scholarly journals Cocaine addicted to cytoskeletal change and a fibrosis high

Cytoskeleton ◽  
2019 ◽  
Vol 76 (2) ◽  
pp. 177-185 ◽  
Author(s):  
Avnish Verma ◽  
Jason Bennett ◽  
Ayşe Merve Örme ◽  
Elena Polycarpou ◽  
Brian Rooney
Keyword(s):  
Cytoskeletal Change

scholarly journals Biochemical, Structural, and Biomarker Evidence for Calpain-Mediated Cytoskeletal Change After Diffuse Brain Injury Uncomplicated by Contusion

2009 ◽  
Vol 68 (3) ◽  
pp. 241-249 ◽  
Author(s):  
Melissa J. McGinn ◽  
Brian J. Kelley ◽  
Linnet Akinyi ◽  
Monika W. Oli ◽  
Ming Cheng Liu ◽  
...  
Keyword(s):  
Brain Injury ◽  
Diffuse Brain Injury ◽  
Cytoskeletal Change ◽  
Diffuse Brain

Immunocytochemistrical Studies on Cytoskeletal Change in Cultured Cardiomyocyte of Tilapia

2000 ◽  
Vol 6 (S2) ◽  
pp. 888-889
Author(s):  
L. C. Tung
Keyword(s):  
Culture Medium ◽  
Cultured Cells ◽  
Calf Serum ◽  
Amino Acid Mixture ◽  
Penicillin G ◽  
Acid Mixture ◽  
Minimal Essential Medium ◽  
Cultured Fish ◽  
Cytoskeletal Change

In the present study, the myofibril regeneration in the long-term cultured fish cardiomyocytes was studied with immunocytochemistry.Adult Tilapia heart was dissociated into a single-cell suspension with collagenase and protease-minced tissue method. The culture medium was Eagle's minimal essential medium (MEM) with Earle's salts, supplemented with 10% fetal calf serum, 1 x nonessential amino acid mixture, 100 IU/ml penicillin G, and 100 μg/ml streptomycin. The cultured cells were grown in a humidified CO2 incubator at 28°Cand in a medium without glutamine for eliminating fibroblast contamination. In the initial 24 h culture, the elongated-shape cells gradually shortened from their both ends and rounded up. Over 5 to 6 days postcultivation, the cells attached to the bottom of the culture flask and began to protrude pseudopodia. The cells could not be subcultured and also proliferated indefinitely. The life span of cells in culture was 30 to 60 days.

Transient dynamic actin cytoskeletal change stimulates the osteoblastic differentiation

2009 ◽  
Vol 27 (2) ◽  
pp. 158-167 ◽  
Author(s):  
Chikahisa Higuchi ◽  
Norimasa Nakamura ◽  
Hideki Yoshikawa ◽  
Kazuyuki Itoh
Keyword(s):  
Osteoblastic Differentiation ◽  
Transient Dynamic ◽  
Cytoskeletal Change

Thrombin induced cytoskeletal change in cultured bovine corneal endothelial cells mediated via protein kinase C pathway

1995 ◽  
Vol 14 (1) ◽  
pp. 35-45 ◽  
Author(s):  
Taiji Sakamoto ◽  
David R. Hinton ◽  
Hitomi Sakamoto ◽  
Rayudu Gopalakrishna ◽  
Stephen J. Ryan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Corneal Endothelial Cells ◽  
Kinase C ◽  
Cytoskeletal Change

9J-18 Measurement of Local Cytoskeletal Change in an Osteoblast Induced by Mechanical Stimulation

2011 ◽  
Vol 2010.23 (0) ◽  
pp. 591-592
Author(s):  
Kazuhiro SAKATA ◽  
Toshihiko SHIRAISHI ◽  
Shin MORISHITA ◽  
Ryohei TAKEUCHI
Keyword(s):  
Mechanical Stimulation ◽  
Cytoskeletal Change

scholarly journals Role of Phosphatidylinositol 4,5-Bisphosphate in Ras/Rac-Induced Disruption of the Cortactin-Actomyosin II Complex and Malignant Transformation

1998 ◽  
Vol 18 (7) ◽  
pp. 3829-3837 ◽  
Author(s):  
Hong He ◽  
Takeshi Watanabe ◽  
Xi Zhan ◽  
Cai Huang ◽  
Ed Schuuring ◽  
...  
Keyword(s):  
Actin Cytoskeleton ◽  
Malignant Transformation ◽  
Myosin Ii ◽  
Signal Transduction Pathway ◽  
Dependent Manner ◽  
Transduction Pathway ◽  
Membrane Ruffling ◽  
Oncogenic Ras ◽  
Cytoskeletal Change

ABSTRACT Oncogenic Ras mutants such as v-Ha-Ras cause a rapid rearrangement of actin cytoskeleton during malignant transformation of fibroblasts or epithelial cells. Both PI-3 kinase and Rac are required for Ras-induced malignant transformation and membrane ruffling. However, the signal transduction pathway(s) downstream of Rac that leads to membrane ruffling and other cytoskeletal change(s) as well as the exact biochemical nature of the cytoskeletal change remain unknown. Cortactin/EMS1 is the first identified molecule that is dissociated in a Rac–phosphatidylinositol 4,5-biphosphate (PIP2)-dependent manner from the actin-myosin II complex during Ras-induced malignant transformation; either the PIP2 binder HS1 or the Rac blocker SCH51344 restores the ability of EMS1 to bind the complex and suppresses the oncogenicity of Ras. Furthermore, while PIP2 inhibits the actin-EMS1 interaction, HS1 reverses the PIP2 effect. Thus, we propose that PIP2, an end-product of the oncogenic Ras/PI-3 kinase/Rac pathway, serves as a second messenger in the Ras/Rac-induced disruption of the actin cytoskeleton and discuss the anticancer drug potential of PIP2-binding molecules.

scholarly journals Snake venom cardiotoxin can rapidly induce actin polymerization in intact platelets

1993 ◽  
Vol 290 (2) ◽  
pp. 591-594 ◽  
Author(s):  
R F Liou ◽  
W C Chang ◽  
S T Chu ◽  
Y H Chen
Keyword(s):  
Actin Polymerization ◽  
Cytochalasin B ◽  
Cell Lysis ◽  
Toxin Concentration ◽  
Intact Cells ◽  
Lactate Dehydrogenase Activity ◽  
Rabbit Platelets ◽  
Cytoskeletal Change ◽  
Naja Atra ◽  
Rapid Incorporation

The action of Taiwan cobra (Naja naja atra) venom cardiotoxin on rabbit platelets at 37 degrees C was characterized by observing cytoskeletal alterations and cell lysis. At a concentration of 21.4 microM the toxin produced no cell lysis within 30 s, and less than 5% of the total lactate dehydrogenase activity of intact cells was detected in the suspending medium after the interaction had proceeded for 3 min. The extent of cell lysis was proportional to toxin concentration and interaction time. Before cell lysis, the toxin caused rapid incorporation of actin monomers into cross-linked actin filaments. The actin incorporation could be inhibited by either the presence of cytochalasin B or increased CaCl2 concentration in the suspending medium. However, addition of indomethacin did not influence the toxin-induced cytoskeletal change.

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