about
Desmin is essential for the tensile strength and integrity of myofibrils but not for myogenic commitment, differentiation, and fusion of skeletal muscleWnt5a is required for proper epithelial-mesenchymal interactions in the uterusSerum response factor is required for sprouting angiogenesis and vascular integrityLocally expressed IGF1 propeptide improves mouse heart function in induced dilated cardiomyopathy by blocking myocardial fibrosis and SRF-dependent CTGF induction.Aerobic Exercise and Pharmacological Treatments Counteract Cachexia by Modulating Autophagy in Colon CancerCTIP2 is a negative regulator of P-TEFb.Proteome modulation in H9c2 cardiac cells by microRNAs miR-378 and miR-378.Posttranslational modifications of desmin and their implication in biological processes and pathologies.The receptor tyrosine kinase regulator Sprouty1 is a target of the tumor suppressor WT1 and important for kidney development.Muscle creatine kinase deficiency triggers both actin depolymerization and desmin disorganization by advanced glycation end products in dilated cardiomyopathy.Nicotinamide adenine dinucleotide homeostasis and signalling in heart disease: Pathophysiological implications and therapeutic potential.Regulation of Connective Tissue Growth Factor and Cardiac Fibrosis by an SRF/MicroRNA-133a AxisAn SRF/miR-1 axis regulates NCX1 and annexin A5 protein levels in the normal and failing heart.Mitochondria: a central target for sex differences in pathologies.Micro-RNAs as promising biomarkers in cardiac diseases.Diethylstilbestrol exposure in utero: a paradigm for mechanisms leading to adult disease.Inactivation of serum response factor contributes to decrease vascular muscular tone and arterial stiffness in mice.A crucial role for Pax3 in the development of the hypaxial musculature and the long-range migration of muscle precursors.Selective involvement of serum response factor in pressure-induced myogenic tone in resistance arteries.Voluntary Exercise Improves Cardiac Function and Prevents Cardiac Remodeling in a Mouse Model of Dilated Cardiomyopathy.Temporally controlled onset of dilated cardiomyopathy through disruption of the SRF gene in adult heart.Inducible mouse model of chronic intestinal pseudo-obstruction by smooth muscle-specific inactivation of the SRF gene.Nicotinamide Riboside Preserves Cardiac Function in a Mouse Model of Dilated Cardiomyopathy.Nicotinamide riboside, a form of vitamin B3, protects against excitotoxicity-induced axonal degeneration.Efficacy of epicardially delivered adipose stroma cell sheets in dilated cardiomyopathy.SRF selectively controls tip cell invasive behavior in angiogenesis.Null mutation in the desmin gene gives rise to a cardiomyopathy.[MicroRNAs: what cardiologists should know about them?].Mosaic inactivation of the serum response factor gene in the myocardium induces focal lesions and heart failure.The Oxygen Paradox, the French Paradox, and age-related diseases.SDF-1α/CXCR4 Axis Is Instrumental in Neointimal Hyperplasia and Recruitment of Smooth Muscle Progenitor CellsTransplacental injection of somite-derived cells in mdx mouse embryos for the correction of dystrophin deficiencyN-terminal stretch Arg2, Arg3, Arg4 and Arg5 of human lactoferrin is essential for binding to heparin, bacterial lipopolysaccharide, human lysozyme and DNAStudy of regulation of mitochondrial respiration in vivoAged Nicotinamide Riboside Kinase 2 Deficient Mice Present an Altered Response to Endurance Exercise TrainingRescue of biosynthesis of nicotinamide adenine dinucleotide protects the heart in cardiomyopathy caused by lamin A/C gene mutationInducible Cardiac-Specific Deletion of Sirt1 in Male Mice Reveals Progressive Cardiac Dysfunction and Sensitization of the Heart to Pressure Overload
P50
Q24678638-33C48F83-1465-451F-834C-05DFB5F4F48BQ28255597-298A9C21-BC4E-425C-BF83-A2C732AC8C0EQ28586456-B764F561-A119-455E-98CA-6BE5A1C5AAD5Q36051055-DC149CF6-7410-476F-85CD-D62B313080BEQ36950475-CF4D759F-B3EE-4FC6-A0F2-3607DAD545DCQ37068686-F53093FA-3596-44FD-A86E-53AC01BFC2FFQ37428826-8996CBA5-2B26-4331-8AB2-CFBDD35AB188Q38148976-A7601710-64E7-4295-A3CF-569BC1881482Q38352220-071BF0BD-4FB0-4FC5-BD2C-B774ECF9F7E8Q38621809-44160AA4-56B1-4274-A0EC-523ECF29751DQ38680388-CA4D17E4-04BE-434E-B106-1033AA10B257Q38830036-498772CD-4085-4F77-9D39-302A0B1CF248Q39189258-52E116FE-33F2-48E9-8539-98A3963B0A82Q39251093-44FE6C7B-6956-4360-9BFC-46997F88A385Q41908255-36C41E12-6CDC-4394-899E-6BA95AF79462Q45306829-E1EFE0DF-87D6-4C7D-BEAF-74A035E702B5Q45806437-90353215-C6DA-47B4-9987-E186890567F9Q46176856-5E890D4B-CE86-4888-B62C-9E195D00D92EQ46527655-A02B5A11-1F70-4FF0-8ED4-85D9722D7186Q46745145-2981D958-794B-4CCD-A155-DA6600210FFCQ46783976-0281FF91-60F8-41C9-9F27-3F9F78DD7052Q46869935-25869B9B-0198-4DCC-9A53-C999094EC4B4Q47348192-C82C55DD-CB26-49C3-9A7F-A4F088B53571Q48139519-B8F832F4-3D89-41E2-902A-32FA6107CDA6Q50478885-BD9FF70F-48DB-46F2-A8B9-F6FC46B871EFQ50744342-87700A37-B445-45DD-921E-659A72E02B0CQ52526996-332E07F7-1C57-4FA4-AACD-AD015895FBE1Q53624716-3037219E-3981-4B9E-9590-636183036885Q54531651-BB52B426-3037-4218-95E5-068DED6D9A20Q55384244-0BEA0443-499A-4DF8-9461-9563292BC820Q56921714-A682AA3E-3485-4D93-AC5F-672982B28E41Q56921723-F639D365-FB40-4D45-A16F-E7031784B60CQ56921730-188EDF4D-0EE9-40BF-8808-7D77CC7798B2Q56921738-53D802BC-3E8C-4414-8B03-1A461E101C70Q57072981-D9FA3872-3CA6-4723-86C3-C9B52F076A3EQ63531097-454CBA5F-05E4-4115-8F70-BB9EEFE3C736Q90972339-06C65086-12CA-4525-AB89-7F2DAF96E68D
P50
description
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Mathias MERICSKAY
@ast
Mathias MERICSKAY
@es
Mathias Mericskay
@en
Mathias Mericskay
@nl
type
label
Mathias MERICSKAY
@ast
Mathias MERICSKAY
@es
Mathias Mericskay
@en
Mathias Mericskay
@nl
prefLabel
Mathias MERICSKAY
@ast
Mathias MERICSKAY
@es
Mathias Mericskay
@en
Mathias Mericskay
@nl
P1053
M-3477-2018
P106
P21
P31
P3829
P496
0000-0002-6779-092X