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Journal Article
Cellular Signalling, ISSN 0898-6568, 05/2015, Volume 27, Issue 5, pp. 908 - 922
Hypertrophy increases the risk of heart failure and arrhythmia. Prevention or reversal of the maladaptive hypertrophic phenotype has thus been proposed to... 
protein kinase A (PKA) | Compartmentalized signaling | A-kinase anchoring protein (AKAP) | cardiomyocyte hypertrophy | 3′,5′-cyclic monophosphate (cAMP) | Phosphodiesterase 4 (PDE4) activation | 3',5'-cyclic monophosphate (cAMP) | Cardiomyocyte hypertrophy | Protein kinase A (PKA) | MAP KINASE | HEART-FAILURE | CELL BIOLOGY | SIGNAL-TRANSDUCTION | 3 ',5 '-cyclic monophosphate (cAMP) | CYCLIC-AMP | KINASE ANCHORING PROTEINS | CARDIAC-HYPERTROPHY | PKA PHOSPHORYLATION | PHOSPHATIDIC-ACID | RYANODINE-RECEPTOR | CAMP | Humans | Molecular Sequence Data | Cardiomegaly - pathology | Protein Isoforms - metabolism | Protein Isoforms - chemistry | HEK293 Cells | Phosphorylation - drug effects | Cyclic Nucleotide Phosphodiesterases, Type 4 - metabolism | Cyclic AMP - metabolism | Cyclic Nucleotide Phosphodiesterases, Type 4 - chemistry | A Kinase Anchor Proteins - metabolism | Cyclic AMP-Dependent Protein Kinases - metabolism | Amino Acid Sequence | Peptides - chemistry | Cardiomegaly - drug therapy | Cells, Cultured | Rats | Enzyme Activation - drug effects | Peptides - pharmacology | Myocytes, Cardiac - pathology | Animals | Myocytes, Cardiac - drug effects | Signal Transduction - drug effects | Myocytes, Cardiac - metabolism | Cardiomegaly - metabolism | Protein binding | Hypertrophy | Heart | Proteins | Receptors | Upstream | Stimulation | Kinases | Failure | Anchoring | compartmentalized signaling | 3′, 5′-cyclic monophosphate (cAMP) | A-Kinase Anchoring Protein (AKAP)-Lbc
Journal Article
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 2013, Volume 66, pp. 27 - 40
Abstract The objective of this study was to determine the role of A-Kinase Anchoring Protein (AKAP)-Lbc in the development of heart failure, by investigating... 
Cardiovascular | A-Kinase Anchoring Protein (AKAP) | Heart failure | Cardiac hypertrophy | Protein kinase D | COMPLEX | CARDIAC & CARDIOVASCULAR SYSTEMS | ANCHORING PROTEINS | PROTEIN-KINASE-D | HEART-FAILURE | PKA | D ACTIVATION | NUCLEAR EXPORT | IDENTIFICATION | CELL BIOLOGY | PRESSURE | EXPRESSION | Protein Kinase C - genetics | Minor Histocompatibility Antigens | Cardiomegaly - pathology | Male | A Kinase Anchor Proteins - chemistry | A Kinase Anchor Proteins - genetics | Phenylephrine - adverse effects | Guanine Nucleotide Exchange Factors - metabolism | Protein Kinase C - metabolism | Myocardium - metabolism | Female | Collagen - genetics | Angiotensin II - adverse effects | A Kinase Anchor Proteins - metabolism | Protein Structure, Tertiary | Guanine Nucleotide Exchange Factors - genetics | Histone Deacetylases - genetics | Signal Transduction | Gene Expression Regulation | Heart Failure - genetics | Histone Deacetylases - metabolism | Mice, Transgenic | Myocardium - pathology | Heart Failure - metabolism | Heart Failure - pathology | Aorta - pathology | Collagen - metabolism | Animals | Cardiomegaly - chemically induced | Mice | Cardiomegaly - genetics | Heart Failure - chemically induced | Apoptosis | Cardiomegaly - metabolism | Guanine Nucleotide Exchange Factors - chemistry | Heart | Heart enlargement | Analysis | Angiotensin | heart failure | protein kinase D | cardiac hypertrophy
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2013, Volume 8, Issue 4, p. e62705
A-kinase anchoring proteins (AKAPs) are scaffolding molecules that coordinate and integrate G-protein signaling events to regulate development, physiology, and... 
Proteins | Heart | Purines | Heart enlargement | Electrocardiogram | Physiological aspects | Electrocardiography | Protein kinases | Protein binding
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2013, Volume 8, Issue 4, p. e62705
Background: A-kinase anchoring proteins (AKAPs) are scaffolding molecules that coordinate and integrate G-protein signaling events to regulate development,... 
