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animals (25) 25
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1. Full Text HSP27 is a partner of JAK2-STAT5 and a potential therapeutic target in myelofibrosis
by Sevin, Margaux and Kubovcakova, Lucia and Pernet, Nicolas and Causse, Sébastien and Vitte, Franck and Villeval, Jean Luc and Lacout, Catherine and Cordonnier, Marine and Rodrigues-Lima, Fernando and Chanteloup, Gaétan and Mosca, Matthieu and Chrétien, Marie-Lorraine and Bastie, Jean Noël and Audia, Sylvain and Sagot, Paul and Ramla, Selim and Martin, Laurent and Gleave, Martin and Mezger, Valérie and Skoda, Radek and Plo, Isabelle and Garrido, Carmen and Girodon, François and De Thonel, Aurélie
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 1431 - 13
Heat shock protein 27 (HSP27/HSPB1) is a stress-inducible chaperone that facilitates cancer development by its proliferative and anti-apoptotic functions. The... 
EXTRACELLULAR HSP27 | POLYCYTHEMIA-VERA | HSP90 INHIBITOR | ACTIVATION | SHOCK-PROTEIN 27 | MULTIDISCIPLINARY SCIENCES | MYELOPROLIFERATIVE NEOPLASMS | SERUM | MESENCHYMAL TRANSITION | TYROSINE-PHOSPHATASE | BONE-MARROW FIBROSIS | Leukocytes - pathology | Whole-Body Irradiation | Humans | STAT5 Transcription Factor - immunology | Primary Myelofibrosis - pathology | Molecular Targeted Therapy | HSP27 Heat-Shock Proteins - genetics | Leukocytes - immunology | STAT5 Transcription Factor - genetics | Thrombopoietin - immunology | Oligonucleotides - pharmacology | Bone Marrow Cells - immunology | Bone Marrow Transplantation | HEK293 Cells | Female | Disease Models, Animal | Primary Myelofibrosis - drug therapy | Janus Kinase 2 - immunology | Transduction, Genetic | Mice, Inbred C57BL | Primary Myelofibrosis - immunology | Bone Marrow Cells - pathology | Janus Kinase 2 - genetics | Mice, Transgenic | HSP27 Heat-Shock Proteins - immunology | Thrombopoietin - genetics | Primary Myelofibrosis - genetics | Animals | K562 Cells | Cell Line, Tumor | Leukocytes - drug effects | Mice | Mutation | Spleen | CD34 antigen | Cell proliferation | Animal models | Myelofibrosis | Therapeutic applications | Lung diseases | Heat shock proteins | Antisense oligonucleotides | Stat5 protein | Disease control | Patients | Neoplasms | Thrombopoietin | Janus kinase 2 | Hsp27 protein | Fibrosis | Weight reduction | Apoptosis | Cancer | Heat shock | Tumors | Life Sciences
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2. Full Text Myeloproliferative neoplasms can be initiated from a single hematopoietic stem cell expressing JAK2-V617F
by Lundberg, Pontus and Takizawa, Hitoshi and Kubovcakova, Lucia and Guo, Guoji and Hao-Shen, Hui and Dirnhofer, Stephan and Orkin, Stuart H and Manz, Markus G and Skoda, Radek C
Journal of Experimental Medicine, ISSN 0022-1007, 2014, Volume 211, Issue 11, pp. 2213 - 2230
The majority of patients with myeloproliferative neoplasms (MPNs) carry a somatic JAK2-V617F mutation. Because additional mutations can precede JAK2-V617F, it... 
PROGENITOR CELLS | V617F MUTATION | MEDICINE, RESEARCH & EXPERIMENTAL | POLYCYTHEMIA-VERA | ACTIVATING MUTATION | GAIN-OF-FUNCTION | TYROSINE KINASE JAK2 | IMMUNOLOGY | ESSENTIAL THROMBOCYTHEMIA | CLONAL ANALYSIS | MYELOID METAPLASIA | SOMATIC MUTATIONS | Cell Cycle - genetics | Hematopoietic Stem Cells - pathology | Gene Expression Profiling | Proto-Oncogene Proteins c-kit - metabolism | Myeloproliferative Disorders - genetics | Cell Transformation, Neoplastic - genetics | Bone Marrow Transplantation | Antigens, Surface - metabolism | Antigens, Ly - metabolism | Female | Membrane Proteins - metabolism | Cell Lineage - genetics | Biomarkers - metabolism | Gene Expression | Janus Kinase 2 - genetics | Immunophenotyping | Hematopoietic Stem Cells - metabolism | Transplantation Chimera | Mice, Knockout | Phenotype | Animals | Alleles | Mice | DNA Damage | Mutation | Cluster Analysis
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3. Full Text Deletion of Stat3 in hematopoietic cells enhances thrombocytosis and shortens survival in a JAK2-V617F mouse model of MPN
by Grisouard, Jean and Shimizu, Takafumi and Duek, Adrian and Kubovcakova, Lucia and Hao-Shen, Hui and Dirnhofer, Stephan and Skoda, Radek C
Blood, ISSN 0006-4971, 03/2015, Volume 125, Issue 13, pp. 2131 - 2140
The acquired somatic JAK2-V617F mutation is present in >80% of patients with myeloproliferative neoplasms (MPNs). Stat3 plays a role in hematopoietic... 
