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Juan F. Santibanez

Researcher at University of Belgrade

Publications -  115
Citations -  3577

Juan F. Santibanez is an academic researcher from University of Belgrade. The author has contributed to research in topics: Transforming growth factor & Mesenchymal stem cell. The author has an hindex of 30, co-authored 102 publications receiving 2929 citations. Previous affiliations of Juan F. Santibanez include University of Chile & Spanish National Research Council.

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TGF-β/TGF-β receptor system and its role in physiological and pathological conditions

TL;DR: The knowledge about the mechanisms involved in TGF-β signal transduction has allowed a better understanding of the disease pathogenicity as well as the identification of several molecular targets with great potential in therapeutic interventions.
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Interaction and functional interplay between endoglin and ALK‐1, two components of the endothelial transforming growth factor‐β receptor complex

TL;DR: It is found that the extracellular and cytoplasmic domains of the auxiliary TGF‐β receptor endoglin interact with ALK‐1 (a type I TGF•β receptor), and this results suggest that the functional association ofendoglin with ALk‐1 is critical for the endothelial responses to T GF‐β.
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ROS-NFkappaB mediates TGF-beta1-induced expression of urokinase-type plasminogen activator, matrix metalloproteinase-9 and cell invasion.

TL;DR: ROS-NFκΒ acts as the crucial signal in TGF-β1-induced uPA and MMP-9 expression thereby mediating the enhancement of cellular malignity by TGF -β1.
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Transforming Growth Factor-Beta and Oxidative Stress Interplay: Implications in Tumorigenesis and Cancer Progression

TL;DR: The mutual collaboration of TGF-β and ROS in tumorigenesis is highly complex, and, due to their differential roles in tumor progression, careful consideration should be taken when thinking of combinatorial targeting in cancer therapies.
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Transforming growth factor-beta and matrix metalloproteinases: functional interactions in tumor stroma-infiltrating myeloid cells.

TL;DR: This review will focus on the compartment of myeloid stroma cells, such as tumor-associated macrophages, neutrophils, and dendritic and mast cells, which are potently regulated by TGF-β and produce large amounts of MMPs.