About: Collaborative Research Centre (CRC) 1002: "Modulatory Units in Heart Failure"

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Attributes	Values
rdf:type	Item
rdfs:label	Sonderforschungsbereich (SFB) 1002: Modulatorische Einheiten bei Herzinsuffizienz (de) Collaborative Research Centre (CRC) 1002: "Modulatory Units in Heart Failure" (en)
skos:prefLabel	Sonderforschungsbereich (SFB) 1002: Modulatorische Einheiten bei Herzinsuffizienz (de) Collaborative Research Centre (CRC) 1002: "Modulatory Units in Heart Failure" (en)
name	Sonderforschungsbereich (SFB) 1002: Modulatorische Einheiten bei Herzinsuffizienz (de) Collaborative Research Centre (CRC) 1002: "Modulatory Units in Heart Failure" (en)
title	wds:Q48693816-1b0db149-4a55-b3bc-31ad-2223dc23b7e2 wds:Q48693816-2728bee4-4b3d-00d7-9324-8a1f8d68cd6b
title	Modulatorische Einheiten bei Herzinsuffizienz (de) Modulatory Units in Heart Failure (en)
instance of	wds:Q48693816-7a821590-4cc1-e383-7e79-f53970685164
instance of	Collaborative Research Centre
country	wds:Q48693816-ce01efcd-49f7-1f43-6140-3216a4adf513
country	Germany
has part(s)	wds:Q48693816-44958f08-44f1-4121-f79c-23861acedceb wds:Q48693816-4af02e18-418b-9205-9e97-06fc68a296a6 wds:Q48693816-6a7c99fc-41b7-54d9-bd6a-b6352fd27041 wds:Q48693816-cd538b98-464c-800e-2908-8e97a25d932f wds:Q48693816-d8893fb5-4a2b-0a3b-9299-fba24a33f0d1
has part(s)	Max Planck Institute for Biophysical Chemistry Max Planck Institute for Dynamics and Self-Organization Universitätsmedizin Göttingen Department of Medical Informatics Göttingen Department of Molecular Biology Göttingen
GEPRIS project ID	wds:Q48693816-52C48612-7C5C-4809-9AFE-8D7D5DC194F9
skos:altLabel	CRC 1002 (en) CRC1002 (en) SFB 1002 (de) SFB1002 (de) crc 1002 (en) crc1002 (en) sfb 1002 (de) sfb1002 (de)
located in the adm...erritorial entity	wds:Q48693816-74143f09-4b25-8e9c-95af-bcf8cd798716
official website	wds:Q48693816-920f3f95-485f-102e-6ab0-255e46142b23
sponsor	wds:Q48693816-ed174843-42c1-83b7-fe0d-014ad23f7a11
located in the adm...erritorial entity	Göttingen
official website	https://sfb1002.med.uni-goettingen.de/
sponsor	German Research Foundation
GEPRIS project ID	193793266
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q48693816
is Wikidata property example of	GEPRIS project ID
is Wikidata property example of	wds:P4870-DC4F5187-0310-494F-8CC2-F9CCC86D7E31
is affiliation of	Harald Kusch
is affiliation of	wds:Q48794779-135579f2-4b49-a64d-6279-498d4c6acc23
is part of of	Max Planck Institute for Biophysical Chemistry Max Planck Institute for Dynamics and Self-Organization Enhancing and extending the CRC 1002 information infrastructure for basic and clinical research (INF)
is part of of	wds:Q836125-ce755b66-4f99-2618-3fd0-dd526b59da19 wds:Q277098-c8b61141-47e4-0c3b-6356-bed02c5e578f wds:Q56701905-415b9785-42f6-6f0d-4386-f7f14d99de26
is main subject of	Wikidata as semantic representation platform of the scientific achievements of the biomedical Collaborative Research Centre 1002
is main subject of	wds:Q56235886-807324fc-4880-b5c6-a17a-1ed146e15072
is sponsor of	Cooperation between COA6 and SCO2 in COX2 maturation during cytochrome c oxidase assembly links two mitochondrial cardiomyopathies COX16 promotes COX2 metallation and assembly during respiratory complex IV biogenesis. Extracellular matrix secretion by cardiac fibroblasts: role of microRNA-29b and microRNA-30c Crucial role for Ca2(+)/calmodulin-dependent protein kinase-II in regulating diastolic stress of normal and failing hearts via titin phosphorylation Physiologic force-frequency response in engineered heart muscle by electromechanical stimulation Human Engineered Heart Muscles Engraft and Survive Long Term in a Rodent Myocardial Infarction Model The role of promoter hypermethylation in fibroblast activation and fibrogenesis RAnoLazIne for the treatment of diastolic heart failure in patients with preserved ejection fraction: the RALI-DHF proof-of-concept study S-glutathionylation of cryptic cysteines enhances titin elasticity by blocking protein