MyD88 mediated inflammatory signaling leads to CaMKII oxidation, cardiac hypertrophy and death after myocardial infarction. - Wikidata - wikimedia - TriplyDB

MyD88 mediated inflammatory signaling leads to CaMKII oxidation, cardiac hypertrophy and death after myocardial infarction.

MyD88 mediated inflammatory signaling leads to CaMKII oxidation, cardiac hypertrophy and death after myocardial infarction.

http://www.wikidata.org/entity/Q35892464

about

Ca(2+) signaling in the myocardium by (redox) regulation of PKA/CaMKII CaMKII oxidative activation and the pathogenesis of cardiac disease Calmodulin-dependent protein kinase II: linking heart failure and arrhythmias Toll-like receptors and hypertension New therapeutic targets in cardiology: arrhythmias and Ca2+/calmodulin-dependent kinase II (CaMKII)Heart-resident CCR2+ macrophages promote neutrophil extravasation through TLR9/MyD88/CXCL5 signaling.Protein methionine oxidation augments reperfusion injury in acute ischemic stroke Phagocyte-myocyte interactions and consequences during hypoxic wound healing.Loss of MD1 exacerbates pressure overload-induced left ventricular structural and electrical remodelling.Conditional knockout of prolyl hydroxylase domain protein 2 attenuates high fat-diet-induced cardiac dysfunction in mice.β-arrestin2 in infiltrated macrophages inhibits excessive inflammation after myocardial infarction The immune system and hypertension.CaMKII is essential for the proasthmatic effects of oxidation.Melatonin protects against myocardial hypertrophy induced by lipopolysaccharide.Dual Activation of TRIF and MyD88 Adaptor Proteins by Angiotensin II Evokes Opposing Effects on Pressure, Cardiac Hypertrophy, and Inflammatory Gene Expression.Atrial remodelling in atrial fibrillation: CaMKII as a nodal proarrhythmic signal Retinol-Binding Protein 4 Induces Cardiomyocyte Hypertrophy by Activating TLR4/MyD88 Pathway.Structural studies on the regulation of Ca2+/calmodulin dependent protein kinase II Oxidant stress promotes disease by activating CaMKII.Macrophage-dependent IL-1β production induces cardiac arrhythmias in diabetic mice.Oxidized CaMKII promotes asthma through the activation of mast cells.Toll-interacting protein (Tollip) negatively regulates pressure overload-induced ventricular hypertrophy in mice Regulation of connexin- and pannexin-based channels by post-translational modifications.Role of toll-like receptors in systemic sclerosis.Myocyte signalling in leucocyte recruitment to the heart.Pathophysiology of Myocardial Infarction.The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis.Recent advances of adapter proteins in the regulation of heart diseases.S100A8/MYD88/NF-қB: a novel pathway involved in cardiomyocyte hypertrophy driven by thyroid hormone.CaMKII is a nodal signal for multiple programmed cell death pathways in heart.CaMKIIδ subtypes differentially regulate infarct formation following ex vivo myocardial ischemia/reperfusion through NF-κB and TNF-α.Exosomes as critical agents of cardiac regeneration triggered by cell therapy.Ca2+/Calmodulin-dependent protein kinase II δ mediates myocardial ischemia/reperfusion injury through nuclear factor-κB.CaMKII: The molecular villain that aggravates cardiovascular disease.Transplantation of Isl1+ cardiac progenitor cells in small intestinal submucosa improves infarcted heart function.Toll-like receptor-mediated, enhanced production of profibrotic TIMP-1 in monocytes from patients with systemic sclerosis: role of serum factors.Insights into innate immune signalling in controlling cardiac remodelling.The Role of Toll-Like Receptor Signaling in the Progression of Heart Failure.Physiological and unappreciated roles of CaMKII in the heart.Empagliflozin normalizes the size and number of mitochondria and prevents reduction in mitochondrial size after myocardial infarction in diabetic hearts.

