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Acute cholesterol depletion impairs functional expression of tissue factor in fibroblasts: modulation of tissue factor activity by membrane cholesterol.
The data presented herein suggest that membrane cholesterol functions as a positive regulator of TF function by maintaining TF receptors, probably in noncaveolar lipid rafts, in a high-affinity state for VIIa binding.
Identification of amino acid residues in protein SRP72 required for binding to a kinked 5e motif of the human signal recognition particle RNA
In agreement with biochemical data and results from chymotryptic digestion experiments, molecular modeling of SRP72 implied that the invariant W577 was located inside the predicted structure of an RNA binding domain, similar to how other K-turn recognizing proteins interact with RNA.
Mutagenesis studies toward understanding allostery in thrombin.
- S. Qureshi, Likui Yang, C. Manithody, A. Iakhiaev, A. Rezaie
- Biology, ChemistryBiochemistry
- 1 September 2009
Results suggest that, while exosite-2 of thrombin is an independent cofactor binding-site, both Na(+)-binding andExosite-1 are energetically linked to each other and to the active site.
Catabolism of Factor VIIa Bound to Tissue Factor in Fibroblasts in the Presence and Absence of Tissue Factor Pathway Inhibitor*
- A. Iakhiaev, U. Pendurthi, J. Voigt, M. Ezban, L. Rao
- Biology, ChemistryThe Journal of Biological Chemistry
- 24 December 1999
The data support the concept that F VIIa bound to cell surface TF was endocytosed by two different pathways, and TFPI·Xa-mediated internalization of FVIIa was associated with the depletion of TF from the cell surface.
Active Site Blockade of Factor VIIa Alters Its Intracellular Distribution*
The present data reveal that despite the common pathway of tissue factor-mediated processing, considerable differences exist in the trafficking of factor VIIa and active site-inhibitedfactor VIIa in fibroblasts.
Thrombomodulin-mediated catabolism of protein C by pleural mesothelial and vascular endothelial cells.
The thrombin-TM-mediated degradation of PC by both cell types suggest a previously unrecognized mechanism, which can contribute to PC consumption, and may be pathophysiologically relevant and contribute to an acquired PC deficiency in conditions characterized by sustainedThrombin generation.
Possible mechanisms contributing to oxidative inactivation of activated protein C: molecular dynamics study.
It is found that treatment of APC with these oxidants markedly inhibits the cleavage of the APC-specific chromogenic substrate, suggesting that oxidants can induce changes in the structure of the active site ofAPC.
Activation and Degradation of Protein C by Primary Rabbit Pleural Mesothelial Cells
Observations indicate that sustained expression of PC during evolving pleurodesis induced by TCN is subject to regulation by resident pleural cells: both RPMC and lung fibroblasts.
The role of catalytic cleft and exosite residues of factor VIIa for complex formation with tissue factor pathway inhibitor.
The masking of the mutational effect by the presence of phospholipid shows a critical importance of Xa Gla-domain interactions in stabilizing the quaternary TF-VIIa-Xa-TFPI complex.
Asbestos Induces Tissue Factor in Beas-2BHuman Lung Bronchial Epithelial Cells In Vitro
It is demonstrated that asbestos induces TF expression in lung epithelial cells in vitro, representing a newly recognized potential mechanism by which asbestos may modulate epithelial cell responses germane to lung remodeling.