Lisak 2015 Cell Death Differ: Difference between revisions
(Created page with "{{Publication |title=Lisak D, Schacht T, Gawlitza A, Albrecht P, Aktas O, Koop B, Gliem M, Hofstetter HH, Zanger K, Bultynck G, Parys JB, De Smedt H, Kindler T, Adams-Quack P, Ha...") Β |
No edit summary |
||
| Line 1: | Line 1: | ||
{{Publication | {{Publication | ||
|title=Lisak D, Schacht T, Gawlitza A, Albrecht P, Aktas O, Koop B, Gliem M, Hofstetter HH, Zanger K, Bultynck G, Parys JB, De Smedt H, Kindler T, Adams-Quack P, Hahn M, Waisman A, Reed JC, HΓΆvelmeyer N, Methner A (2015) BAX inhibitor-1 is a Ca<sup>2+</sup> channel critically important for immune cell function and survival. Cell Death Differ [Epub ahead of print]. Β | |title=Lisak D, Schacht T, Gawlitza A, Albrecht P, Aktas O, Koop B, Gliem M, Hofstetter HH, Zanger K, Bultynck G, Parys JB, De Smedt H, Kindler T, Adams-Quack P, Hahn M, Waisman A, Reed JC, HΓΆvelmeyer N, Methner A (2015) BAX inhibitor-1 is a Ca<sup>2+</sup> channel critically important for immune cell function and survival. Cell Death Differ [Epub ahead of print]. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/26470731 PMID: 26470731] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/26470731 PMID: 26470731] | ||
|authors=Lisak D, Schacht T, Gawlitza A, Albrecht P, Aktas O, Koop B, Gliem M, Hofstetter HH, Zanger K, Bultynck G, Parys JB, De Smedt H, Kindler T, Adams-Quack P, Hahn M, Waisman A, Reed JC, Hoevelmeyer N, Methner A | |authors=Lisak D, Schacht T, Gawlitza A, Albrecht P, Aktas O, Koop B, Gliem M, Hofstetter HH, Zanger K, Bultynck G, Parys JB, De Smedt H, Kindler T, Adams-Quack P, Hahn M, Waisman A, Reed JC, Hoevelmeyer N, Methner A | ||
| Line 6: | Line 6: | ||
|journal=Cell Death Differ | |journal=Cell Death Differ | ||
|abstract=The endoplasmic reticulum (ER) serves as the major intracellular Ca<sup>2+</sup> store and has a role in the synthesis and folding of proteins. BAX (BCL2-associated X protein) inhibitor-1 (BI-1) is a Ca<sup>2+</sup> leak channel also implicated in the response against protein misfolding, thereby connecting the Ca<sup>2+</sup> store and protein-folding functions of the ER. We found that BI-1-deficient mice suffer from leukopenia and erythrocytosis, have an increased number of splenic marginal zone B cells and higher abundance and nuclear translocation of NF-ΞΊB (nuclear factor-ΞΊ light-chain enhancer of activated B cells) proteins, correlating with increased cytosolic and ER Ca<sup>2+</sup> levels. When put into culture, purified knockout T cells and even more so B cells die spontaneously. This is preceded by increased activity of the mitochondrial initiator caspase-9 and correlated with a significant surge in mitochondrial Ca<sup>2+</sup> levels, suggesting an exhausted mitochondrial Ca<sup>2+</sup> buffer capacity as the underlying cause for cell death ''in vitro''. ''In vivo'', T-cell-dependent experimental autoimmune encephalomyelitis and B-cell-dependent antibody production are attenuated, corroborating the ''ex vivo'' results. These results suggest that BI-1 has a major role in the functioning of the adaptive immune system by regulating intracellular Ca<sup>2+</sup> homeostasis in lymphocytes. | |abstract=The endoplasmic reticulum (ER) serves as the major intracellular Ca<sup>2+</sup> store and has a role in the synthesis and folding of proteins. BAX (BCL2-associated X protein) inhibitor-1 (BI-1) is a Ca<sup>2+</sup> leak channel also implicated in the response against protein