EXC 229: Cellular Stress Responses in Aging-Associated Diseases
Final Report Abstract
Modern societies are facing a dramatic demographic change with an ever-increasing life expectancy that is concomitant with increased risk of age-associated diseases, e.g. diabetes and obesity, as well as skin, kidney, and neurodegenerative disorders, thus posing an enormous challenge for both individuals and their societies. The landmark discovery that modification of specific signaling pathways can extend lifespan and reduce the incidence of age-associated diseases formed the scientific foundation of the Cologne Cluster of Excellence on Cellular Stress Responses in Agingassociated Diseases (CECAD) – to define the molecular and cellular mechanisms underlying the aging process as potential novel targets for prevention, early diagnosis, and treatment of ageassociated diseases. CECAD has actively recruited top basic researchers and clinician scientists who work in concert at the University of Cologne (UoC), the Max Planck Institutes for Biology of Ageing (MPI AGE) and for Metabolism Research (MPI MR), as well as the German Center for Neurodegenerative Diseases (DZNE). Further, CECAD together with the UoC has effected massive infrastructural changes, which have firmly established this Cluster as one of the leading aging research centers worldwide. Moreover, CECAD’s strategic recruitment policy has generated an international and inclusive research environment where female representation is high. In parallel, we have built up educational measures to better train the best global scientific talent at all academic levels. Together, these developments led to a very rapid increase in research momentum, that thereby enabled CECAD scientists through highly collaborative efforts in unravelling novel fundamental principles underlying aging and aging-associated diseases and identifying potential novel targets for intervention. While work initially focused on defining the role of cell autonomous quality control pathways in aging and aging-aging associated diseases, recent studies from the second period have highlighted the importance of interorgan communication and signals originating from the environment that control longevity and health, thereby opening up a new channel for identifying novel therapeutic targets. For the future CECAD will therefore expand its research program and supporting core structures and educational programs in these areas while at the same time enhancing its translational studies through inclusion of unique human cohorts. Collectively, these efforts of CECAD PIs and its participating institutions will not only enable CECAD to continue to be at the forefront of world-class aging research, but also provide a leading training site for aging researchers at all academic levels.
Link to the final report
https://dx.doi.org/10.2314/GBV:1697037887
Publications
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(2008) Endothelial cell-specific NF-kappaB inhibition protects mice from atherosclerosis. Cell Metab 8: 372-83
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(2011) MTERF4 regulates translation by targeting the methyltransferase NSUN4 to the mammalian mitochondrial ribosome. Cell Metab 13: 527-39
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(2011) Role for insulin signaling in catecholaminergic neurons in control of energy homeostasis. Cell Metab 13: 720-8
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(2012) A steroid receptor-microRNA switch regulates life span in response to signals from the gonad. Science 338: 1472-6
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(2012) Intramitochondrial transport of phosphatidic acid in yeast by a lipid transfer protein. Science 338: 815-8
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(2013) DNA damage in germ cells induces an innate immune response that triggers systemic stress resistance. Nature 501: 416-20
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(2013) Insulin/IGF-1 controls epidermal morphogenesis via regulation of FoxO-mediated p63 inhibition. Dev Cell 26: 176-87
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(2013) The actin cross-linker Filamin/Cheerio mediates tumor malignancy downstream of JNK signaling. J Cell Sci 126: 927-38
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(2013) TRIAP1/PRELI complexes prevent apoptosis by mediating intramitochondrial transport of phosphatidic acid. Cell Metab 18: 287-95
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(2014) CLUH regulates mitochondrial biogenesis by binding mRNAs of nuclear-encoded mitochondrial proteins. J Cell Biol 207: 213-23
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(2014) Hexosamine pathway metabolites enhance protein quality control and prolong life. Cell 156: 1167-78
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(2014) Neonatal insulin action impairs hypothalamic neurocircuit formation in response to maternal high-fat feeding. Cell 156: 495-509
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(2014) Signaling by IL-6 promotes alternative activation of macrophages to limit endotoxemia and obesity-associated resistance to insulin. Nat Immunol 15: 423-30
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(2014) The i-AAA protease YME1L and OMA1 cleave OPA1 to balance mitochondrial fusion and fission. J Cell Biol 204: 919-29
