Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG10470)
Regulator Name Neuronal pentraxin-2 (NPTX2)
Synonyms
Neuronal pentraxin II
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Gene Name NPTX2
Gene ID 4885
Regulator Type Protein coding
Uniprot ID P47972
Sequence
MLALLAASVALAVAAGAQDSPAPGSRFVCTALPPEAVHAGCPLPAMPMQGGAQSPEEELR
AAVLQLRETVVQQKETLGAQREAIRELTGKLARCEGLAGGKARGAGATGKDTMGDLPRDP
GHVVEQLSRSLQTLKDRLESLEHQLRANVSNAGLPGDFREVLQQRLGELERQLLRKVAEL
EDEKSLLHNETSAHRQKTESTLNALLQRVTELERGNSAFKSPDAFKVSLPLRTNYLYGKI
KKTLPELYAFTICLWLRSSASPGIGTPFSYAVPGQANEIVLIEWGNNPIELLINDKVAQL
PLFVSDGKWHHICVTWTTRDGMWEAFQDGEKLGTGENLAPWHPIKPGGVLILGQEQDTVG
GRFDATQAFVGELSQFNIWDRVLRAQEIVNIANCSTNMPGNIIPWVDNNVDVFGGASKWP
VETCEERLLDL

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Function
Likely to play role in the modification of cellular properties that underlie long-term plasticity. Binds to agar matrix in a calcium-dependent manner (By similarity).

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HGNC ID
HGNC:7953
KEGG ID hsa:4885
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
NPTX2 can regulate the following target(s), and cause disease/drug response(s). You can browse detail information of target(s) or disease/drug response(s).
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Unspecific Target [Unspecific Target]
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Responsed Disease Glioblastoma ICD-11: 2A00
 Disease Info 
Responsed Drug Boric Acid Investigative
 Drug Info 
Pathway Response Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell apoptosis
In Vitro Model
 C6 cells Malignant glioma Rattus norvegicus CVCL_0194
Response regulation Our hypothesis and results provided proof that boric acid prevent tumor progression by regulation of ferroptosis, apoptosis and semaphorin signaling pathway. BA was found to have more effective on SEMA3F/NP2 upregulated against C6 untreated cells. What's more, the novel anticancer candidate drug effect of BA were principally associated with the ACSL4/GPX4, TOS/TAS biochemical marker and SEMA3F/NP2 signaling pathways. Dose-decently BA induced oxidative and ferroptosis Glioblastoma multiform.
Glioblastoma [ICD-11: 2A00]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Neuronal pentraxin-2 (NPTX2) Protein coding
 Regulator Info 
Responsed Drug Boric Acid Investigative
 Drug Info 
Pathway Response Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell apoptosis
In Vitro Model
 C6 cells Malignant glioma Rattus norvegicus CVCL_0194
Response regulation Our hypothesis and results provided proof that boric acid prevent tumor progression by regulation of ferroptosis, apoptosis and semaphorin signaling pathway. BA was found to have more effective on SEMA3F/NP2 upregulated against C6 untreated cells. What's more, the novel anticancer candidate drug effect of BA were principally associated with the ACSL4/GPX4, TOS/TAS biochemical marker and SEMA3F/NP2 signaling pathways. Dose-decently BA induced oxidative and ferroptosis Glioblastoma multiform.
Boric Acid [Investigative]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response [1]
Drug for Ferroptosis Inducer
Response Target Unspecific Target
Responsed Disease Glioblastoma ICD-11: 2A00
 Disease Info 
Pathway Response Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell apoptosis
In Vitro Model
 C6 cells Malignant glioma Rattus norvegicus CVCL_0194
Response regulation Our hypothesis and results provided proof that boric acid prevent tumor progression by regulation of ferroptosis, apoptosis and semaphorin signaling pathway. BA was found to have more effective on SEMA3F/NP2 upregulated against C6 untreated cells. What's more, the novel anticancer candidate drug effect of BA were principally associated with the ACSL4/GPX4, TOS/TAS biochemical marker and SEMA3F/NP2 signaling pathways. Dose-decently BA induced oxidative and ferroptosis Glioblastoma multiform.
References
Ref 1 The dual role of boron in vitro neurotoxication of glioblastoma cells via SEMA3F/NRP2 and ferroptosis signaling pathways. Environ Toxicol. 2023 Jan;38(1):70-77. doi: 10.1002/tox.23662. Epub 2022 Sep 22.