P2860

Q26796230-59AC34B3-FE16-4B0F-BBB1-317A74681983 Q26998988-8F8DFE2D-536F-4D28-A799-F945F1518672 Q26999872-36ECD3CA-614C-4E4C-895E-3359EFD7B263 Q27004654-6FE7184B-EAE9-4B11-B5D3-9A8C0EE4A3E8 Q27016402-DB33C2D8-F74F-4ABE-A9A8-A448725CB1CB Q27333707-BDBF472C-5797-4DED-A4C3-7A975D2D9BCD Q27333918-B7314E30-65F5-4E91-A85C-325D57D6E4A6 Q27690914-851A4936-AB39-4E87-A862-0D1D6857C480 Q33894807-6E3ABC2B-69C4-4142-A7C7-8B87E2D56ADB Q34784334-6C3EBE49-62BE-41AA-8594-AF5F48A089E1 Q34827316-1726C757-4050-4A43-A6CB-24BCEA52CFC4 Q35038155-EDE919AC-1658-4A50-9537-0E091AE68EAE Q35091137-9C48DF8E-955C-467A-85FC-3CA02BEDF84D Q35490630-A21C40A0-F5C1-4CBD-82DB-9CFD1270EA4E Q35956355-FCB850CF-4BBF-42DB-8633-0E05F39529B1 Q36650585-B93C135B-51C4-4828-9D59-955B853271C3 Q36965244-CE2E80E9-A398-44D5-BE5E-632AC8E73768 Q37210184-64A129CD-7A3A-49D2-83DC-B2A9CC8B7E43 Q37358999-F139A3A9-9D38-4E26-BEE7-E5DF94142189 Q37439581-B06687FC-C6EA-46F6-8337-C8939798BFBC Q37558095-F7F212D6-1F93-43D2-BBA3-9D1144037BB6 Q37669879-D2EED81D-DE1F-4427-8DEA-A52B1EE13B7A Q38110305-DA0314CE-7CD2-48A5-AC31-16F3C8C594FA Q38132298-8F516136-D27F-43BB-929A-B9DD471A6E93 Q38185647-C4EE0524-F736-4315-AA7A-E407295D919C Q38596702-1DA6E048-55F7-499D-9A9A-B004AF6281E4 Q38875774-826F1826-5A14-4C46-8665-823872699C5D Q38953404-CA72D76E-ED58-40CC-9DBF-0C8F6B27196C Q38978641-144B5E5C-9688-4863-BC02-46A1C6A492CF Q39056528-D81F1109-A2BB-4DB3-AF10-81FF5D85B18F Q40385305-C3C15BF1-89C4-494C-B2F4-7D95F7DCC22A Q40477633-EFC46655-04CD-4309-B44C-BDE5455D97CA Q41584910-6BD883B0-E070-4996-983B-1A73B72CA057 Q42290634-45E870CE-ADC8-447D-9D32-72D48314ACA0 Q42379231-3B39EBA9-1607-4291-A717-833265EC033F Q43091811-A9D492B8-244D-4E80-AE56-43D73FA5A634 Q52448624-9FC5EE22-F40C-47FD-942F-23AAE2A0680C Q52632607-C898DB11-81B5-4D0F-B2E1-8C0B9893E41A Q55381387-23810031-CF59-4EF3-A198-BCA46484106C Q55384960-CDC3BBB0-3B90-4609-B7B1-C1E93EA0AD75

P2860

MyD88 mediated inflammatory signaling leads to CaMKII oxidation, cardiac hypertrophy and death after myocardial infarction.

http://www.wikidata.org/entity/Q35892464

description

2012 nî lūn-bûn

@nan

2012年の論文

@ja

2012年論文

@yue

2012年論文

@zh-hant

2012年論文

@zh-hk

2012年論文

@zh-mo

2012年論文

@zh-tw

2012年论文

@wuu

2012年论文

@zh

2012年论文

@zh-cn

name

MyD88 mediated inflammatory si ...... h after myocardial infarction.

@ast

MyD88 mediated inflammatory si ...... h after myocardial infarction.

@en

type

label

MyD88 mediated inflammatory si ...... h after myocardial infarction.

@ast

MyD88 mediated inflammatory si ...... h after myocardial infarction.

@en

prefLabel

MyD88 mediated inflammatory si ...... h after myocardial infarction.

@ast

MyD88 mediated inflammatory si ...... h after myocardial infarction.

