Molecule Information
General Information of the Molecule (ID: Mol04432)
| Name |
Acidic leucine-rich nuclear phosphoprotein 32 family member E (ANP32E)
,Homo sapiens
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| Synonyms |
LANP-like protein
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| Molecule Type |
Protein
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| Gene Name |
ANP32E
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| Gene ID | |||||
| Sequence |
MEMKKKINLELRNRSPEEVTELVLDNCLCVNGEIEGLNDTFKELEFLSMANVELSSLARL
PSLNKLRKLELSDNIISGGLEVLAEKCPNLTYLNLSGNKIKDLSTVEALQNLKNLKSLD L FNCEITNLEDYRESIFELLQQITYLDGFDQEDNEAPDSEEEDDEDGDEDDEEEEENEA GP PEGYEEEEEEEEEEDEDEDEDEDEAGSELGEGEEEVGLSYLMKEEIQDEEDDDDYVE EGE EEEEEEEGGLRGEKRKRDAEDDGEEEDD Click to Show/Hide
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| Function |
Histone chaperone that specifically mediates the genome-wideremoval of histone H2A.Z/H2AZ1 from the nucleosome: removes H2A.Z/H2AZ1from its normal sites of deposition, especially from enhancer andinsulator regions. Not involved in deposition of H2A.Z/H2AZ1 in thenucleosome. May stabilize the evicted H2A.Z/H2AZ1-H2B dimer, thusshifting the equilibrium towards dissociation and the off-chromatinstate . Inhibits activity of protein phosphatase 2A. Does not inhibit protein phosphatase 1. May play a role incerebellar development and synaptogenesis.{ECO:0000269|PubMed:24463511}.
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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 Sensitivity Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Oesophagus adenocarcinoma [ICD-11: 2B70.0] | [1] | |||
| Sensitive Disease | Oesophagus adenocarcinoma [ICD-11: 2B70.0] | |||
| Sensitive Drug | Paclitaxel | |||
| Molecule Alteration | Expression | Down-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| Cell Pathway Regulation | Ferroptosis signaling pathway | Activation | hsa04216 | |
| In Vitro Model | KYSE150 cells | Esophagus | Homo sapiens (Human) | CVCL_1348 |
| Experiment for Molecule Alteration |
Western blot assay | |||
| Experiment for Drug Resistance |
CCK8 assay; Colony formation assay | |||
| Mechanism Description | Repression of ANP32E increases the responsiveness of EC to PTX, and the concurrent use of erastin with PTX enhances their anti-cancer effectiveness. These findings provide support for the efficacy of inducing ferroptosis as a potential therapeutic approach to enhance the cytotoxic effects of PTX. ANP32E regulates EC progression and ferroptosis through the p53/SLC7A11 axis, offering a potential molecular target for overcoming PTX resistance in EC treatment. | |||
| Disease Class: Oesophagus adenocarcinoma [ICD-11: 2B70.0] | [1] | |||
| Sensitive Disease | Oesophagus adenocarcinoma [ICD-11: 2B70.0] | |||
| Sensitive Drug | Paclitaxel | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| Cell Pathway Regulation | Ferroptosis signaling pathway | Activation | hsa04216 | |
| In Vitro Model | KYSE-30 cells | Esophagus | Homo sapiens (Human) | CVCL_1351 |
| Experiment for Molecule Alteration |
Western blot assay | |||
| Experiment for Drug Resistance |
CCK8 assay; Colony formation assay | |||
| Mechanism Description | Repression of ANP32E increases the responsiveness of EC to PTX, and the concurrent use of erastin with PTX enhances their anti-cancer effectiveness. These findings provide support for the efficacy of inducing ferroptosis as a potential therapeutic approach to enhance the cytotoxic effects of PTX. ANP32E regulates EC progression and ferroptosis through the p53/SLC7A11 axis, offering a potential molecular target for overcoming PTX resistance in EC treatment. | |||
Patented Agent(s)
1 drug(s) in total
| Drug Sensitivity Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Oesophagus adenocarcinoma [ICD-11: 2B70.0] | [1] | |||
| Sensitive Disease | Oesophagus adenocarcinoma [ICD-11: 2B70.0] | |||
| Sensitive Drug | Erastin | |||
| Molecule Alteration | Expression | Down-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| Cell Pathway Regulation | Ferroptosis signaling pathway | Activation | hsa04216 | |
| In Vitro Model | KYSE150 cells | Esophagus | Homo sapiens (Human) | CVCL_1348 |
| KYSE-30 cells | Esophagus | Homo sapiens (Human) | CVCL_1351 | |
| Experiment for Molecule Alteration |
Western blot assay | |||
| Experiment for Drug Resistance |
CCK8 assay; Colony formation assay | |||
| Mechanism Description | Repression of ANP32E increases the responsiveness of EC to PTX, and the concurrent use of erastin with PTX enhances their anti-cancer effectiveness. These findings provide support for the efficacy of inducing ferroptosis as a potential therapeutic approach to enhance the cytotoxic effects of PTX. ANP32E regulates EC progression and ferroptosis through the p53/SLC7A11 axis, offering a potential molecular target for overcoming PTX resistance in EC treatment. | |||
References
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