Thymosin β4 Is an Endogenous Iron Chelator and Molecular Switcher of Ferroptosis.
NMR
TEM
ferroptosis
mRNA
metal chelation
molecular dynamics
thymosine beta 4
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
04 Jan 2022
04 Jan 2022
Historique:
received:
13
12
2021
revised:
01
01
2022
accepted:
03
01
2022
entrez:
11
1
2022
pubmed:
12
1
2022
medline:
8
2
2022
Statut:
epublish
Résumé
Thymosin β4 (Tβ4) was extracted forty years agofrom calf thymus. Since then, it has been identified as a G-actin binding protein involved in blood clotting, tissue regeneration, angiogenesis, and anti-inflammatory processes. Tβ4 has also been implicated in tumor metastasis and neurodegeneration. However, the precise roles and mechanism(s) of action of Tβ4 in these processes remain largely unknown, with the binding of the G-actin protein being insufficient to explain these multi-actions. Here we identify for the first time the important role of Tβ4 mechanism in ferroptosis, an iron-dependent form of cell death, which leads to neurodegeneration and somehow protects cancer cells against cell death. Specifically, we demonstrate four iron
Identifiants
pubmed: 35008976
pii: ijms23010551
doi: 10.3390/ijms23010551
pmc: PMC8745404
pii:
doi:
Substances chimiques
Iron Chelating Agents
0
thymosin beta(4)
549LM7U24W
Thymosin
61512-21-8
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Regione Autonoma della Sardegna
ID : RASSR79857
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