folding Emerging importance of oxidative stress in regulating striated muscle elasticity Deranged myofilament phosphorylation and function in experimental heart failure with preserved ejection fraction. Ca2+/calmodulin-dependent protein kinase II and protein kinase A differentially regulate sarcoplasmic reticulum Ca2+ leak in human cardiac pathology. Redox regulation of sodium and calcium handling Cardiolipin deficiency affects respiratory chain function and organization in an induced pluripotent stem cell model of Barth syndrome Role of late sodium current as a potential arrhythmogenic mechanism in the progression of pressure-induced heart disease Ionizing radiation regulates cardiac Ca handling via increased ROS and activated CaMKII. Control of cytoplasmic and nuclear protein kinase A by phosphodiesterases and phosphatases in cardiac myocytes Enhanced expression of β3-adrenoceptors in cardiac myocytes attenuates neurohormone-induced hypertrophic remodeling through nitric oxide synthase Role of oxidants on calcium and sodium movement in healthy and diseased cardiac myocytes Stimulated emission depletion live-cell super-resolution imaging shows proliferative remodeling of T-tubule membrane structures after myocardial infarction Gigantic business: titin properties and function through thick and thin Sensing Cardiac Electrical Activity With a Cardiac Myocyte--Targeted Optogenetic Voltage Indicator. Compartmentation of cAMP signalling in cardiomyocytes in health and disease Biophysical techniques for detection of cAMP and cGMP in living cells In vivo model with targeted cAMP biosensor reveals changes in receptor-microdomain communication in cardiac disease. Lysine methyltransferase Smyd2 regulates Hsp90-mediated protection of the sarcomeric titin springs and cardiac function Cardiac CaM Kinase II genes δ and γ contribute to adverse remodeling but redundantly inhibit calcineurin-induced myocardial hypertrophy Ion channelopathies in human induced pluripotent stem cell derived cardiomyocytes: a dynamic clamp study with virtual IK1. Reactive oxygen species and excitation-contraction coupling in the context of cardiac pathology Tubulin polymerization disrupts cardiac β-adrenergic regulation of late INa. Oxidized Ca(2+)/calmodulin-dependent protein kinase II triggers atrial fibrillation. NADPH oxidase 2 mediates angiotensin II-dependent cellular arrhythmias via PKA and CaMKII. Ca(2+) /calmodulin-dependent protein kinase II equally induces sarcoplasmic reticulum Ca(2+) leak in human ischaemic and dilated cardiomyopathy. Enhanced late INa induces proarrhythmogenic SR Ca leak in a CaMKII-dependent manner. Increased concentration of circulating angiogenesis and nitric oxide inhibitors induces endothelial to mesenchymal transition and myocardial fibrosis in patients with chronic kidney disease. Epigenetic balance of aberrant Rasal1 promoter methylation and hydroxymethylation regulates cardiac fibrosis Diabetes increases mortality after myocardial infarction by oxidizing CaMKII Induction of Tet3-dependent Epigenetic Remodeling by Low-dose Hydralazine Attenuates Progression of Chronic Kidney Disease Urocortin 2 stimulates nitric oxide production in ventricular myocytes via Akt- and PKA-mediated phosphorylation of eNOS at serine 1177. Comparative study of human-induced pluripotent stem cells derived from bone marrow cells, hair keratinocytes, and skin fibroblasts The ryanodine receptor leak: how a tattered receptor plunges the failing heart into crisis Titin-truncating variants affect heart function in disease cohorts and the general population. Axial tubule junctions control rapid calcium signaling in atria Phosphodiesterase-2 is up-regulated in human failing hearts and blunts β-adrenergic responses in cardiomyocytes HEART DISEASE. Titin mutations in iPS cells define sarcomere insufficiency as a cause of dilated cardiomyopathy The Function of Rho-Associated Kinases ROCK1 and ROCK2 in the Pathogenesis of Cardiovascular Disease

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