@en

P1433

Q35892464-07A9FDE3-3FC0-443B-A0B8-5CAB4FE3E8E2

P1476

Q35892464-37F4BAA3-8863-43A9-8BA5-644D1F860D3D

P2093

Q35892464-12888AB9-4699-4496-BE10-824B28780607

Q35892464-17F181FD-C5C7-4A95-9B0C-DBFB59912E3E

Q35892464-3401838B-A563-4F15-BC0E-98A6B5A21F4E

Q35892464-6221297E-491D-4907-B215-5248082DABA5

Q35892464-7DE85B6B-218E-4E1C-9759-ED0068AC5D6A

P2860

Q35892464-0D058AB8-326D-4769-B11D-2C7C0D852C9E

Q35892464-0D720798-3C93-4EF2-85AD-86D2603920FF

Q35892464-115E7E02-91FA-4818-B9CA-5A477CD556A8

Q35892464-117B7FF5-4A1A-4F3E-B876-A9A8A22C90C9

Q35892464-196AE246-487C-4E06-9D86-69539D602BFF

Q35892464-201B26D0-95FD-47BA-8A01-EBF126026301

Q35892464-3131032E-9322-43A4-A517-75D4620F8AB0

Q35892464-36043038-7013-47B2-946C-4E3334240030

Q35892464-3C084E28-68E7-4CE1-A8F6-AA1E3DEDED14

Q35892464-3CEF2EE7-93A9-47E1-ABAD-005ED9FAC15F

P304

Q35892464-812B7D70-B76E-491B-A968-BE7294FAD100

P31

Q35892464-4ACF0980-5A58-46D2-8FB8-52788496CECF

P356

Q35892464-96CF6D78-DB55-4C3A-843D-1FB1DC44B241

P433

Q35892464-53BF4A14-C5FE-47CC-8FB4-0AD84E88C27C

P478

Q35892464-AFFEFD08-6D99-4AF9-8876-38BE379EA0C4

P50

Q35892464-44D0DA2B-237A-4B5C-8206-9DE2A90DA59B

P577

Q35892464-65FC9773-4A70-421C-A7BD-B3FA56FBE4E3

P5875

Q35892464-5E1DA8BA-1F59-4E21-ADF5-95CF7D4B1E7A

P698

Q35892464-948C52A6-E848-4B53-8B50-977F04DD2FE8

P921

Q35892464-953A9870-458D-4EC1-B8C9-BB9FB5AF7032

P932

Q35892464-83DF6AF7-B4F0-4E99-AA30-62B26C494599

P356

J.YJMCC.2012.01.021

P1433

Journal of Molecular and Cellular Cardiology

P1476

MyD88 mediated inflammatory si ...... th after myocardial infarction

@en

P2093

Elizabeth D Luczak

http://www.w3.org/2001/XMLSchema#string

Mark E Anderson

http://www.w3.org/2001/XMLSchema#string

Paari D Swaminathan

http://www.w3.org/2001/XMLSchema#string

Robert M Weiss

http://www.w3.org/2001/XMLSchema#string

W Kutschke

http://www.w3.org/2001/XMLSchema#string

P2860

The deltaC isoform of CaMKII is activated in cardiac hypertrophy and induces dilated cardiomyopathy and heart failure

NF-kappa B functions in synaptic signaling and behavior

Role of adaptor TRIF in the MyD88-independent toll-like receptor signaling pathway

Origin and physiological roles of inflammation

Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function

A dynamic pathway for calcium-independent activation of CaMKII by methionine oxidation

Phospholamban: protein structure, mechanism of action, and role in cardiac function.

Ca2+/calmodulin-dependent protein kinase IV stimulates nuclear factor-kappa B transactivation via phosphorylation of the p65 subunit.

Inflammation 2010: new adventures of an old flame.

The inflammatory response in myocardial infarction.

P304

1135-1144

http://www.w3.org/2001/XMLSchema#string

P31

scholarly article

P356

10.1016/J.YJMCC.2012.01.021

http://www.w3.org/2001/XMLSchema#string

P433

5

http://www.w3.org/2001/XMLSchema#string

P478

52

http://www.w3.org/2001/XMLSchema#string

P50

P577

2012-02-03T00:00:00Z

http://www.w3.org/2001/XMLSchema#dateTime

P5875

221825298

http://www.w3.org/2001/XMLSchema#string

P698

22326848

http://www.w3.org/2001/XMLSchema#string

P921

P932

3327770

http://www.w3.org/2001/XMLSchema#string