misfolding, thereby connecting the Ca<sup>2+</sup> store and protein-folding functions of the ER. We found that BI-1-deficient mice suffer from leukopenia and erythrocytosis, have an increased number of splenic marginal zone B cells and higher abundance and nuclear translocation of NF-ΞΊB (nuclear factor-ΞΊ light-chain enhancer of activated B cells) proteins, correlating with increased cytosolic and ER Ca<sup>2+</sup> levels. When put into culture, purified knockout T cells and even more so B cells die spontaneously. This is preceded by increased activity of the mitochondrial initiator caspase-9 and correlated with a significant surge in mitochondrial Ca<sup>2+</sup> levels, suggesting an exhausted mitochondrial Ca<sup>2+</sup> buffer capacity as the underlying cause for cell death ''in vitro''. ''In vivo'', T-cell-dependent experimental autoimmune encephalomyelitis and B-cell-dependent antibody production are attenuated, corroborating the ''ex vivo'' results. These results suggest that BI-1 has a major role in the functioning of the adaptive immune system by regulating intracellular Ca<sup>2+</sup> homeostasis in lymphocytes. | ||
|mipnetlab=DE Mainz Methner A | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
Revision as of 17:27, 18 November 2015
| [[Has title::Lisak D, Schacht T, Gawlitza A, Albrecht P, Aktas O, Koop B, Gliem M, Hofstetter HH, Zanger K, Bultynck G, Parys JB, De Smedt H, Kindler T, Adams-Quack P, Hahn M, Waisman A, Reed JC, HΓΆvelmeyer N, Methner A (2015) BAX inhibitor-1 is a Ca2+ channel critically important for immune cell function and survival. Cell Death Differ [Epub ahead of print].]] |
Β» [[Has info::PMID: 26470731]]
Lisak D, Schacht T, Gawlitza A, Albrecht P, Aktas O, Koop B, Gliem M, Hofstetter HH, Zanger K, Bultynck G, Parys JB, De Smedt H, Kindler T, Adams-Quack P, Hahn M, Waisman A, Reed JC, Hoevelmeyer N, Methner A (2015) Cell Death Differ
Abstract: The endoplasmic reticulum (ER) serves as the major intracellular Ca2+ store and has a role in the synthesis and folding of proteins. BAX (BCL2-associated X protein) inhibitor-1 (BI-1) is a Ca2+ leak channel also implicated in the response against protein misfolding, thereby connecting the Ca2+ store and protein-folding functions of the ER. We found that BI-1-deficient mice suffer from leukopenia and erythrocytosis, have an increased number of splenic marginal zone B cells and higher abundance and nuclear translocation of NF-ΞΊB (nuclear factor-ΞΊ light-chain enhancer of activated B cells) proteins, correlating with increased cytosolic and ER Ca2+ levels. When put into culture, purified knockout T cells and even more so B cells die spontaneously. This is preceded by increased activity of the mitochondrial initiator caspase-9 and correlated with a significant surge in mitochondrial Ca2+ levels, suggesting an exhausted mitochondrial Ca2+ buffer capacity as the underlying cause for cell death in vitro. In vivo, T-cell-dependent experimental autoimmune encephalomyelitis and B-cell-dependent antibody production are attenuated, corroborating the ex vivo results. These results suggest that BI-1 has a major role in the functioning of the adaptive immune system by regulating intracellular Ca2+ homeostasis in lymphocytes.
β’ O2k-Network Lab: DE Mainz Methner A
Labels: MiParea: Respiration, Genetic knockout;overexpression
Pathology: Obesity
Organism: Mouse
Preparation: Intact cells
Regulation: Calcium Coupling state: LEAK, ROUTINE, ETS
HRR: Oxygraph-2k
Labels
