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The N-terminal ABD1 of TLN blocks actin filament barbed-end elongation, whereas ABD2 and ABD3 do not show any activity.
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Expression of ecotopic viral integration site 1 (EVI1) is positively correlated with talin1 (TLN1) in both chronic myeloid leukemia (CML)-chronic phase (CP) and CML-blast crisis (BC) cases.
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Low TLN1 expression is associated with invasion and metastasis in Hepatocellular Carcinoma.
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Calpain small subunit 1 (Capn4) overexpression increased the protein level of cleaved talin and and activated the focal adhesion kinase (FAK)/AKT/MAPK signaling in 786-O cells, while Capn4 silencing decreased the protein level of cleaved talin in Caki-1 cells.
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Talin-1 induces proliferation and migration of vascular smooth muscle cells obtained from patients with thoracic aortic dissection.
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Here, the authors show that cortical microtubule stabilization sites containing CLASPs, KIF21A, LL5beta and liprins are recruited to focal adhesions by the adaptor protein KANK1, which directly interacts with the major adhesion component, talin. Structural studies showed that the conserved KN domain in KANK1 binds to the talin rod domain R7.
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Vinculin head-tail interaction is required on soft substrates to destabilize vinculin and talin in FAs, and to allow hMSCs branching. Another module involves paxillin and FAK, which soft substrates also destabilize, but independently of vinculin head-tail interaction. This multi-modularity may be key to allow a versatile response to complex biomechanical cues.
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The central role of talin and vinculin in cell adhesions suggests that the disintegration of the tissue in atherosclerosis could be partially driven by downregulation of these genes, leading to loosening of cell-ECM interactions and remodeling of the tissue.
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Application of these techniques to new talin biosensors reveals an intramolecular tension gradient across talin-1 that is established upon integrin-mediated cell adhesion. The tension gradient is actomyosin- and vinculin-dependent and sensitive to the rigidity of the extracellular environment
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Our findings confirm the role of Talin-1 in carcinogenesis and provided a set of novel therapeutic targets for the treatment of hepatocellular carcinoma
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These data show that TLN1 can act as a viral restriction factor that suppresses hepatitis B virus replication, and suggest that the HBx relieves this restriction by inducing TLN1 degradation.
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The ERK pathway was responsible for these promoting effects of Talin1 knockdown in HCC cells.
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This study showed that serum sTalin-1 levels were associated with a sustained increase in disability after MS attack but not with serum anti-Talin-1 antibody levels.
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The Rap1-RIAM-talin axis of integrin activation and blood cell function
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These findings suggested that Talin-1 protein was significantly upregulated in PCa tissues compared with that of BPH tissue and Talin-1 expression was an independent predictor for lymph node metastasis and biochemical recurrence of PCa.
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Serum talin-1 had 97.7% sensitivity.
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Both TLN-1 and TLN-2 levels correlate with tumorigenicity in human HCC, indicating that these molecules constitute important molecular targets for the diagnosis and/or treatment of hepatocellular carcinoma .
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TLN1 significantly increases in refractory glioblastoma multiforme
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Applying correlative imaging to link live cell and fixed immunofluorescence data on a single cell basis, we related per cell talin-1 levels to per cell measures quantitatively defining an array of cellular properties.
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Disruption of the RIAM/lamellipodin-integrin-talin complex markedly impairs cell migration.
