ArticleScientific reports2017
The molecular basis of talin2's high affinity toward β1-integrin.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- A Review of Talin- and Integrin-Dependent Molecular Mechanisms in Cancer Invasion and Metastasis.International journal of molecular sciences · 2025Review
- Talin2 binds to non-muscle myosin IIa and regulates cell attachment and fibronectin secretion.Scientific reports · 2024Article
- A possible molecular mechanism for mechanotransduction at cellular focal adhesion complexes.Biophysical reports · 2021Article
- LOXL3 Silencing Affected Cell Adhesion and Invasion in U87MG Glioma Cells.International journal of molecular sciences · 2021Article
- Synergistic Beneficial Effect of Docosahexaenoic Acid (DHA) and Docetaxel on the Expression Level of Matrix Metalloproteinase-2 (MMP-2) and MicroRNA-106b in Gastric Cancer.Journal of gastrointestinal cancer · 2020Article
- PtdIns(4,5)P2 and PtdIns(3,4,5)P3 dynamics during focal adhesions assembly and disassembly in a cancer cell line.Turkish journal of biology = Turk biyoloji dergisi · 2020Article
- The tale of two talins - two isoforms to fine-tune integrin signalling.FEBS letters · 2018Review
- The role of talin2 in breast cancer tumorigenesis and metastasis.Oncotarget · 2017Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Talin interacts with β-integrin tails and actin to control integrin activation, thus regulating focal adhesion dynamics and cell migration. There are two talin genes, Tln1 and Tln2, which encode talin1 and talin2, and it is generally believed that talin2 functions redundantly with talin1. However, we show here that talin2 has a higher affinity to β1-integrin tails than talin1. Mutation of talin2 S339 to leucine, which can cause Fifth Finger Camptodactyly, a human genetic disease, completely disrupted its binding to β-integrin tails. Also, substitution of talin1 C336 with Ser enhanced the affinity of talin1, whereas substitution of talin2 S339 with Cys diminished that of talin2. Further computational modeling analysis shows that talin2 S339 formed a hydrogen bond with E353, which is critical for inducing key hydrogen bonds between talin2 N326 and β1-integrin R760, and between talin2 K327 and β1-integrin D759. Mutation at any of these residues significantly diminished the interaction of talin2 with β1- integrin tails. These hydrogen bonds were not observed in talin1/β1-integrin, but did exist in talin1
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