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Τετάρτη 27 Ιουνίου 2018

CXCL13 produced by macrophages due to Fli1 deficiency may contribute to the development of tissue fibrosis, vasculopathy, and immune activation in systemic sclerosis

Experimental Dermatology, Volume 0, Issue ja, -Not available-.


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Cancers, Vol. 10, Pages 218: The Osteoclast in Bone Metastasis: Player and Target

Cancers, Vol. 10, Pages 218: The Osteoclast in Bone Metastasis: Player and Target

Cancers doi: 10.3390/cancers10070218

Authors: Antonio Maurizi Nadia Rucci

Bone metastases are frequently the final fate of breast and prostate cancer patients. According to the definition of metastasis as an incurable disease, to date there are no effective treatments for tumor-associated bone metastases and this represents a real challenge for the researchers in the field. The bone is a heterogeneous environment that represents a fertile soil for tumor cells, supporting their growth. Among the different cell types present in the bone, in this review we will focus our attention on the osteoclasts, which are crucial players in the so called “vicious cycle”, a phenomenon triggered by tumor cells eventually leading to both tumor proliferation as well as bone deregulation, thus fueling the development of bone metastasis. The complex network, linking tumor cells to the bone by activating osteoclasts, represents a fruitful target for the treatment of bone metastases. In this review we will describe how tumor cells perturb the bone microenvironment by actively influencing osteoclast formation and activity. Moreover, we will describe the current antiresorptive drugs employed in the treatment of bone metastases as well as new, targeted therapies able to affect both cancer cells and osteoclasts.



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A database of predicted binding sites for cholesterol on membrane proteins, deep in the membrane

The outer membranes of animal cells contain high concentrations of cholesterol of which a small proportion is located deep within the hydrophobic core of the membrane. An automated docking procedure is described that allows the characterization of binding sites for these deep cholesterol molecules on the membrane-spanning surfaces of membrane proteins and in protein cavities or pores, driven by hydrogen bond formation. A database of this class of predicted binding site is described, covering 397 high resolution structures.

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Lipoprotein particle formation by anti-apoptotic tBid.

The interactions of Bcl-2 family proteins with intracellular lipids are essential for the regulation of apoptosis, a mechanism of programmed cell death that is central for the health and development of multicellular organisms. Bid and its caspase-8 cleavage product, tBid, promote permeabilization of the mitochondrial outer membrane (MOM) and sequester anti-apoptotic Bcl-2 proteins to counter their cyto-protective activity. Bid and tBid also promote lipid exchange, a characteristic trait of apoptosis.

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