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(2014) Tissue-specific loss of DARS2 activates stress responses independently of respiratory chain deficiency in the heart. Cell Metab 19: 458-69
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(2014) Unexpected role of the steroid-deficiency protein ecdysoneless in pre-mRNA splicing. PloS Genet 10: e1004287
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(2015) A synergistic interaction between Chk1- and MK2 inhibitors in KRAS-mutant cancer. Cell Jul 2, 162(1): 146-159
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(2015) Hypothalamic Agrp neurons drive stereotypic behaviors beyond feeding. Cell 160: 1222-32
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(2015) Hypothalamic POMC neurons promote cannabinoidinduced feeding. Nature 519: 45-50
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(2015) Hypothalamic UDP Increases in Obesity and Promotes Feeding via P2Y6-Dependent Activation of AgRP Neurons. Cell 162: 1404-17
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(2016) AgRP Neurons Control Systemic Insulin Sensitivity via Myostatin Expression in Brown Adipose Tissue. Cell 165: 125-138
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(2016) Mechanical regulation of transcription drives Polycomb mediated gene silence during lineage I. Nat Cell Biol 18: 864-75
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(2016) Mondo complexes regulate TFEB via TOR inhibition to promote longevity in response to gonadal signals. Nat Commun 7: 10944
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(2016) mTORC1 and mTORC2 regulate skin morphogenesis and epidermal barrier formation. Nat Commun 7: 13226
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(2016) Myeloid-Cell-Derived VEGF Maintains Brain Glucose Uptake and Limits Cognitive Impairment in Obesity. Cell 165: 882-95
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(2016) On the dependency of cellular protein levels on mRNA abundance. Cell 165: 535-50
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(2016) Restricted diet delays accelerated ageing and genomic stress in HAT-repair-deficient mice. Nature 537: 427-431
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(2016) RIPK1 counteracts ZBP1-mediated necroptosis to inhibit inflammation. Nature 540: 124-128
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(2016) Somatic increase of CCT8 mimics proteostasis of human pluripotent stem cells and extends C. elegans lifespan. Nat Commun 7: 13649
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(2016) The Mitochondrial m-AAA Protease Prevents Demyelination and Hair Greying. PloS Genet 12: e1006463
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(2016) The ubiquitin ligase Ubr4 controls stability of podocin/MEC-2 supercomplexes. Hum Mol Genet 25: 1328-44
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(2016). Loss of OMA1 delays neurodegeneration by preventing stress-induced OPA1 processing in mitochondria. J Cell Biol. 212, 157-166
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(2017) A microRNA screen reveals that elevated hepatic ectodysplasin A expression contributes to obesity-induced insulin resistance in skeletal muscle. Nat Med 23: 1466-1473
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(2017) A post-transcriptional program coordinated by CSDE1 prevents intrinsic neural differentiation of human embryonic stem cells. Nat Commun 8: 1456
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(2017) DARS2 protects against neuroinflammation and apoptotic neuronal loss, but is dispensable for myelin producing cells. Hum Mol Genet 26: 4181-4189
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(2017) Dynamic changes in the mouse skeletal muscle proteome during denervation-induced atrophy. Dis Model Mech 10: 881-896
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(2017) E-cadherin integrates mechanotransduction and EGFR signaling to control junctional tissue polarization and tight junction positioning. Nat Commun 8: 1250
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(2017) Energy imbalance alters Ca2+ handling and excitability of POMC neurons. Elife 6
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(2017) Gamma oscillations organize top-down signalling to hypothalamus and enable food seeking. Nature 542: 232-236
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(2017) IL-6/Stat3-Dependent Induction of a Distinct, Obesity-Associated NK Cell Subpopulation Deteriorates Energy and Glucose Homeostasis. Cell Metab 26: 171-184
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(2017) Inflammation and metabolism in tissue repair and regeneration. Science 356: 1026-1030
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(2017) Multilayered Reprogramming in Response to Persistent HAT Damage in C. elegans. Cell Rep 20: 2026-2043
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(2017) Retrograde transport of TrkB-containing autophagosomes via the adaptor AP-2 mediates neuronal complexity and prevents neurodegeneration. Nat Commun 8: 14819
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(2017) Small nucleoli are a cellular hallmark of longevity. Nat Commun 8: 16083
Tiku V, Jain C, Raz Y, Nakamura S, Heestand B, Liu W, Spath M, Suchiman HED, Müller RU, Slagboom PE, Partridge L, Antebi A
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