His primary areas of investigation include Cell biology, Endoplasmic reticulum, Receptor, Inositol and Calcium signaling. His study in Cell biology is interdisciplinary in nature, drawing from both Apoptosis, Calcium-binding protein and Voltage-dependent calcium channel. Humbert De Smedt has researched Endoplasmic reticulum in several fields, including Programmed cell death and Homeostasis.
His Receptor study combines topics from a wide range of disciplines, such as Mechanism of action and Gene isoform. His studies deal with areas such as Ruthenium red, Calcium, Biophysics, Fusion protein and Binding site as well as Inositol. His biological study spans a wide range of topics, including Autophagy, Unfolded protein response, Downregulation and upregulation and Mitochondrion.
Humbert De Smedt spends much of his time researching Cell biology, Receptor, Inositol, Biochemistry and Endoplasmic reticulum. The various areas that Humbert De Smedt examines in his Cell biology study include Inositol trisphosphate receptor and Voltage-dependent calcium channel. His work in Receptor addresses issues such as Binding site, which are connected to fields such as Plasma protein binding.
His Inositol research incorporates themes from Amino acid, Ruthenium red, Stimulation and Adenosine triphosphate. His study in Biochemistry is interdisciplinary in nature, drawing from both Biophysics and Calcium. In the field of Endoplasmic reticulum, his study on Thapsigargin overlaps with subjects such as SERCA.
His scientific interests lie mostly in Cell biology, Endoplasmic reticulum, Intracellular, Apoptosis and Receptor. His Cell biology research is multidisciplinary, incorporating elements of Autophagy, Cellular homeostasis and Inositol trisphosphate receptor. His Inositol trisphosphate receptor research is multidisciplinary, relying on both Peptide sequence, Function, Binding site and Voltage-dependent calcium channel.
His Endoplasmic reticulum research integrates issues from Inositol, Peptide and Calcium signaling. The Intracellular study combines topics in areas such as Extracellular, Biophysics and Ion transporter. His Programmed cell death study, which is part of a larger body of work in Apoptosis, is frequently linked to B-cell lymphoma, bridging the gap between disciplines.
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Endoplasmic-Reticulum Calcium Depletion and Disease
Djalila Mekahli;Geert Bultynck;Jan B. Parys;Humbert De Smedt.
Cold Spring Harbor Perspectives in Biology (2011)
Ca2+ release induced by inositol 1,4,5-trisphosphate is a steady-state phenomenon controlled by luminal Ca2+ in permeabilized cells
Ludwig Missiaen;Humbert De Smedt;Guillaume Droogmans;Rik Casteels.
Functional specialization of calreticulin domains.
Kimitoshi Nakamura;Anna Zuppini;Serge Arnaudeau;Jeffery Lynch.
Journal of Cell Biology (2001)
The BH4 domain of Bcl-2 inhibits ER calcium release and apoptosis by binding the regulatory and coupling domain of the IP3 receptor
Yi Ping Rong;Geert Bultynck;Ademuyiwa S. Aromolaran;Fei Zhong.
Proceedings of the National Academy of Sciences of the United States of America (2009)
Targeting Bcl-2-IP3 receptor interaction to reverse Bcl-2's inhibition of apoptotic calcium signals
Yi Ping Rong;Ademuyiwa S. Aromolaran;Geert Bultynck;Fei Zhong.
Molecular Cell (2008)
Phosphorylation of inositol 1,4,5-trisphosphate receptors by protein kinase B/Akt inhibits Ca2+ release and apoptosis.
Tania Szado;Veerle Vanderheyden;Jan B. Parys;Humbert De Smedt.
Proceedings of the National Academy of Sciences of the United States of America (2008)
A dual role for the anti-apoptotic Bcl-2 protein in cancer: mitochondria versus endoplasmic reticulum
Haidar Akl;Tamara Vervloessem;Santeri Kiviluoto;Mart Bittremieux.
Biochimica et Biophysica Acta (2014)
Expression and function of ryanodine receptors in nonexcitable cells.
Deborah L. Bennett;Timothy R. Cheek;Michael J. Berridge;Humbert De Smedt.
Journal of Biological Chemistry (1996)
Intracellular Ca2+ storage in health and disease: a dynamic equilibrium.
Eva Sammels;Jan B. Parys;Ludwig Missiaen;Humbert De Smedt.
Cell Calcium (2010)
Regulation of inositol 1,4,5-trisphosphate-induced Ca2+ release by reversible phosphorylation and dephosphorylation.
Veerle Vanderheyden;Benoit Devogelaere;Ludwig Missiaen;Humbert De Smedt.
Biochimica et Biophysica Acta (2009)
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