenic trioxide | |||
Molecule Alteration | Expression | Up-regulation |
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Experimental Note | Revealed Based on the Cell Line Data | |||
Cell Pathway Regulation | Cell apoptosis | Inhibition | hsa04210 | |
Nrf2 signaling pathway | Activation | hsa05208 | ||
In Vitro Model | A549 cells | Lung | Homo sapiens (Human) | CVCL_0023 |
Experiment for Molecule Alteration |
Immunoblotting assay | |||
Experiment for Drug Resistance |
MTT Assay | |||
Mechanism Description | miR155 mediates arsenic trioxide resistance by activating Nrf2 and suppressing apoptosis in lung cancer cells. miR155 mediated ATO resistance by upregulating the Nrf2 signaling pathway, but downregulating cellular apoptosis in lung cancer cells. |
Conivaptan
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Unusual Activation of Pro-survival Pathway (UAPP) | ||||
Disease Class: Solid tumour/cancer | [2] | |||
Resistant Disease | Solid tumour/cancer [ICD-11: 2A00-2F9Z] | |||
Resistant Drug | Conivaptan | |||
Molecule Alteration | Function | Inhibition |
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Experimental Note | Revealed Based on the Cell Line Data | |||
In Vitro Model | ATCC 293T cells | Fetal kidney | Homo sapiens (Human) | CVCL_0063 |
Experiment for Molecule Alteration |
Resazurin assay | |||
Mechanism Description | HMOX1, PRKCA, and NEIL2 contribute to anthracycline resistance within the more complex MDR phenotype, while P-glycoprotein/ABCB1 overexpression causes not only anthracycline resistance but also resistance to other anticancer drug classes. Conivaptan has the potential to be used as the dual inhibitor of HMOX1 and PRKCA, whereas bexarotene has the potential as an HMOX1 inhibitor and desloratadine as a PRKCA inhibitor. |
Disease- and Tissue-specific Abundances of This Molecule
ICD Disease Classification 02
Lung cancer [ICD-11: 2C25]
Differential expression of molecule in resistant diseases | ||
The Studied Tissue | Lung | |
The Specified Disease | Lung cancer | |
The Expression Level of Disease Section Compare with the Healthy Individual Tissue | p-value: 4.25E-17; Fold-change: -4.73E-01; Z-score: -5.23E-01 | |
The Expression Level of Disease Section Compare with the Adjacent Tissue | p-value: 2.29E-10; Fold-change: -7.41E-01; Z-score: -6.45E-01 | |
Molecule expression in the normal tissue adjacent to the diseased tissue of patients
Molecule expression in the diseased tissue of patients
Molecule expression in the normal tissue of healthy individuals
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Disease-specific Molecule Abundances | Click to View the Clearer Original Diagram | |
Tissue-specific Molecule Abundances in Healthy Individuals
References
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