scholarly journals Computational study of the putative active form of protein Z (PZa): Sequence design and structural modeling

2008 ◽  
Vol 17 (8) ◽  
pp. 1354-1361 ◽  
Author(s):  
Vasu Chandrasekaran ◽  
Chang Jun Lee ◽  
Robert E. Duke ◽  
Lalith Perera ◽  
Lee G. Pedersen
Keyword(s):  
Computational Study ◽  
Active Form ◽  
Structural Modeling ◽  
Protein Z ◽  
Sequence Design

Exploring the binding properties of agonists interacting with human TGR5 using structural modeling, molecular docking and dynamics simulations

RSC Advances ◽  
2015 ◽  
Vol 5 (19) ◽  
pp. 14202-14213 ◽  
Author(s):  
Thangaraj Sindhu ◽  
Pappu Srinivasan
Keyword(s):  
Molecular Docking ◽  
Binding Site ◽  
Type Ii Diabetes ◽  
Computational Study ◽  
Structural Modeling ◽  
Type Ii ◽  
Binding Properties ◽  
Pharmacological Target ◽  
Dynamics Simulations ◽  
Molecular Docking And Dynamics

TGR5, act as a potential pharmacological target in the treatment of type II diabetes. In the computational study, structural modeling and binding site prediction of TGR5 receptor was performed. Two well-known agonists of TGR5 used to investigate the mode and mechanism of binding.

Comprehensive structural modeling and preparation of human 5‐HT 2A G‐protein coupled receptor in functionally active form

Biopolymers ◽  
2019 ◽  
Vol 111 (1) ◽  
Author(s):  
Sukanya Mozumder ◽  
Aritra Bej ◽  
Krishnamoorthi Srinivasan ◽  
Sujoy Mukherjee ◽  
Jayati Sengupta
Keyword(s):  
G Protein ◽  
Active Form ◽  
Structural Modeling ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled

scholarly journals Trans-(−)-Kusunokinin: A Potential Anticancer Lignan Compound against HER2 in Breast Cancer Cell Lines?

Molecules ◽  
2021 ◽  
Vol 26 (15) ◽  
pp. 4537
Author(s):  
Thidarath Rattanaburee ◽  
Tanotnon Tanawattanasuntorn ◽  
Tienthong Thongpanchang ◽  
Varomyalin Tipmanee ◽  
Potchanapond Graidist
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Computational Study ◽  
Active Form ◽  
Dynamics Simulation ◽  
Breast Cancer Cell Lines ◽  
Interfering Rna ◽  
Further Development ◽  
Mcf 7

Trans-(−)-kusunokinin, an anticancer compound, binds CSF1R with low affinity in breast cancer cells. Therefore, finding an additional possible target of trans-(−)-kusunokinin remains of importance for further development. Here, a computational study was completed followed by indirect proof of specific target proteins using small interfering RNA (siRNA). Ten proteins in breast cancer were selected for molecular docking and molecular dynamics simulation. A preferred active form in racemic trans-(±)-kusunokinin was trans-(−)-kusunokinin, which had stronger binding energy on HER2 trans-(+)-kusunokinin; however, it was weaker than the designed HER inhibitors (03Q and neratinib). Predictively, trans-(−)-kusunokinin bound HER2 similarly to a reversible HER2 inhibitor. We then verified the action of (±)-kusunokinin compared with neratinibon breast cancer cells (MCF-7). (±)-Kusunokinin exhibited less cytotoxicity on normal L-929 and MCF-7 than neratinib. (±)-Kusunokinin and neratinib had stronger inhibited cell proliferation than siRNA-HER2. Moreover, (±)-kusunokinin decreased Ras, ERK, CyclinB1, CyclinD and CDK1. Meanwhile, neratinib downregulated HER, MEK1, ERK, c-Myc, CyclinB1, CyclinD and CDK1. Knocking down HER2 downregulated only HER2. siRNA-HER2 combination with (±)-kusunokinin suppressed HER2, c-Myc, CyclinB1, CyclinD and CDK1. On the other hand, siRNA-HER2 combination with neratinib increased HER2, MEK1, ERK, c-Myc, CyclinB1, CyclinD and CDK1 to normal levels. We conclude that trans-(±)-kusunokinin may bind HER2 with low affinity and had a different action from neratinib.

