Colchicine-like action of sevine on human embryonic fibroblasts in vitro

1972 ◽  
Vol 73 (6) ◽  
pp. 703-705
Author(s):  
A. F. Vasilos ◽  
V. D. Dmitrienko ◽  
I. G. Shroit
2007 ◽  
Vol 10 (2) ◽  
pp. 157-172 ◽  
Author(s):  
Magda Katsiki ◽  
Niki Chondrogianni ◽  
Ioanna Chinou ◽  
A. Jennifer Rivett ◽  
Efstathios S. Gonos

1982 ◽  
Vol 37 (1) ◽  
pp. 33-37 ◽  
Author(s):  
M. Matsuo ◽  
K. Kaji ◽  
T. Utakoji ◽  
K. Hosoda

2009 ◽  
Vol 23 (2) ◽  
pp. 169-175 ◽  
Author(s):  
Kenichi Miyako ◽  
Laura J. Cobb ◽  
Malik Francis ◽  
Alden Huang ◽  
Bonnie Peng ◽  
...  

Abstract IGF-binding proteins (IGFBPs) have multiple cellular effects, which occur by both IGF-dependent and -independent mechanisms. IGFBP-2 is involved in the regulation of both normal and carcinogenic cell growth. To further understand the actions of IGFBP-2, we carried out a yeast two-hybrid screen to search for intracellular partner proteins using a human prostate cDNA library. We isolated Pim-1-associated protein-1 (PAP-1)-associated protein-1 (PAPA-1) as an IGFBP-2-binding protein, whose expression and subcellular localization is regulated by both IGFBP-2 and androgens. Coimmunoprecipitation and glutathione S-transferase pull-down assay confirmed the interaction in vitro, and confocal microscopy showed the colocalization of IGFBP-2 and PAPA-1 in the nucleus. Suppression of PAPA-1 by small interfering RNA treatment enhanced the growth-promoting effect of IGFBP-2. Conversely, IGFBP-2-promoted bromodeoxyuridine incorporation into LNCaP cells was abrogated by the simultaneous overexpression of myc-hPAPA-1. Mouse embryonic fibroblasts from IGFBP-2 knockout mouse showed diminished growth activity compared with wild type, and expression of FLAG-mPAPA-1 decreased cell proliferation in IGFBP-2 knockout, but not control mouse embryonic fibroblasts. These studies suggest that the growth-promoting role of IGFBP-2 in prostate cancer is inhibited by its intracellular interaction with PAPA-1.


1974 ◽  
Vol 24 (2) ◽  
pp. 237-246 ◽  
Author(s):  
G. Barbanti-Brodano ◽  
A. Mannini-Palenzona ◽  
O. Varoli ◽  
M. Portolani ◽  
M. La Placa

2018 ◽  
Vol 115 (31) ◽  
pp. 7973-7978 ◽  
Author(s):  
Xiaobai Patrinostro ◽  
Pallabi Roy ◽  
Angus Lindsay ◽  
Christopher M. Chamberlain ◽  
Lauren J. Sundby ◽  
...  

The highly similar cytoplasmic β- and γ-actins differ by only four functionally similar amino acids, yet previous in vitro and in vivo data suggest that they support unique functions due to striking phenotypic differences between Actb and Actg1 null mouse and cell models. To determine whether the four amino acid variances were responsible for the functional differences between cytoplasmic actins, we gene edited the endogenous mouse Actb locus to translate γ-actin protein. The resulting mice and primary embryonic fibroblasts completely lacked β-actin protein, but were viable and did not present with the most overt and severe cell and organismal phenotypes observed with gene knockout. Nonetheless, the edited mice exhibited progressive high-frequency hearing loss and degeneration of actin-based stereocilia as previously reported for hair cell-specific Actb knockout mice. Thus, β-actin protein is not required for general cellular functions, but is necessary to maintain auditory stereocilia.


1970 ◽  
Vol 132 (6) ◽  
pp. 1055-1070 ◽  
Author(s):  
Irun R. Cohen ◽  
Lary Stavy ◽  
Michael Feldman

We studied the influence of glucocorticoids on the sensitization phase as well as on the cytolytic effector phase of an in vitro lymphocyte-mediated immune reaction. Lymphocytes obtained from the spleens or lymph nodes of unimmunized inbred rats were sensitized against foreign rat or mouse embryonic fibroblasts in cell culture. The capacity of the sensitized lymphocytes to produce a cytolytic effect was tested by transferring them to target fibroblast cultures. Injury to target fibroblasts was measured by release of radioactive 51Cr from previously labeled fibroblasts or by direct count of viable fibroblasts after incubation with sensitized lymphocytes. Various concentrations of water-soluble hydrocortisone or prednisolone were added to cell cultures during the 5 day sensitization phase and/or during the subsequent cytolytic effector phase and the influence of these hormones on the number and cytolytic capacity of the lymphocytes was measured. During the sensitization phase, the presence of glucocorticoid hormones, at concentrations of about 1 µg/ml, led to a profound decrease in the total number of recoverable lymphocytes. However, the per cent of large transformed lymphocytes was much greater in these treated cultures. The antigen-specific cytolytic capacity per cell of the glucocorticoid-treated lymphocytes, after the hormone was removed, was several times greater than that of lymphocytes sensitized in the absence of added hormones. Glucocorticoids influenced the effector phase of the reaction by inhibiting lymphocyte-mediated injury to target fibroblasts. The hormones, at concentrations of about 1 µg/ml, inhibited the cytolytic effect by about 50% without reducing the viability of the sensitized lymphocytes. Dose-dependent toxicity to lymphocytes and increasing inhibition of cytolytic effect appeared at higher concentrations of hormones. Thus, hydrocortisone and prednisolone, at concentrations of about 1 µg/ml, did not suppress the induction of sensitization, a process which they seem to facilitate in vitro. However, similar concentrations of these hormones appear to inhibit the cytolytic effector mechanism of sensitized lymphocytes. These findings may be relevant to the use of glucocorticoids as immunosuppressive agents in vivo.


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