https://wiki.oroboros.at/index.php?title=Ale-Agha_2018_PLOS_Biol&feed=atom&action=historyAle-Agha 2018 PLOS Biol - Revision history2024-03-29T10:42:21ZRevision history for this page on the wikiMediaWiki 1.36.1https://wiki.oroboros.at/index.php?title=Ale-Agha_2018_PLOS_Biol&diff=161406&oldid=prevPlangger Mario: Plangger Mario moved page Ale-Agha 2018 PLoS Biol to Ale-Agha 2018 PLOS Biol without leaving a redirect2018-08-23T13:45:44Z<p>Plangger Mario moved page <a href="/index.php?title=Ale-Agha_2018_PLoS_Biol&action=edit&redlink=1" class="new" title="Ale-Agha 2018 PLoS Biol (page does not exist)">Ale-Agha 2018 PLoS Biol</a> to <a href="/index.php/Ale-Agha_2018_PLOS_Biol" title="Ale-Agha 2018 PLOS Biol">Ale-Agha 2018 PLOS Biol</a> without leaving a redirect</p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<tr class="diff-title" lang="en">
<td colspan="1" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="1" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 13:45, 23 August 2018</td>
</tr><tr><td colspan="2" class="diff-notice" lang="en"><div class="mw-diff-empty">(No difference)</div>
</td></tr></table>Plangger Mariohttps://wiki.oroboros.at/index.php?title=Ale-Agha_2018_PLOS_Biol&diff=161405&oldid=prevPlangger Mario at 13:45, 23 August 20182018-08-23T13:45:30Z<p></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 13:45, 23 August 2018</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l1">Line 1:</td>
<td colspan="2" class="diff-lineno">Line 1:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{Publication</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{Publication</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>|title=Ale-Agha N, Goy C, Jakobs P, Spyridopoulos I, Gonnissen S, Dyballa-Rukes N, Aufenvenne K, von Ameln F, Zurek M, Spannbrucker T, Eckermann O, Jakob S, Gorressen S, Abrams M, Grandoch M, Fischer JW, Köhrer K, Deenen R, Unfried K, Altschmied J, Haendeler J (2018) CDKN1B/p27 is localized in mitochondria and improves respiration-dependent processes in the cardiovascular system - New mode of action for caffeine. <del style="font-weight: bold; text-decoration: none;">PLoS </del>Biol 6:e2004408.</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>|title=Ale-Agha N, Goy C, Jakobs P, Spyridopoulos I, Gonnissen S, Dyballa-Rukes N, Aufenvenne K, von Ameln F, Zurek M, Spannbrucker T, Eckermann O, Jakob S, Gorressen S, Abrams M, Grandoch M, Fischer JW, Köhrer K, Deenen R, Unfried K, Altschmied J, Haendeler J (2018) CDKN1B/p27 is localized in mitochondria and improves respiration-dependent processes in the cardiovascular system - New mode of action for caffeine. <ins style="font-weight: bold; text-decoration: none;">PLOS </ins>Biol 6:e2004408.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|info=[https://www.ncbi.nlm.nih.gov/pubmed/29927970 PMID: 29927970 Open Access]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|info=[https://www.ncbi.nlm.nih.gov/pubmed/29927970 PMID: 29927970 Open Access]</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|authors=Ale-Agha N, Goy C, Jakobs P, Spyridopoulos I, Gonnissen S, Dyballa-Rukes N, Aufenvenne K, von Ameln F, Zurek M, Spannbrucker T, Eckermann O, Jakob S, Gorressen S, Abrams M, Grandoch M, Fischer JW, Koehrer K, Deenen R, Unfried K, Altschmied J, Haendeler J</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|authors=Ale-Agha N, Goy C, Jakobs P, Spyridopoulos I, Gonnissen S, Dyballa-Rukes N, Aufenvenne K, von Ameln F, Zurek M, Spannbrucker T, Eckermann O, Jakob S, Gorressen S, Abrams M, Grandoch M, Fischer JW, Koehrer K, Deenen R, Unfried K, Altschmied J, Haendeler J</div></td></tr>
</table>Plangger Mariohttps://wiki.oroboros.at/index.php?title=Ale-Agha_2018_PLOS_Biol&diff=161403&oldid=prevPlangger Mario at 13:44, 23 August 20182018-08-23T13:44:33Z<p></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 13:44, 23 August 2018</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l4">Line 4:</td>
