Toward Computing Relative Configurations:  16-epi-Latrunculin B, a New Stereoisomer of the Actin Polymerization Inhibitor Latrunculin B

2002 ◽  
Vol 124 (25) ◽  
pp. 7405-7410 ◽  
Author(s):  
Thomas R. Hoye ◽  
Seif-Eldin N. Ayyad ◽  
Brian M. Eklov ◽  
Nadia E. Hashish ◽  
W. Thomas Shier ◽  
...  
Keyword(s):  
Actin Polymerization ◽  
Latrunculin B ◽  
Polymerization Inhibitor

Effect of Actin Polymerization Inhibitor During Oocyte Maturation on Parthenogenetic Embryo Development and Ploidy in Capra hircus

2013 ◽  
Vol 51 (11-12) ◽  
pp. 944-953 ◽  
Author(s):  
R. Ranjan ◽  
R. K. Singh ◽  
T. Yasotha ◽  
Manish Kumar ◽  
Gopal Puri ◽  
...  
Keyword(s):  
Embryo Development ◽  
Oocyte Maturation ◽  
Actin Polymerization ◽  
Capra Hircus ◽  
Polymerization Inhibitor ◽  
Parthenogenetic Embryo

scholarly journals Effects of bistheonellide A, an Actin-polymerization Inhibitor, on Chinese Hamster V79 Cells and on IL-8 Production in PMA-stimulated HL-60 Cells

Marine Drugs ◽  
2006 ◽  
Vol 4 (1) ◽  
pp. 22-27 ◽  
Author(s):  
Taiko Oda ◽  
Jinzhong Xu ◽  
Ayako Fujita ◽  
Masataka Mochizuki ◽  
Michio Namikoshi
Keyword(s):  
Actin Polymerization ◽  
Chinese Hamster ◽  
V79 Cells ◽  
Polymerization Inhibitor ◽  
Chinese Hamster V79 Cells

Latrunculin B modulates electrophysiological characteristics and arrhythmogenesis in pulmonary vein cardiomyocytes

2016 ◽  
Vol 130 (9) ◽  
pp. 721-732 ◽  
Author(s):  
Yen-Yu Lu ◽  
Yung-Kuo Lin ◽  
Zhi-Hong Wen ◽  
Yao-Chang Chen ◽  
Shih-Ann Chen ◽  
...  
Keyword(s):  
Pulmonary Vein ◽  
Actin Polymerization ◽  
Latrunculin B

Lat-B inhibits actin polymerization and Ca2+regulation. Lat-B regulates PV electrophysiology and Ca2+ homeostasis. Lat-B may attenuate PV-initiated AF during stretch.

scholarly journals Cellular Changes of Rat Embryonic Fibroblasts by an Actin-Polymerization Inhibitor, Bistheonellide A, from a Marine Sponge.

1996 ◽  
Vol 21 (3) ◽  
pp. 199-212 ◽  
Author(s):  
Shugo Watabe ◽  
Shun-ichi Wada ◽  
Shin-ya Saito ◽  
Shigeki Matsunaga ◽  
Nobuhiro Fusetani ◽  
...  
Keyword(s):  
Marine Sponge ◽  
Actin Polymerization ◽  
Embryonic Fibroblasts ◽  
Cellular Changes ◽  
Polymerization Inhibitor ◽  
Rat Embryonic Fibroblasts

Anti-HLA-DR Monoclonal Antibody Evokes a Novel Non-Apoptotic Cell Death Pathway In Acute Lymphoblastic Leukemia

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3245-3245
Author(s):  
Khimara Naidoo ◽  
Waleed Alduaij ◽  
Jamie Honeychurch ◽  
Eleanor Cheadle ◽  
Seema Alexander ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Flow Cytometry ◽  
Cell Death ◽  
Acute Lymphoblastic Leukemia ◽  
Cell Lines ◽  
Actin Polymerization ◽  
Lymphoblastic Leukemia ◽  
Cell Contact ◽  
Latrunculin B ◽  
Hla Dr