POLYCYTHEMIA-VERA | INTERFERON | MYELOPROLIFERATIVE DISORDERS | MUTATION | MICE | PHENOTYPES | JAK2 | HEMATOLOGY | MEGAKARYOPOIESIS | IL-6 | Mice, Inbred C57BL | Janus Kinase 2 - genetics | Mice, Transgenic | Hematopoietic Stem Cells - metabolism | Bone Marrow Neoplasms - genetics | Myeloproliferative Disorders - genetics | Disease Progression | Animals | Bone Marrow Neoplasms - metabolism | Phenylalanine - genetics | Bone Marrow - metabolism | Gene Deletion | Myeloproliferative Disorders - metabolism | Valine - genetics | Mice | Bone Marrow Neoplasms - mortality | Myeloproliferative Disorders - mortality | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Amino Acid Substitution | Disease Models, Animal | Thrombocytosis - genetics
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4. Full Text Loss of Ezh2 synergizes with JAK2-V617F in initiating myeloproliferative neoplasms and promoting myelofibrosis
by Shimizu, Takafumi and Kubovcakova, Lucia and Nienhold, Ronny and Zmajkovic, Jakub and Meyer, Sara C and Hao-Shen, Hui and Geier, Florian and Dirnhofer, Stephan and Guglielmelli, Paola and Vannucchi, Alessandro M and Milosevic Feenstra, Jelena D and Kralovics, Robert and Orkin, Stuart H and Skoda, Radek C
Journal of Experimental Medicine, ISSN 0022-1007, 07/2016, Volume 213, Issue 8, pp. 1479 - 1496
Myeloproliferative neoplasm (MPN) patients frequently show co-occurrence of JAK2-V617F and mutations in epigenetic regulator genes, including EZH2. In this... 
GROUP GENE EZH2 | MEDICINE, RESEARCH & EXPERIMENTAL | POLYCYTHEMIA-VERA | ACTIVATING MUTATION | HEMATOPOIETIC STEM-CELLS | TYROSINE KINASE JAK2 | IMMUNOLOGY | WORLD-HEALTH-ORGANIZATION | MYELOID METAPLASIA | SOMATIC MUTATIONS | MYELODYSPLASTIC SYNDROMES | REPRESSIVE COMPLEX 2
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5. Full Text Estrogen Signaling Selectively Induces Apoptosis of Hematopoietic Progenitors and Myeloid Neoplasms without Harming Steady-State Hematopoiesis
by Sánchez-Aguilera, Abel and Arranz, Lorena and Martín-Pérez, Daniel and García-García, Andrés and Stavropoulou, Vaia and Kubovcakova, Lucia and Isern, Joan and Martín-Salamanca, Sandra and Langa, Xavier and Skoda, Radek C and Schwaller, Jürg and Méndez-Ferrer, Simón
Cell Stem Cell, ISSN 1934-5909, 12/2014, Volume 15, Issue 6, pp. 791 - 804
Estrogens are potent regulators of mature hematopoietic cells; however, their effects on primitive and malignant hematopoietic cells remain unclear. Using... 