<td colspan="2" class="diff-lineno">Line 4:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|authors=Ale-Agha N, Goy C, Jakobs P, Spyridopoulos I, Gonnissen S, Dyballa-Rukes N, Aufenvenne K, von Ameln F, Zurek M, Spannbrucker T, Eckermann O, Jakob S, Gorressen S, Abrams M, Grandoch M, Fischer JW, Koehrer K, Deenen R, Unfried K, Altschmied J, Haendeler J</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|authors=Ale-Agha N, Goy C, Jakobs P, Spyridopoulos I, Gonnissen S, Dyballa-Rukes N, Aufenvenne K, von Ameln F, Zurek M, Spannbrucker T, Eckermann O, Jakob S, Gorressen S, Abrams M, Grandoch M, Fischer JW, Koehrer K, Deenen R, Unfried K, Altschmied J, Haendeler J</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|year=2018</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|year=2018</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>|journal=<del style="font-weight: bold; text-decoration: none;">PLoS </del>Biol</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>|journal=<ins style="font-weight: bold; text-decoration: none;">PLOS </ins>Biol</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|abstract=We show that the cyclin-dependent kinase inhibitor 1B (CDKN1B)/p27, previously known as a cell cycle inhibitor, is also localized within mitochondria. The migratory capacity of endothelial cells, which need intact mitochondria, is completely dependent on mitochondrial p27. Mitochondrial p27 improves mitochondrial membrane potential, increases adenosine triphosphate (ATP) content, and is required for the promigratory effect of caffeine. Domain mapping of p27 revealed that the N-terminus and C-terminus are required for those improvements. Further analysis of those regions revealed that the translocation of p27 into the mitochondria and its promigratory activity depend on serine 10 and threonine 187. In addition, mitochondrial p27 protects cardiomyocytes against apoptosis. Moreover, mitochondrial p27 is necessary and sufficient for cardiac myofibroblast differentiation. In addition, p27 deficiency and aging decrease respiration in heart mitochondria. Caffeine does not increase respiration in p27-deficient animals, whereas aged mice display improvement after 10 days of caffeine in drinking water. Moreover, caffeine induces transcriptome changes in a p27-dependent manner, affecting mostly genes relevant for mitochondrial processes. Caffeine also reduces infarct size after myocardial infarction in prediabetic mice and increases mitochondrial p27. Our data characterize mitochondrial p27 as a common denominator that improves mitochondria-dependent processes and define an increase in mitochondrial p27 as a new mode of action of caffeine.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|abstract=We show that the cyclin-dependent kinase inhibitor 1B (CDKN1B)/p27, previously known as a cell cycle inhibitor, is also localized within mitochondria. The migratory capacity of endothelial cells, which need intact mitochondria, is completely dependent on mitochondrial p27. Mitochondrial p27 improves mitochondrial membrane potential, increases adenosine triphosphate (ATP) content, and is required for the promigratory effect of caffeine. Domain mapping of p27 revealed that the N-terminus and C-terminus are required for those improvements. Further analysis of those regions revealed that the translocation of p27 into the mitochondria and its promigratory activity depend on serine 10 and threonine 187. In addition, mitochondrial p27 protects cardiomyocytes against apoptosis. Moreover, mitochondrial p27 is necessary and sufficient for cardiac myofibroblast differentiation. In addition, p27 deficiency and aging decrease respiration in heart mitochondria. Caffeine does not increase respiration in p27-deficient animals, whereas aged mice display improvement after 10 days of caffeine in drinking water. Moreover, caffeine induces transcriptome changes in a p27-dependent manner, affecting mostly genes relevant for mitochondrial processes. Caffeine also reduces infarct size after myocardial infarction in prediabetic mice and increases mitochondrial p27. Our data characterize mitochondrial p27 as a common denominator that improves mitochondria-dependent processes and define an increase in mitochondrial p27 as a new mode of action of caffeine.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|editor=[[Plangger M]], [[Kandolf G]],</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|editor=[[Plangger M]], [[Kandolf G]],</div></td></tr>
</table>Plangger Mariohttps://wiki.oroboros.at/index.php?title=Ale-Agha_2018_PLOS_Biol&diff=161400&oldid=prevPlangger Mario at 13:30, 23 August 20182018-08-23T13:30:08Z<p></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 13:30, 23 August 2018</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l1">Line 1:</td>
