about
Altered glucose homeostasis in mice with liver-specific deletion of Src homology phosphatase 2Effects of hepatic protein tyrosine phosphatase 1B and methionine restriction on hepatic and whole-body glucose and lipid metabolism in mice.Fenretinide mediated retinoic acid receptor signalling and inhibition of ceramide biosynthesis regulates adipogenesis, lipid accumulation, mitochondrial function and nutrient stress signalling in adipocytes and adipose tissue.Fenretinide treatment prevents diet-induced obesity in association with major alterations in retinoid homeostatic gene expression in adipose, liver, and hypothalamus.Neuronal human BACE1 knockin induces systemic diabetes in mice.Elevated Fibroblast growth factor 21 (FGF21) in obese, insulin resistant states is normalised by the synthetic retinoid Fenretinide in mice.Myeloid-cell protein tyrosine phosphatase-1B deficiency in mice protects against high-fat diet and lipopolysaccharide-induced inflammation, hyperinsulinemia, and endotoxemia through an IL-10 STAT3-dependent mechanism.Photoperiod- and Triiodothyronine-dependent Regulation of Reproductive Neuropeptides, Proinflammatory Cytokines, and Peripheral Physiology in Siberian Hamsters (Phodopus sungorus).Executive functions predict conceptual learning of science.A key role for PTP1B in dendritic cell maturation, migration, and T cell activation.Myeloid protein tyrosine phosphatase 1B (PTP1B) deficiency protects against atherosclerotic plaque formation in the ApoE-/- mouse model of atherosclerosis with alterations in IL10/AMPKα pathway.Direct comparison of methionine restriction with leucine restriction on the metabolic health of C57BL/6J mice.Hepatic protein tyrosine phosphatase 1B (PTP1B) deficiency protects against obesity-induced endothelial dysfunction.Methionine restriction restores a younger metabolic phenotype in adult mice with alterations in fibroblast growth factor 21.In vivo differential effects of fasting, re-feeding, insulin and insulin stimulation time course on insulin signaling pathway components in peripheral tissues.Deletion of myeloid-PTP1B decreases MHC Class I expression and peptide presentation through an IL-10 dependent mechanism in response to LPS challenge.Correction: Adipocyte-Specific Protein Tyrosine Phosphatase 1B Deletion Increases Lipogenesis, Adipocyte Cell Size and Is a Minor Regulator of Glucose Homeostasis.Deficiency in Protein Tyrosine Phosphatase PTP1B Shortens Lifespan and Leads to Development of Acute Leukemia.Methionine restriction improves renal insulin signalling in aged kidneys.Pharmacological inhibition of protein tyrosine phosphatase 1B protects against atherosclerotic plaque formation in the LDLR-/- mouse model of atherosclerosis.Response to comment by Moxon et al.Adipose specific disruption of seipin causes early-onset generalised lipodystrophy and altered fuel utilisation without severe metabolic disease.Inducible liver-specific knockdown of protein tyrosine phosphatase 1B improves glucose and lipid homeostasis in adult mice.Fenretinide prevents obesity in aged female mice in association with increased retinoid and estrogen signaling.Regulation of growth hormone induced JAK2 and mTOR signalling by hepatic protein tyrosine phosphatase 1B.Susceptibility to diet-induced obesity and glucose intolerance in the APP (SWE)/PSEN1 (A246E) mouse model of Alzheimer's disease is associated with increased brain levels of protein tyrosine phosphatase 1B (PTP1B) and retinol-binding protein 4 (RBP4Female adipose tissue-specific Bscl2 knockout mice develop only moderate metabolic dysfunction when housed at thermoneutrality and fed a high-fat dietAblation of Bscl2/seipin in hepatocytes does not cause metabolic dysfunction in congenital generalised lipodystrophyEffects of Liraglutide and Fenretinide treatments on the diabetic phenotype of neuronal human BACE1 knock-in miceKnock-in of Mutated hTAU Causes Insulin Resistance, Inflammation and Proteostasis Disturbance in a Mouse Model of Frontotemporal Dementia
P50
Q34400843-9DF3D462-4CE0-4F5A-A127-97C4A259E186Q35322235-0698A524-0126-4741-908D-4755014E4819Q36604243-C4C7F7B3-2408-43F6-8D06-3ED7A1037643Q36635330-655C71B5-0C58-4677-8375-DE3D639B4170Q36990153-96720D30-BDAE-423E-AC39-8040DFB77968Q37678960-6B59510D-9045-4DBD-8AE5-32F8015607C9Q39067449-9F868C8F-32F5-48FB-8260-8ADAC36B2568Q39914230-9E53F164-6153-49F1-973F-78BB6B86533BQ40123429-01EE6CD0-6917-4A4B-8E51-35E001C15786Q40847594-D1102BE8-EB43-4844-9400-9890CAC16C1BQ41069361-76BD351F-5920-46A8-83C2-F41654B2EB0CQ41563870-16D44F73-043B-4BFD-A310-E743418E2FF8Q41753143-60B5C989-DAF9-4503-9216-3C1DB80C7428Q42566497-E8CA60D4-9FFF-40AE-A4EF-04B8EB7CE64EQ42910284-70E78566-A0E3-4B69-A07A-1E7C12498E6BQ45958243-41B1ED76-7B49-4984-BD59-8FF0730A1E89Q45976942-30DEFA03-13B8-400C-AF67-C9AEDD53D9A4Q47419511-C0CC0AEA-89B2-418A-8235-74D48CA57EB0Q47611789-3DD3F551-A0B1-4B54-B264-CCD425047645Q47814899-5D4EF97C-4A67-4F0A-8B76-B65446E7CFDCQ49358806-E7A16384-8140-4DEE-91D6-24D9511A4AE7Q49833789-AAB38392-A0E4-441C-BB1F-86812BB7E1CAQ50854047-35C05F54-1F70-408E-89CB-4FB68B9AFB39Q51005071-318D6D4A-A799-46D9-B70D-9EDE282EA5EAQ51132944-5FBC14C8-F394-4C55-99A4-39FEA9481D9CQ51373857-3904366D-EEBF-4B86-815E-19BE79253FDAQ60302320-BA276B12-6FB1-4005-BB49-6279E219E774Q92057005-740CA194-5533-4F9F-8A4B-B5022DB49D63Q92134642-796E661F-4C78-4C98-A1BC-0C13670F99BCQ92515239-0A2817EB-C7F6-47E7-83F7-50C34B9539C4
P50
description
investigador
@es
researcher
@en
wetenschapper
@nl
name
M Delibegovic
@en
M Delibegovic
@nl
type
label
M Delibegovic
@en
M Delibegovic
@nl
prefLabel
M Delibegovic
@en
M Delibegovic
@nl
P108
P31
P496
0000-0001-6193-3152