About: E. Dale Abel

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An Entity of Type : wikibase:Item, within Data Space : wikidata.demo.openlinksw.com associated with source document(s)

American endocrinologist

Attributes	Values
rdf:type	Item
owl:sameAs	E. Dale Abel
description	ikertzailea (eu) 연구원 (ko) 研究者 (ja) wetenschapper (nl) дослідник (uk) эрдэмтэн (mn) باحت (ary) изилдөөчү (ky) 研究者 (zh) American endocrinologist (en)
rdfs:label	E. Dale Abel (en) E. Dale Abel (es) E. Dale Abel (nl) E. Dale Abel (ast)
skos:prefLabel	E. Dale Abel (en) E. Dale Abel (es) E. Dale Abel (nl) E. Dale Abel (ast)
name	E. Dale Abel (en) E. Dale Abel (es) E. Dale Abel (nl) E. Dale Abel (ast)
Scopus author ID	wds:Q59100279-2E1B2277-6B67-4BF4-A513-2BAA63E6C880
Scopus author ID	7202417444
given name	wds:Q59100279-84FF14B9-8900-428C-8023-9DE068D6DAFF
given name	E.
image	wds:Q59100279-A9D268C1-EE87-4C2E-B239-6AC725A1C6CD
instance of	wds:Q59100279-0E1F9EF2-3888-4263-B74F-920DA867B7A8
image
instance of	Homo sapiens
award received	wds:Q59100279-25FBD238-E78A-4EFC-82A8-E15022C2CDF3
award received	Rhodes Scholarship
Google Knowledge Graph ID	wds:Q59100279-8C10B864-5F47-409F-9A15-C7F75582EB49
Google Knowledge Graph ID	http://g.co/kg/g/11f0yrc8jw
Google Knowledge Graph ID	/g/11f0yrc8jw
skos:altLabel	Evan Dale Abel (en)
occupation	wds:Q59100279-0ED07557-E3AD-4639-AB96-5BD8E82B3D7D wds:Q59100279-5f6a4297-4cb7-2b24-59d4-8e08a83cd3cf
employer	wds:Q59100279-13B361A4-8F74-414B-9B08-59B6BBFF89D8 wds:Q59100279-267E172A-5AB6-47EE-951B-EF7AD371522B wds:Q59100279-302D1548-66E6-416A-9432-3551065C2E2F wds:Q59100279-50673E4D-287F-4B9D-9032-06AE7CFF5FE1 wds:Q59100279-650C7558-3E4F-4676-9A7A-D97546664F3F wds:Q59100279-79D1EE7C-5681-4CC2-B81F-7486E4729132 wds:Q59100279-B8E8E904-3970-4EE2-99FD-3B5C9D713CC7 wds:Q59100279-C2D3678C-1F08-4CA4-88F5-43D44BE533D5
sex or gender	wds:Q59100279-16ffcd95-4cdf-6005-001a-b7230130dca4
VIAF ID	wds:Q59100279-F830A401-76D9-479D-A61C-8263A2D18495
GND ID	wds:Q59100279-538bbe65-62cd-416b-8b87-68d39fea8c6f
date of birth	wds:Q59100279-8bcfab76-2d92-417d-a95f-add3bd89d099
educated at	wds:Q59100279-B76A5580-30AC-467E-B5FD-45EDA846C089
VIAF ID	http://viaf.org/viaf/62604676
GND ID	https://d-nb.info/gnd/1056158700
occupation	endocrinologist researcher
employer	UCLA Ronald Reagan Medical Center McLean Hospital Beth Israel Deaconess Medical Center University of Iowa University of the West Indies Brigham and Women's Hospital Harvard Medical School University of Utah
sex or gender	male
VIAF ID	62604676
GND ID	1056158700
date of birth	1963-01-01 00:00:00Z (xsd:dateTime)
educated at	Green College, Oxford
ORCID iD	wds:Q59100279-245B6F67-4323-4A9B-823C-C6E76E68B3AB
ORCID iD	https://orcid.org/0000-0001-5290-0738
ORCID iD	0000-0001-5290-0738
is about of	E. Dale Abel https://www.wikidata.org/wiki/Special:EntityData/Q59100279 E. Dale Abel
is author of	Disruption of the circadian clock within the cardiomyocyte influences myocardial contractile function, metabolism, and gene expression. Mitochondrial energetics in the heart in obesity-related diabetes: direct evidence for increased uncoupled respiration and activation of uncoupling proteins. Dilated cardiomyopathy resulting from high-level myocardial expression of Cre-recombinase. Inefficient reprogramming of fibroblasts into cardiomyocytes using Gata4, Mef2c, and Tbx5 Contribution of insulin and Akt1 signaling to endothelial nitric oxide synthase in the regulation of endothelial function and blood pressure Nuclear receptor SHP, a death receptor that targets mitochondria, induces apoptosis and inhibits tumor growth. Mitochondrial uncoupling: a key contributor to reduced cardiac efficiency in diabetes. Endothelial nitric oxide synthase phosphorylation in treadmill-running mice: role of vascular signalling kinases. Loss of bradykinin signaling does not accelerate the development of cardiac dysfunction in type 1 diabetic akita mice. Rodent models of diabetic cardiomyopathy. Molecular mechanisms of diabetic cardiomyopathy. Mitochondria in the diabetic heart Contractile dysfunction in hypertrophied hearts with deficient insulin receptor signaling: possible role of reduced capillary density. The glucose transporter Glut1 is selectively essential for CD4 T cell activation and effector function Modulation of glucose transporter 1 (GLUT1) expression levels alters mouse mammary tumor cell growth in vitro and in vivo. Mitochondrial Calpain-1 Disrupts ATP Synthase and Induces Superoxide Generation in Type 1 Diabetic Hearts: A Novel Mechanism Contributing to Diabetic Cardiomyopathy Targeted deletion of BMK1/ERK5 in adult mice perturbs vascular integrity and leads to endothelial failure. PAS kinase is required for normal cellular energy balance An unliganded thyroid hormone receptor causes severe neurological dysfunction Cardiac metabolism in heart failure: implications beyond ATP production. Lipids, lysosomes, and autophagy. Podocyte-specific GLUT4-deficient mice have fewer and larger podocytes and are protected from diabetic nephropathy. Cardiac remodeling in obesity. Ceramide mediates vascular dysfunction in diet-induced obesity by PP2A-mediated dephosphorylation of the eNOS-Akt complex

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