scholarly journals HIV-1 protein induced modulation of primary human osteoblast differentiation and function via a Wnt/β-catenin-dependent mechanism

2012 ◽  
Vol 31 (2) ◽  
pp. 218-226 ◽  
Author(s):  
Joseph S. Butler ◽  
Eilis C. Dunning ◽  
David W. Murray ◽  
Peter P. Doran ◽  
John M. O'Byrne

1994 ◽  
Vol 55 (5) ◽  
pp. 356-362 ◽  
Author(s):  
S. -L. Cheng ◽  
S. -F. Zhang ◽  
T. L. Nelson ◽  
P. M. Warlow ◽  
R. Civitelli


2010 ◽  
Vol 11 (1) ◽  
Author(s):  
Joseph S Butler ◽  
Joseph M Queally ◽  
Brian M Devitt ◽  
David W Murray ◽  
Peter P Doran ◽  
...  


Author(s):  
Abdulhafez A. Selim ◽  
Samir M. Abdelmagid ◽  
Reem A. Kanaan ◽  
Steven L. Smock ◽  
Thomas A. Owen ◽  
...  


Cell ◽  
1998 ◽  
Vol 92 (6) ◽  
pp. 809-818 ◽  
Author(s):  
Julius Kahn ◽  
Bruce Walcheck ◽  
Grace I Migaki ◽  
Mark A Jutila ◽  
Takashi Kei Kishimoto


2012 ◽  
Vol 227 (6) ◽  
pp. 2677-2685 ◽  
Author(s):  
Fengchang Zhu ◽  
Michael S. Friedman ◽  
Weijun Luo ◽  
Peter Woolf ◽  
Kurt D. Hankenson


2020 ◽  
Author(s):  
Ada Nowosad ◽  
Pauline Jeannot ◽  
Caroline Callot ◽  
Justine Creff ◽  
Renaud T. Perchey ◽  
...  

SummaryAutophagy is a catabolic process whereby cytoplasmic components are degraded within lysosomes, allowing cells to maintain energy homeostasis during nutrient depletion. Several studies have shown that the CDK inhibitor p27Kip1 promotes starvation-induced autophagy. However, the underlying mechanism remains unknown. Here, we report that in amino acid deprived cells, p27 controls autophagy via an mTORC1-dependent mechanism. During prolonged amino acid starvation, a fraction of p27 is recruited to lysosomes where it interacts with LAMTOR1, a component of the Ragulator complex required for mTORC1 lysosomal localization and activation. p27 binding to LAMTOR1 prevents Ragulator assembly and function and subsequent mTORC1 activation, thereby promoting autophagy. Conversely, upon amino acid withdrawal, p27−/− cells exhibit elevated mTORC1 signaling, impaired lysosomal activity and autophagy, and resistance to apoptosis. This is associated with sequestration of TFEB in the cytoplasm, preventing the induction of lysosomal genes required for lysosomal function. Silencing of LAMTOR1 or mTOR inhibition restores autophagy and induces apoptosis in p27−/− cells. Together, these results reveal a direct, coordinated regulation between the cell cycle and cell growth machineries.



Blood ◽  
1988 ◽  
Vol 71 (3) ◽  
pp. 672-676
Author(s):  
SA Cannistra ◽  
E Vellenga ◽  
P Groshek ◽  
A Rambaldi ◽  
JD Griffin

Human colony-stimulating factors (CSF) exert multiple effects on the proliferation, differentiation, and function of myeloid lineage cells. In this study, the effects of three recombinant human CSFs (granulocyte- monocyte CSF [GM-CSF], interleukin 3 [IL-3], and granulocyte CSF [G- CSF]) on antibody-independent monocyte tumoricidal activity were investigated by using WEHI 164 fibrosarcoma cells as monocyte-sensitive targets. None of the CSFs directly induced monocyte cytotoxicity, although both GM-CSF and IL-3 were found to significantly enhance monocyte killing in response to a second stimulatory event (endotoxin). No effect was seen with G-CSF. Antitumor necrosis factor antibody completely abolished CSF-enhanced monocyte cytotoxicity, which suggests that this effect was mediated through increased release of tumor necrosis factor (TNF). As previously shown for GM-CSF, IL-3 was found to induce cytoplasmic accumulation of TNF messenger RNA (mRNA) after 18 hours of exposure. These results suggest that GM-CSF and IL-3 may stimulate monocyte killing indirectly by enhancing expression of TNF mRNA, thereby leading to augmented TNF protein secretion in response to a second activation signal.



Author(s):  
Flávia A. Oliveira ◽  
Adriana A. Matos ◽  
Mariana R. Santesso ◽  
Cintia K. Tokuhara ◽  
Aline L. Leite ◽  
...  


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