Talin2 binds to non-muscle myosin IIa and regulates cell attachment and fibronectin secretion.
Cell adhesion
Fibronectin secretion
MMP1
Non-muscle myosin IIA
Talin-integrin interaction
Talin2
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
30 Aug 2024
30 Aug 2024
Historique:
received:
11
03
2024
accepted:
22
08
2024
medline:
31
8
2024
pubmed:
31
8
2024
entrez:
30
8
2024
Statut:
epublish
Résumé
Talin2 is localized to large focal adhesions and is indispensable for traction force generation, invadopodium formation, cell invasion as well as metastasis. Talin2 has a higher affinity toward β-integrin tails than talin1. Moreover, disruption of the talin2-β-integrin interaction inhibits traction force generation, invadopodium formation and cell invasion, indicating that a strong talin2-β-integrin interaction is required for talin2 to fulfill these functions. Nevertheless, the role of talin2 in mediation of these processes remains unknown. Here we show that talin2 binds to the N-terminus of non-muscle myosin IIA (NMIIA) through its F3 subdomain. Moreover, talin2 co-localizes with NMIIA at cell edges as well as at some cytoplasmic spots. Talin2 also co-localizes with cortactin, an invadopodium marker. Furthermore, overexpression of NMIIA promoted the talin2 head binding to the β1-integrin tail, whereas knockdown of NMIIA reduced fibronectin and matrix metalloproteinase secretion as well as inhibited cell attachment on fibronectin-coated substrates. These results suggest that talin2 binds to NMIIA to control the secretion of extracellular matrix proteins and this interaction modulates cell adhesion.
Identifiants
pubmed: 39215026
doi: 10.1038/s41598-024-70866-w
pii: 10.1038/s41598-024-70866-w
pmc: PMC11364542
doi:
Substances chimiques
Talin
0
Fibronectins
0
Nonmuscle Myosin Type IIA
EC 3.6.1.-
TLN2 protein, human
0
Integrin beta1
0
Cortactin
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
20175Subventions
Organisme : Polish National Science Centre PRELUDIUM
ID : 2018/31/N/ NZ3/02031
Organisme : Academy of Finland
ID : 331946
Organisme : NIH HHS
ID : GM122994
Pays : United States
Informations de copyright
© 2024. The Author(s).
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