PROTEIN-KINASE-A | BREAST-CANCER | CELL INVASIVENESS | MULTIDISCIPLINARY SCIENCES | HEART-FAILURE | MOUSE | EXCHANGE FACTOR AKAP13 | RECEPTOR | INDUCED CARDIOMYOCYTE HYPERTROPHY | ANCHORING PROTEIN | SIGNALING COMPLEX | Embryo, Mammalian | Minor Histocompatibility Antigens | Heart - embryology | Myocardial Contraction - drug effects | Male | A Kinase Anchor Proteins - genetics | Gene Expression Regulation, Developmental | Guanine Nucleotide Exchange Factors - metabolism | Electrocardiography | Female | A Kinase Anchor Proteins - metabolism | Heart - physiopathology | Protein Structure, Tertiary | Guanine Nucleotide Exchange Factors - genetics | Signal Transduction | Breeding | Cardiomegaly - physiopathology | Organ Size | Stroke Volume - drug effects | Mice, Transgenic | Animals | Cardiomegaly - chemically induced | Heart - drug effects | Mice | Isoproterenol - adverse effects | Cardiomegaly - metabolism | Heart | Protein kinase A | Cell culture | Cardiovascular disease | Isoproterenol | Kinases | Guanine | Defects | Eutrophication | Proteins | Embryogenesis | Fertility | Rodents | Physiology | Guanine nucleotide exchange factor | Heart diseases | Anchoring | Pharmaceutical sciences | Heart failure | Contractility | Cardiomyocytes | Pharmacology | Breast cancer | Embryos | Muscle contraction | Signaling | Scaffolding | Isoforms | Mutation | Alzheimers disease | Viability | Binding sites | Hypertrophy | Ejection
Journal Article
Experimental Dermatology, ISSN 0906-6705, 08/2012, Volume 21, Issue 8, pp. 605 - 611
Collagen XVII (COL17), a transmembrane protein expressed in epidermal keratinocytes (EK), is targeted by pathogenic autoantibodies in bullous pemphigoid.... 
junctional epidermolysis bullosa | bullous pemphigoid | inflammation | dermal–epidermal junction | hemidesmosome | Junctional epidermolysis bullosa | Inflammation | Bullous pemphigoid | Dermal-epidermal junction | Hemidesmosome | AUTOANTIBODIES | INTERLEUKIN-8 GENE-EXPRESSION | ACTIVATION | PROTEIN-KINASE | BENIGN EPIDERMOLYSIS-BULLOSA | dermal-epidermal junction | DERMATOLOGY | CULTURED HUMAN KERATINOCYTES | ELEVATED LEVELS | NF-KAPPA-B | SIGNALING CASCADE | BLISTER FLUID | Cell Line | Inflammation - pathology | Autoantigens - metabolism | Tetradecanoylphorbol Acetate - pharmacology | Keratinocytes - radiation effects | Humans | RNA, Small Interfering - pharmacology | Non-Fibrillar Collagens - genetics | NF-kappa B - metabolism | Non-Fibrillar Collagens - deficiency | Autoantigens - genetics | Epidermolysis Bullosa - pathology | Gene Expression Regulation - drug effects | Non-Fibrillar Collagens - metabolism | Tumor Necrosis Factor-alpha - pharmacology | Inflammation - metabolism | Ultraviolet Rays | Keratinocytes - drug effects | Keratinocytes - metabolism | Lipopolysaccharides - pharmacology | Epidermolysis Bullosa - metabolism | Integrin alpha6beta4 - metabolism | Interleukin-18 - metabolism | Autoimmunity | Autoantibodies | Nuclear radiation | Mitogens | Collagen | Integrins | phorbol 12-myristate 13-acetate | Keratinocytes | Lipopolysaccharides | Membrane proteins | NF- Kappa B protein | Tumor necrosis factor | Chemokines | Interleukin 8
Journal Article
Journal Article
American Journal of Physiology-Cell Physiology, ISSN 0363-6143, 09/2019
Severe burn injury results in systemic disruption of metabolic regulations and impaired cardiac function. Restoration of hemodynamic homeostasis utilizing... 
Journal Article
Biological Psychiatry, ISSN 0006-3223, 05/2017, Volume 81, Issue 10, pp. S331 - S332
Journal Article
Biological Psychiatry, ISSN 0006-3223, 2017, Volume 81, Issue 10, pp. S331 - S332
Journal Article
Medical Physics, ISSN 0094-2405, 05/2010, Volume 37, Issue 6, pp. 2457 - 2465
Purpose: To experimentally simulate IMRT delivery using two human cell models in vitro and test the hypothesis that a loss in effective dose resulting from the... 
IMRT | simulation | loss of effectiveness | dose protraction | neutrons | incomplete repair
Journal Article