<td colspan="2" class="diff-lineno">Line 1:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{Publication</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{Publication</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>|title=Ale-Agha N, Goy C, Jakobs P, Spyridopoulos I, Gonnissen S, Dyballa-Rukes N, Aufenvenne K, von Ameln F, Zurek M, Spannbrucker T, Eckermann O, Jakob S, Gorressen S, Abrams M, Grandoch M, Fischer JW, Köhrer K, Deenen R, Unfried K, Altschmied J, Haendeler J (2018) CDKN1B/p27 is localized in mitochondria and improves respiration-dependent processes in the cardiovascular <del style="font-weight: bold; text-decoration: none;">systemÐNew </del>mode of action for caffeine. PLoS Biol 6:e2004408.</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>|title=Ale-Agha N, Goy C, Jakobs P, Spyridopoulos I, Gonnissen S, Dyballa-Rukes N, Aufenvenne K, von Ameln F, Zurek M, Spannbrucker T, Eckermann O, Jakob S, Gorressen S, Abrams M, Grandoch M, Fischer JW, Köhrer K, Deenen R, Unfried K, Altschmied J, Haendeler J (2018) CDKN1B/p27 is localized in mitochondria and improves respiration-dependent processes in the cardiovascular <ins style="font-weight: bold; text-decoration: none;">system - New </ins>mode of action for caffeine. PLoS Biol 6:e2004408.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|info=[https://www.ncbi.nlm.nih.gov/pubmed/29927970 PMID: 29927970 Open Access]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|info=[https://www.ncbi.nlm.nih.gov/pubmed/29927970 PMID: 29927970 Open Access]</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|authors=Ale-Agha N, Goy C, Jakobs P, Spyridopoulos I, Gonnissen S, Dyballa-Rukes N, Aufenvenne K, von Ameln F, Zurek M, Spannbrucker T, Eckermann O, Jakob S, Gorressen S, Abrams M, Grandoch M, Fischer JW, Koehrer K, Deenen R, Unfried K, Altschmied J, Haendeler J</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|authors=Ale-Agha N, Goy C, Jakobs P, Spyridopoulos I, Gonnissen S, Dyballa-Rukes N, Aufenvenne K, von Ameln F, Zurek M, Spannbrucker T, Eckermann O, Jakob S, Gorressen S, Abrams M, Grandoch M, Fischer JW, Koehrer K, Deenen R, Unfried K, Altschmied J, Haendeler J</div></td></tr>
</table>Plangger Mariohttps://wiki.oroboros.at/index.php?title=Ale-Agha_2018_PLOS_Biol&diff=161399&oldid=prevPlangger Mario at 13:00, 23 August 20182018-08-23T13:00:53Z<p></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 13:00, 23 August 2018</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l7">Line 7:</td>
<td colspan="2" class="diff-lineno">Line 7:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|abstract=We show that the cyclin-dependent kinase inhibitor 1B (CDKN1B)/p27, previously known as a cell cycle inhibitor, is also localized within mitochondria. The migratory capacity of endothelial cells, which need intact mitochondria, is completely dependent on mitochondrial p27. Mitochondrial p27 improves mitochondrial membrane potential, increases adenosine triphosphate (ATP) content, and is required for the promigratory effect of caffeine. Domain mapping of p27 revealed that the N-terminus and C-terminus are required for those improvements. Further analysis of those regions revealed that the translocation of p27 into the mitochondria and its promigratory activity depend on serine 10 and threonine 187. In addition, mitochondrial p27 protects cardiomyocytes against apoptosis. Moreover, mitochondrial p27 is necessary and sufficient for cardiac myofibroblast differentiation. In addition, p27 deficiency and aging decrease respiration in heart mitochondria. Caffeine does not increase respiration in p27-deficient animals, whereas aged mice display improvement after 10 days of caffeine in drinking water. Moreover, caffeine induces transcriptome changes in a p27-dependent manner, affecting mostly genes relevant for mitochondrial processes. Caffeine also reduces infarct size after myocardial infarction in prediabetic mice and increases mitochondrial p27. Our data characterize mitochondrial p27 as a common denominator that improves mitochondria-dependent processes and define an increase in mitochondrial p27 as a new mode of action of caffeine.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|abstract=We show that the cyclin-dependent kinase inhibitor 1B (CDKN1B)/p27, previously known as a cell cycle inhibitor, is also localized within mitochondria. The migratory capacity of endothelial cells, which need intact mitochondria, is completely dependent on mitochondrial p27. Mitochondrial p27 improves mitochondrial membrane potential, increases adenosine triphosphate (ATP) content, and is required for the promigratory effect of caffeine. Domain mapping of p27 revealed that the N-terminus and C-terminus are required for those improvements. Further analysis of those regions revealed that the translocation of p27 into the mitochondria and its promigratory activity depend on serine 10 and threonine 187. In addition, mitochondrial p27 protects cardiomyocytes against apoptosis. Moreover, mitochondrial p27 is necessary and sufficient for