Dupuytren's Contracture and Microvessels

1981 ◽  
Vol 39 ◽  
pp. 470-471
Author(s):  
C. W. Klscher ◽  
D. Speer
Keyword(s):  
Hypertrophic Scar ◽  
Active Form ◽  
Scar Tissue ◽  
Vascular Supply ◽  
Fiber Bundles ◽  
Dupuytren’S Contracture ◽  
Palmar Fascia ◽  
Immune Disease ◽  
Dupuytren's Contracture ◽  
Longitudinal Fiber

Dupuytren's Contracture is a nodular proliferation of the longitudinal fiber bundles of palmar fascia with its attendant contraction. The factors attributed to its etiology have included trauma, diabetes, alcoholism, arthritis, and auto-immune disease. The tissue has been observed by electron microscopy and found to contain myofibroblasts.Dupuytren's Contracture constitutes a scar, and as such, excessive collagen can be observed, along with an active form of fibroblast.Previous studies of the hypertrophic scar have led us to propose that integral in the initiation and sustenance of scar tissue is a profusion of microvascular regeneration, much of which becomes and remains occluded producing a hypoxia which stimulates fibroblast synthesis. Thus, when considering a study of Dupuytren's Contracture, we predicted finding occluded microvessels at or near the fascial scarring focus.Three cases of Dupuytren's Contracture yielded similar specimens, which were fixed in Karnovskys fluid for 2 to 20 days. Upon removal of the contracture bands care was taken to include the contiguous fatty and areolar tissue which contain the vascular supply and to identify the junctional area between old and new fascia.

Integrated morphometrical and electron energy loss image analysis in cytochemistry

1989 ◽  
Vol 47 ◽  
pp. 402-403
Author(s):  
W.C. de Bruijn ◽  
A.A.W. de Jong ◽  
C.W.J. Sorber
Keyword(s):  
Image Analysis ◽  
Acid Phosphatase ◽  
Chemical Analysis ◽  
Active Form ◽  
List Type ◽  
Type Number ◽  
Enzyme Cytochemistry ◽  
Related Data ◽  
Endogenous Peroxidase ◽  
Electron Energy Loss

One aspect of enzyme cytochemistry is, whether all macrophage lysosomal hydrolytical enzymes are present in an active form, or are activated upon stimulation. Integrated morphometrical and chemical analysis has been chosen as a tool to illucidate that cytochemical problem. Mouse peritoneal resident macrophages have been used as a model for this complicated integration of morphometrical and element-related data. Only aldehyde-fixed cells were treated with three cytochemical reactions to detect different enzyme activities within one cell (for details see [1,2]). The enzyme-related precipitates anticipated to be differentiated, were:(1).lysosomal barium and sulphur from aryl sulphatase activity,(2).lysosomal cerium and phosphate from acid phosphatase activity and(3).platinum/di-amino-benzidine( D A B) complex from endogenous peroxidase activity.

Correction: Structural modeling and role of HAX-1 as a positive allosteric modulator of human serine protease HtrA2

2020 ◽  
Vol 477 (2) ◽  
pp. 459-459
Author(s):  
Lalith K. Chaganti ◽  
Shubhankar Dutta ◽  
Raja Reddy Kuppili ◽  
Mriganka Mandal ◽  
Kakoli Bose
Keyword(s):  
Serine Protease ◽  
Structural Modeling ◽  
Allosteric Modulator ◽  
Positive Allosteric Modulator

Plasma Levels of Lipoprotein(a) Are Elevated in Patients with the Antiphospholipid Antibody Syndrome

1994 ◽  
Vol 71 (04) ◽  
pp. 424-427 ◽  
Author(s):  
Masahide Yamazaki ◽  
Hidesaku Asakura ◽  
Hiroshi Jokaji ◽  
Masanori Saito ◽  
Chika Uotani ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Active Form ◽  
Plasminogen Activator Inhibitor ◽  
Arterial System ◽  
Control Group ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Lipoprotein A ◽  
Soluble Thrombomodulin ◽  
Relationship Of

SummaryThe mechanisms underlying clinical abnormalities associated with the antiphospholipid antibody syndrome (APAS) have not been elucidated. We measured plasma levels of lipoprotein(a) [Lp(a)], the active form of plasminogen activator inhibitor (active PAI), thrombin-antithrombin III complex (TAT) and soluble thrombomodulin (TM), to investigate the relationship of these factors to thrombotic events in APAS. Mean plasma levels of Lp(a), TAT, active PAI and TM were all significantly higher in patients with aPL than in a control group of subjects. Plasma levels of Lp(a) and active PAI were significantly higher in patients with aPL and arterial thromboses than in patients with aPL but only venous thromboses. There was a significant correlation between plasma levels of Lp(a) and active PAI in patients with aPL. These findings suggest that patients with aPL are in hypercoagulable state. High levels of Lp(a) in plasma may impair the fibrinolytic system resulting in thromboses, especially in the arterial system.

