Molecule Information
General Information of the Molecule (ID: Mol04329)
| Name |
Histone H1.4 (H1-4)
,Homo sapiens
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| Synonyms |
Histone H1b; Histone H1s-4
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| Molecule Type |
Protein
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| Gene Name |
H1-4
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| Gene ID | |||||
| Sequence |
MSETAPAAPAAPAPAEKTPVKKKARKSAGAAKRKASGPPVSELITKAVAASKERSGVSLA
ALKKALAAAGYDVEKNNSRIKLGLKSLVSKGTLVQTKGTGASGSFKLNKKAASGEAKPK A KKAGAAKAKKPAGAAKKPKKATGAATPKKSAKKTPKKAKKPAAAAGAKKAKSPKKAKA AK PKKAPKSPAKAKAVKPKAAKPKTAKPKAAKPKKAAAKKK Click to Show/Hide
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| Function |
Histone H1 protein binds to linker DNA between nucleosomesforming the macromolecular structure known as the chromatin fiber.Histones H1 are necessary for the condensation of nucleosome chainsinto higher-order structured fibers. Also acts as a regulator ofindividual gene transcription through chromatin remodeling, nucleosomespacing and DNA methylation . {ECO:0000250}.
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Type(s) of Resistant Mechanism of This Molecule
Drug Resistance Data Categorized by Drug
Approved Drug(s)
2 drug(s) in total
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Oesophagus adenocarcinoma [ICD-11: 2B70.0] | [1] | |||
| Resistant Disease | Oesophagus adenocarcinoma [ICD-11: 2B70.0] | |||
| Resistant Drug | Docetaxel | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Discovered Using In-vivo Testing Model | |||
| In Vivo Model | Patient-derived esophageal cancer model | Homo sapiens | ||
| Experiment for Molecule Alteration |
Gene expression analysis | |||
| Experiment for Drug Resistance |
Drug sensitivity analysis | |||
| Mechanism Description | The results of drug sensitivity of risk genes showed that the high expression of HIST1H1E made tumor cells resistant to trametinib, selumetinib, RDEA119, Docetaxel and 17-AAG. The high expression of UBE2C makes tumor cells resistant to masitinib. The low expression of ERO1B makes the EC more sensitive to FK866 | |||
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Oesophagus adenocarcinoma [ICD-11: 2B70.0] | [1] | |||
| Resistant Disease | Oesophagus adenocarcinoma [ICD-11: 2B70.0] | |||
| Resistant Drug | Trametinib | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Discovered Using In-vivo Testing Model | |||
| In Vivo Model | Patient-derived esophageal cancer model | Homo sapiens | ||
| Experiment for Molecule Alteration |
Gene expression analysis | |||
| Experiment for Drug Resistance |
Drug sensitivity analysis | |||
| Mechanism Description | The results of drug sensitivity of risk genes showed that the high expression of HIST1H1E made tumor cells resistant to trametinib, selumetinib, RDEA119, Docetaxel and 17-AAG. The high expression of UBE2C makes tumor cells resistant to masitinib. The low expression of ERO1B makes the EC more sensitive to FK866 | |||
Clinical Trial Drug(s)
3 drug(s) in total
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Oesophagus adenocarcinoma [ICD-11: 2B70.0] | [1] | |||
| Resistant Disease | Oesophagus adenocarcinoma [ICD-11: 2B70.0] | |||
| Resistant Drug | Refametinib | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Discovered Using In-vivo Testing Model | |||
| In Vivo Model | Patient-derived esophageal cancer model | Homo sapiens | ||
| Experiment for Molecule Alteration |
Gene expression analysis | |||
| Experiment for Drug Resistance |
Drug sensitivity analysis | |||
| Mechanism Description | The results of drug sensitivity of risk genes showed that the high expression of HIST1H1E made tumor cells resistant to trametinib, selumetinib, RDEA119, Docetaxel and 17-AAG. The high expression of UBE2C makes tumor cells resistant to masitinib. The low expression of ERO1B makes the EC more sensitive to FK866 | |||
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Oesophagus adenocarcinoma [ICD-11: 2B70.0] | [1] | |||
| Resistant Disease | Oesophagus adenocarcinoma [ICD-11: 2B70.0] | |||
| Resistant Drug | Selumetinib | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Discovered Using In-vivo Testing Model | |||
| In Vivo Model | Patient-derived esophageal cancer model | Homo sapiens | ||
| Experiment for Molecule Alteration |
Gene expression analysis | |||
| Experiment for Drug Resistance |
Drug sensitivity analysis | |||
| Mechanism Description | The results of drug sensitivity of risk genes showed that the high expression of HIST1H1E made tumor cells resistant to trametinib, selumetinib, RDEA119, Docetaxel and 17-AAG. The high expression of UBE2C makes tumor cells resistant to masitinib. The low expression of ERO1B makes the EC more sensitive to FK866 | |||
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Oesophagus adenocarcinoma [ICD-11: 2B70.0] | [1] | |||
| Resistant Disease | Oesophagus adenocarcinoma [ICD-11: 2B70.0] | |||
| Resistant Drug | Tanespimycin | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Discovered Using In-vivo Testing Model | |||
| In Vivo Model | Patient-derived esophageal cancer model | Homo sapiens | ||
| Experiment for Molecule Alteration |
Gene expression analysis | |||
| Experiment for Drug Resistance |
Drug sensitivity analysis | |||
| Mechanism Description | The results of drug sensitivity of risk genes showed that the high expression of HIST1H1E made tumor cells resistant to trametinib, selumetinib, RDEA119, Docetaxel and 17-AAG. The high expression of UBE2C makes tumor cells resistant to masitinib. The low expression of ERO1B makes the EC more sensitive to FK866 | |||
References
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