cardiac myofibroblast differentiation. In addition, p27 deficiency and aging decrease respiration in heart mitochondria. Caffeine does not increase respiration in p27-deficient animals, whereas aged mice display improvement after 10 days of caffeine in drinking water. Moreover, caffeine induces transcriptome changes in a p27-dependent manner, affecting mostly genes relevant for mitochondrial processes. Caffeine also reduces infarct size after myocardial infarction in prediabetic mice and increases mitochondrial p27. Our data characterize mitochondrial p27 as a common denominator that improves mitochondria-dependent processes and define an increase in mitochondrial p27 as a new mode of action of caffeine.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|editor=[[Plangger M]], [[Kandolf G]],</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|editor=[[Plangger M]], [[Kandolf G]],</div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">|mipnetlab=DE Duesseldorf Haendeler J</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>}}</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>}}</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{Labeling</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{Labeling</div></td></tr>
</table>Plangger Mariohttps://wiki.oroboros.at/index.php?title=Ale-Agha_2018_PLOS_Biol&diff=161398&oldid=prevPlangger Mario: Created page with "{{Publication |title=Ale-Agha N, Goy C, Jakobs P, Spyridopoulos I, Gonnissen S, Dyballa-Rukes N, Aufenvenne K, von Ameln F, Zurek M, Spannbrucker T, Eckermann O, Jakob S, Gorr..."2018-08-23T12:58:23Z<p>Created page with "{{Publication |title=Ale-Agha N, Goy C, Jakobs P, Spyridopoulos I, Gonnissen S, Dyballa-Rukes N, Aufenvenne K, von Ameln F, Zurek M, Spannbrucker T, Eckermann O, Jakob S, Gorr..."</p>
<p><b>New page</b></p><div>{{Publication<br />
|title=Ale-Agha N, Goy C, Jakobs P, Spyridopoulos I, Gonnissen S, Dyballa-Rukes N, Aufenvenne K, von Ameln F, Zurek M, Spannbrucker T, Eckermann O, Jakob S, Gorressen S, Abrams M, Grandoch M, Fischer JW, Köhrer K, Deenen R, Unfried K, Altschmied J, Haendeler J (2018) CDKN1B/p27 is localized in mitochondria and improves respiration-dependent processes in the cardiovascular systemÐNew mode of action for caffeine. PLoS Biol 6:e2004408.<br />
|info=[https://www.ncbi.nlm.nih.gov/pubmed/29927970 PMID: 29927970 Open Access]<br />
|authors=Ale-Agha N, Goy C, Jakobs P, Spyridopoulos I, Gonnissen S, Dyballa-Rukes N, Aufenvenne K, von Ameln F, Zurek M, Spannbrucker T, Eckermann O, Jakob S, Gorressen S, Abrams M, Grandoch M, Fischer JW, Koehrer K, Deenen R, Unfried K, Altschmied J, Haendeler J<br />
|year=2018<br />
|journal=PLoS Biol<br />
|abstract=We show that the cyclin-dependent kinase inhibitor 1B (CDKN1B)/p27, previously known as a cell cycle inhibitor, is also localized within mitochondria. The migratory capacity of endothelial cells, which need intact mitochondria, is completely dependent on mitochondrial p27. Mitochondrial p27 improves mitochondrial membrane potential, increases adenosine triphosphate (ATP) content, and is required for the promigratory effect of caffeine. Domain mapping of p27 revealed that the N-terminus and C-terminus are required for those improvements. Further analysis of those regions revealed that the translocation of p27 into the mitochondria and its promigratory activity depend on serine 10 and threonine 187. In addition, mitochondrial p27 protects cardiomyocytes against apoptosis. Moreover, mitochondrial p27 is necessary and sufficient for cardiac myofibroblast differentiation. In addition, p27 deficiency and aging decrease respiration in heart mitochondria. Caffeine does not increase respiration in p27-deficient animals, whereas aged mice display improvement after 10 days of caffeine in drinking water. Moreover, caffeine induces transcriptome changes in a p27-dependent manner, affecting mostly genes relevant for mitochondrial processes. Caffeine also reduces infarct size after myocardial infarction in prediabetic mice and increases mitochondrial p27. Our data characterize mitochondrial p27 as a common denominator that improves mitochondria-dependent processes and define an increase in mitochondrial p27 as a new mode of action of caffeine.<br />
|editor=[[Plangger M]], [[Kandolf G]],<br />
}}<br />
{{Labeling<br />
|area=Respiration, nDNA;cell genetics, Pharmacology;toxicology<br />
|organism=Mouse<br />
|tissues=Heart<br />
|preparations=Isolated mitochondria<br />
|couplingstates=OXPHOS<br />
|pathways=N, S, CIV<br />
|instruments=Oxygraph-2k<br />
|additional=Labels, 2018-08,<br />
}}</div>Plangger Mario