Immunological Relationship Between Plasminogen Activator Inhibitors from Different Sources

1987 ◽  
Vol 57 (01) ◽  
pp. 029-034 ◽  
Author(s):  
Göran Urdén ◽  
Joanna Chmielewska ◽  
Tomas Carlsson ◽  
Björn Wiman
Keyword(s):  
Plasminogen Activator ◽  
Polyclonal Antibodies ◽  
Active Form ◽  
Polyclonal Antiserum ◽  
The Other ◽  
Hep G2 ◽  
Inhibitor Activity ◽  
Tissue Plasminogen ◽  
Immunological Relationship ◽  
Different Sources

SummaryPolyclonal antibodies have been raised against the inhibitor moiety in the purified complex between tissue plasminogen activator and its fast inhibitor (PA-inhibitor) in human plasma/ serum. A radioimmunoassay for quantitation of PA-inhibitor antigen was developed. The polyclonal antiserum and a previously described monoclonal antibody against the PA-inhibitor (14) have been used to study the immunological relationship between PA-inhibitors from plasma, serum, platelets, placenta extract and conditioned media from Hep G2 and HT 1080 cells. It was demonstrated that the ratio between PA-inhibitor activity and antigen varied considerably between the different sources. In the plasma samples studied, similar activity and antigen concentrations were found, suggesting that the PA-inhibitor in these samples mainly was in an active form. On the other hand the other sources seemed to contain variable amounts of inactive PA-inhibitor forms. Immunoadsorption experiments revealed that the PA-inhibitor (activity and antigen) from all the sources were specifically bound to the insolubilized antibodies (polyclonal and monoclonal). In no case, however, could active PA-inhibitor be eluted from the immunoadsorption columns. Also the competitive radioimmunoassays suggested that the PA-inhibitors from the different sources studied, were closely immunologically related.

Processing and Characterization of Recombinant von Willebrand Factor Expressed in Different Cell Types Using a Vaccinia Virus Vector

1992 ◽  
Vol 67 (01) ◽  
pp. 154-160 ◽  
Author(s):  
P Meulien ◽  
M Nishino ◽  
C Mazurier ◽  
K Dott ◽  
G Piétu ◽  
...  
Keyword(s):  
Vaccinia Virus ◽  
Von Willebrand Factor ◽  
Human Fibroblasts ◽  
Active Form ◽  
Cell Types ◽  
Biologically Active ◽  
L Cells ◽  
Von Willebrand ◽  
Different Cell Types ◽  
Willebrand Factor

SummaryThe cloning of the cDNA encoding von Willebrand factor (vWF) has revealed that it is synthesized as a large precursor (pre-pro-vWF) molecule and it is now clear that the prosequence or vWAgll is responsible for the intracellular multimerization of vWF. We have cloned the complete vWF cDNA and expressed it using a recombinant vaccinia virus as vector. We have characterized the structure and function of the recombinant vWF (rvWF) secreted from five different cell types: baby hamster kidney (BHK), Chinese hamster ovary (CHO), human fibroblasts (143B), mouse fibroblasts (L) and primary embryonic chicken cells. Forty-eight hours after infection, the quantity of vWF antigen found in the cell supernatant varied from 3 to 12 U/dl depending on the cell type. By SDS-agarose gel electrophoresis, the percentage of high molecular weight forms of vWF varied from 39 to 49% relative to normal plasma for BHK, CHO, 143B and chicken cells but was less than 10% for L cells. In all cell types, the two anodic subbands of each multimer were missing. The two cathodic subbands were easily detected only in BHK and L cells. By SDS-PAGE of reduced samples, pro-vWF was present in similar quantity to the fully processed vWF subunit in L cells, present in moderate amounts in BHK and CHO and in very low amounts in 143B and chicken cells. rvWF from all cells bound to collagen and to platelets in the presence of ristocetin, the latter showing a high correlation between binding efficiency and degree of multimerization. rvWF from all cells was also shown to bind to purified FVIII and in this case binding appeared to be independent of the degree of multimerization. We conclude that whereas vWF is naturally synthesized only by endothelial cells and megakaryocytes, it can be expressed in a biologically active form from various other cell types.

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