Disease relevance of Tln1

• In addition, approximately half of WF megakaryocytes showed an increased peripheral localization of talin, often associated with membrane blebs, with decreased talin in the cytoplasmic interior [1].
• At 10 mg/kg, prednisolone markedly suppressed IL-beta and TNF-alpha transcription and calpain mu activation and talin degradation, consistent with the improved 7-day survival after total hepatic ischemia (75% vs. 25% in control group, P = 0.039) [2].
• Talin and vinculin markedly and diffusely immunostained the neuroma [3].
• The present study investigated the immunoreactivity of vinculin, talin and paxillin following stab wounds in the cortex and the underlying white matter of adult rats [4].
• Recent studies have shown significant reduction in the activity of nerve growth factor (NGF) and in the amount of talin cytoskeleton protein immunoreactivity in the perineurium in patients with diabetic neuropathy [5].

High impact information on Tln1

• Western blot analyses were performed for cytoskeletal proteins (talin, alpha-actinin, and vinculin) and the intermediate (activated) and proactivated forms of calpain mu [6].
• In contrast, talin and paxillin remained localized to focal adhesions, suggesting that activation of PI 3-kinase induced a restructuring of the plaque rather than complete dispersion [7].
• The cytoskeleton Type 3 PKC staining closely resembles that of the focal contact protein vinculin and colocalizes with another focal contact protein, talin [8].
• Furthermore, we demonstrate a matrix protein-dependent association of CEACAM1-L with talin, an important regulator of integrin function [9].
• Talin was associated with plasma membranes, membranes of the surface-connected canalicular system, and with alpha-granule membranes of both normal and WF rat platelets, but as in WF megakaryocytes, talin was absent from the large membrane complexes of WF platelets [10].

Biological context of Tln1

• In the presence of TPA (24 and 48 h exposure) the level of colocalization of both talin and phosphoserine residues was the same in the treated cells and in the control cells, but the level of talin phosphorylation was higher in the treated cells [11].
• We also demonstrated that the expression of talin during satellite cell differentiation was constant in both the control and TPA-treated cells [11].
• Increased talin-membrane interaction may be implicated in DA-induced maintenance of a round phenotype in lactotrope cells [12].
• Cell detachment was preceded by a complete loss of the alpha-actinin binding protein talin from the focal adhesions, which was directly associated with F-actin disorganization [13].

Anatomical context of Tln1

• As expected, the rounded cells showed disruption of actin stress fibers and of vinculin and talin at focal contacts [14].
• Talin plays a key role in anchoring actin filaments to integrins as well as to the plasma membrane in focal contacts [11].
• Talin distribution during the differentiation of satellite cells isolated from rat skeletal muscle [11].
• We found that in myotubes from TPA treated cultures (144 h exposure to TPA), talin had localized near the cell membrane in the absence of phosphoserine residues, and that the level of talin phosphorylation was lower than in the control cells [11].
• Talin and alpha-actinin were degraded in a time-dependent manner, although no apparent changes of actin filament were observed [6].

Associations of Tln1 with chemical compounds

• We demonstrated that there is a colocalization of talin and phosphoserine residues during the differentiation of satellite cells, and that it changes after TPA (a protein kinase C activator) treatment, and showed that talin existing in the cell-extracellular matrix and cell-cell contact area was not phosphorylated [11].
• Activation of calcium-dependent proteases during Triton X-100 extraction caused conversion of the 235-Kd antigen into a major fragment of 200 Kd and minor fragments ranging to 115 Kd, identical in mobility to fragments of rat platelet talin produced in the same samples [1].
• Nitric-oxide synthase is a mechanical signal transducer that modulates talin and vinculin expression [15].
• When screening for proteins present in the distal filopodial phosphotyrosine complexes of beta1B cells, p130Cas and the filopodia proteins vasodilator-stimulated phosphoprotein and talin were found, whereas the typical focal complex proteins focal adhesion kinase, paxillin, and vinculin were not [16].
• Other muscle proteins were also present within electrocytes: Actin and sarcomeric alpha-actinin were found within the subsynaptic membrane beneath the plasmalemma of the electrocytes, and talin and acetylcholine receptors were detected both at the innervated posterior face and at the non-innervated anterior face [17].

Enzymatic interactions of Tln1

• In addition, we show that other focal adhesion proteins such as talin and vinculin do not become tyrosine-phosphorylated under the same conditions of cell spreading on extracellular matrix proteins [18].

Other interactions of Tln1

• During the transformation of HSC to myofibroblasts, LAP and LTBP become strongly colocalized with other components of the cytoskeletal network like smooth muscle--actin, desmin, and talin [19].
• Within the peripheral FA, Keap1 was present in distinct foci along the length of the FA and these foci were different from vinculin, talin, paxillin, and phospho-tyrosine rich regions of the FA [20].
• Biochemical analysis has shown a correlation between tyrosine-specific phosphorylation of the fibronectin receptor and the loss of surface-bound fibronectin, but no such correlation with phosphorylation of vinculin or talin [21].
• Dp116, talin, vinculin and vimentin immunoreactivities following nerve transection [3].
• In this study, immunoblot analysis was used to study the expression of N-cadherin, alpha-catenin, beta-catenin, vinculin, talin, and laminin in rat cardiac muscles at embryonic days 15 and 19, the day of birth (postnatal day 0), postnatal weeks 1, 2, 3, and 4, and in the adult [22].

Analytical, diagnostic and therapeutic context of Tln1

• Immunofluorescence labeling with monoclonal antibodies against vinculin and clathrin, and with an antiserum to talin, showed that these proteins are also associated with AChR aggregates; however, their labeling patterns did not correspond closely to the AChR-enriched domains [23].
• Enzyme-linked immunosorbent assay revealed increased concentration of talin, a protein of focal adhesion plaques, and alpha-actin, a marker of VSMC differentiation, in cells on ion-implanted surfaces [24].
• After 60 minutes of intermittent ischemia followed by 2 hours of reperfusion, cell membrane bleb formation, calpain mu activation, and talin degradation were detected in groups 2 and 3 but not in group 1 [25].
• Immunohistochemistry and in situ RT-PCR showed that talin and its mRNA are concentrated and colocalized at myotendinous junctions [26].
• MATERIALS AND METHODS: Post-embedding immunogold electron microscopy using monoclonal antibody against talin in combination with quantitative procedures was employed to localize talin-like immunoreactivity in the sciatic nerve of normal, diabetic and NGF treated diabetic rats [5].

References