Abstract Abstract 3245 Whilst modern treatment approaches cure a high number of patients with acute lymphoblastic leukemia (ALL), little progress has been made in the treatment of refractory and relapsed ALL and new treatment approaches are needed. We recently demonstrated that anti-HLA-DR class II monoclonal antibody (mAb) L243 induces a novel non-apoptotic mode of cell death in B-cell lymphoma lines, defined by homotypic adhesion (HA), actin reorganisation and lysosomal activity (Ivanov et al. J Clin Invest, 2009). Here, we extend these important observations and examine whether this novel form of mAb induced cell death occurs in pre-B ALL cell lines. Expression of HLA-DR was determined using flow cytometry in a panel of ALL cell lines (REH, SupB15 and SD1). HLA-DR was expressed at high levels on each of the cell lines. The ability of L243 to induce HA and cell death (Annexin V/PI positivity) was assessed using microscopy and flow cytometry respectively. L243 was able to evoke both strong HA and cell death in all of the ALL cell lines (e.g. in SupB15 cells 46±1.7% death versus 7±0.5% in controls, p<0.001 by Student's t-test). Inhibitors of actin polymerization (cytochalasin D, latrunculin B) were used to assess the role of actin in cell death and HA induced by L243. These inhibitors of actin polymerization inhibited both HA and cell death elicited by L243 (e.g. in SupB15 cells 24±0.5% death versus 10.3±0.8% with Latrunculin B, p<0.001), demonstrating the dependence of HA and cell death on actin reorganisation. The importance of cell to cell contact in this form of antibody induced cell death was confirmed by the addition of low-melting point agarose which physically blocked cell to cell contact and markedly attenuated cell death induced by L243. In contrast using the pan-caspase inhibitor QVD OPH had no effect on cell death induced by L243, indicating that this mode of death is non-apoptotic. These findings demonstrate that anti-HLA DR mAb L243 induces a novel model of cell death in ALL cell lines that is independent of caspase activation and dependent on actin reorganization. This data suggests that this novel mAb induced death pathway is independent of apoptosis and potentially exploitable in the clinic in leukemias resistant to chemotherapy apoptosis induction. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Actin depolymerization is sufficient to induce programmed cell death in self-incompatible pollen

2006 ◽  
Vol 174 (2) ◽  
pp. 221-229 ◽  
Author(s):  
Steven G. Thomas ◽  
Shanjin Huang ◽  
Shutian Li ◽  
Christopher J. Staiger ◽  
Vernonica E. Franklin-Tong
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Actin Polymerization ◽  
Caspase 3 ◽  
Tip Growth ◽  
Causal Link ◽  
Actin Dynamics ◽  
Latrunculin B ◽  
Actin Depolymerization ◽  
Incompatible Pollen

Self-incompatibility (SI) prevents inbreeding through specific recognition and rejection of incompatible pollen. In incompatible Papaver rhoeas pollen, SI triggers a Ca2+ signaling cascade, resulting in the inhibition of tip growth, actin depolymerization, and programmed cell death (PCD). We investigated whether actin dynamics were implicated in regulating PCD. Using the actin-stabilizing and depolymerizing drugs jasplakinolide (Jasp) and latrunculin B, we demonstrate that changes in actin filament levels or dynamics play a functional role in initiating PCD in P. rhoeas pollen, triggering a caspase-3–like activity. Significantly, SI-induced PCD in incompatible pollen was alleviated by pretreatment with Jasp. This represents the first account of a specific causal link between actin polymerization status and initiation of PCD in a plant cell and significantly advances our understanding of the mechanisms involved in SI.

scholarly journals Identification of seco-clavilactone B as a small-molecule actin polymerization inhibitor

FEBS Letters ◽  
2016 ◽  
Vol 590 (8) ◽  
pp. 1163-1173 ◽  
Author(s):  
So Miyazaki ◽  
Yukiko Sasazawa ◽  
Takuma Mogi ◽  
Takehiro Suzuki ◽  
Keisuke Yoshida ◽  
...  
Keyword(s):  
Small Molecule ◽  
Actin Polymerization ◽  
Polymerization Inhibitor

scholarly journals Identification of actin nucleation activity and polymerization inhibitor in ameboid cells: their regulation by chemotactic stimulation.

1989 ◽  
Vol 109 (5) ◽  
pp. 2207-2213 ◽  
Author(s):  
A L Hall ◽  
V Warren ◽  
S Dharmawardhane ◽  
J Condeelis
Keyword(s):  
Dictyostelium Discoideum ◽  
Actin Polymerization ◽  
Developmental Regulation ◽  
Reversible Inhibitor ◽  
Actin Nucleation ◽  
Low Speed ◽  
Polymerization Inhibitor ◽  
Nucleation Activity ◽  
Triton X

Actin polymerization occurs in amebae of Dictyostelium discoideum after chemotactic stimulation (Hall, A. L., A. Schlein, and J. Condeelis. 1988. J. Cell. Biochem. 37:285-299). When cells are lysed with Triton X-100 during stimulation, an actin nucleation activity is detected in lysates by measuring the rate of pyrene-labeled actin polymerization. This stimulated nucleation activity is closely correlated with actin polymerization observed in vivo in its kinetics, developmental regulation, and cytochalasin D sensitivity. Actin polymerization is coordinate with pseudopod extension in synchronized populations of cells and is correlated with the accumulation of F actin in pseudopods. The stimulated actin nucleation activity is present in low-speed pellets from Triton lysates (cytoskeletons) within 3 s of stimulation and is stable compared with the nucleation activity of whole cell lysates. Low-speed supernatants contain a reversible inhibitor of the actin nucleation activity that is itself regulated by chemotactic stimulation. Neither activity requires Ca2+ and both are fully expressed in 10 mM EGTA. Fractions containing the inhibitor do not sever actin filaments but do inhibit actin polymerization that is seeded by fragments of purified F actin. These results indicate that chemotactic stimulation of Dictyostelium discoideum generates both an actin-nucleating activity and an actin-polymerization inhibitor, and suggest that the parallel regulation of these two activities leads to the transient phases of actin polymerization observed in vivo. The different compartmentation of these two activities may account for polarized pseudopod extension in gradients of chemoattractant.

scholarly journals Dysregulation of Cytoskeleton Remodeling Drives Invasive Leading Cells Detachment

Cancers ◽  
2021 ◽  
Vol 13 (22) ◽  
pp. 5648
Author(s):  
Jei-Ming Peng ◽  
Wei-Yu Chen ◽  
Jai-Hong Cheng ◽  
Jia-Wun Luo ◽  
Hong-Tai Tzeng
Keyword(s):  
Cell Adhesion ◽  
Focal Adhesion ◽  
Actin Polymerization ◽  
Cell Detachment ◽  
Latrunculin B ◽  
Adhesion Protein ◽  
Initial Tumor ◽  
Cytoskeleton Remodeling ◽  
Focal Adhesion Protein ◽  
Tgf Β1

Detachment of cancer cells is the first step in tumor metastasis and malignancy. However, studies on the balance of initial tumor anchoring and detachment are limited. Herein, we revealed that the regulation of cytoskeleton proteins potentiates tumor detachment. The blockage of TGF-β1 using neutralizing antibodies induced cancer cell detachment in the Boyden chamber and 3D in-gel spheroid models. Moreover, treatment with latrunculin B, an actin polymerization inhibitor, enhanced cell dissociation by abolishing actin fibers, indicating that TGF-β1 mediates the formation of actin stress fibers, and is likely responsible for the dynamics of anchoring and detachment. Indeed, latrunculin B disrupted the formation of external TGF-β1-induced actin fibers and translocation of intracellular vinculin, a focal adhesion protein, resulting in the suppression of cell adhesion. Moreover, the silencing of vimentin substantially reduced cell adhesion and enhanced cell detachment, revealing that cell adhesion and focal adhesion protein translocation stimulated by TGF-β1 require vimentin. Using the 3D in-gel spheroid model, we found that latrunculin B suppressed the cell adhesion promoted by external TGF-β1, increasing the number of cells that penetrated the Matrigel and detached from the tumor spheres. Thus, cytoskeleton remodeling maintained the balance of cell anchoring and detachment, and the TGF-β1/vimentin/focal adhesion protein assembly axis was involved in the control dynamics of initial tumor detachment.

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