GENE NETWORKS | STEM-CELLS | POLYCYTHEMIA-VERA | MYELOPROLIFERATIVE DISORDERS | BONE-MARROW | TYROSINE KINASE JAK2 | SELF-RENEWAL | HIGH-DOSE CHEMOTHERAPY | BREAST-CANCER-CELLS | RECEPTOR-ALPHA | CELL & TISSUE ENGINEERING | CELL BIOLOGY | Oncogene Proteins, Fusion - metabolism | Leukemia - pathology | Apoptosis - drug effects | Humans | Apoptosis - genetics | Leukemia - metabolism | Tamoxifen - administration & dosage | Hematopoiesis - drug effects | Cell Differentiation - genetics | Janus Kinase 2 - metabolism | Hematopoietic Stem Cells - physiology | Estrogen Receptor alpha - metabolism | Hematopoietic Stem Cells - drug effects | Cell Proliferation - genetics | Signal Transduction | Mice, Inbred C57BL | Cells, Cultured | Janus Kinase 2 - genetics | Hematopoietic Stem Cell Transplantation | Leukemia - drug therapy | Hematopoiesis - genetics | Selective Estrogen Receptor Modulators - administration & dosage | Mutation - genetics | Mice, Knockout | Xenograft Model Antitumor Assays | Animals | Estrogen Receptor alpha - genetics | Myeloid Progenitor Cells - drug effects | Myeloid Progenitor Cells - physiology | Cell Differentiation - drug effects | Cell Proliferation - drug effects | Mice
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6. Full Text Ruxolitinib-induced defects in DNA repair cause sensitivity to PARP inhibitors in myeloproliferative neoplasms
by Nieborowska-Skorska, Margaret and Maifrede, Silvia and Dasgupta, Yashodhara and Sullivan, Katherine and Flis, Sylwia and Le, Bac Viet and Solecka, Martyna and Belyaeva, Elizaveta A and Kubovcakova, Lucia and Nawrocki, Morgan and Kirschner, Martin and Zhao, Huaqing and Prchal, Josef T and Piwocka, Katarzyna and Moliterno, Alison R and Wasik, Mariusz and Koschmieder, Steffen and Green, Tony R and Skoda, Radek C and Skorski, Tomasz
Blood, ISSN 0006-4971, 12/2017, Volume 130, Issue 26, pp. 2848 - 2859
Myeloproliferative neoplasms (MPNs) often carry JAK2(V617F), MPL(W515L), or CALR (del52) mutations. Current treatment options for MPNs include cytoreduction by... 
GENOMIC INSTABILITY | POLYCYTHEMIA-VERA | REPLICATION FORKS | EPITHELIAL-CELLS | HEMATOPOIETIC STEM-CELLS | IN-VIVO | ACUTE MYELOID-LEUKEMIA | HOMOLOGOUS RECOMBINATION | HEMATOLOGY | MYELODYSPLASTIC SYNDROME | DAMAGE | Cell Line | DNA Repair - drug effects | Humans | Janus Kinase 2 - genetics | Myeloproliferative Disorders - drug therapy | Calreticulin - genetics | Myeloproliferative Disorders - genetics | Piperazines - pharmacology | Neoplasms - drug therapy | Drug Synergism | Phthalazines - pharmacology | Poly(ADP-ribose) Polymerase Inhibitors - pharmacology | Receptors, Thrombopoietin - genetics | Animals | Heterografts | Neoplasms - genetics | Mice | Tumor Cells, Cultured | Pyrazoles - pharmacology | Myeloid Neoplasia
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7. Full Text JAK2 exon 12 mutant mice display isolated erythrocytosis and changes in iron metabolism favoring increased erythropoiesis
by Grisouard, Jean and Li, Sai and Kubovcakova, Lucia and Rao, Tata Nageswara and Meyer, Sara C and Lundberg, Pontus and Hao-Shen, Hui and Romanet, Vincent and Murakami, Masato and Radimerski, Thomas and Dirnhofer, Stephan and Skoda, Radek C
Blood, ISSN 0006-4971, 08/2016, Volume 128, Issue 6, pp. 839 - 851
Mutations in JAK2 exon 12 are frequently found in patients with polycythemia vera (PV) that do not carry a JAK2-V617F mutation. The majority of these patients... 
MYELOFIBROSIS | JAK2 EXON-12 MUTATIONS | MOUSE MODEL | TYROSINE KINASE JAK2 | JAK2-V617F | MYELOPROLIFERATIVE NEOPLASMS | DISORDERS | JAK2V617F-NEGATIVE POLYCYTHEMIA-VERA | ESSENTIAL THROMBOCYTHEMIA | HEMATOLOGY | SOMATIC MUTATIONS | Erythropoiesis | Polycythemia - genetics | Exons | Mice, Inbred C57BL | Janus Kinase 2 - genetics | Mice, Transgenic | Iron - metabolism | Animals | Base Sequence | Polycythemia - metabolism | Erythrocytes - pathology | Mice | Polycythemia - physiopathology | Mutation
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8. Full Text Loss of Stat1 decreases megakaryopoiesis and favors erythropoiesis in a JAK2-V617F-driven mouse model of MPNs
by Duek, Adrian and Lundberg, Pontus and Shimizu, Takafumi and Grisouard, Jean and Karow, Axel and Kubovcakova, Lucia and Hao-Shen, Hui and Dirnhofer, Stephan and Skoda, Radek C
Blood, ISSN 0006-4971, 06/2014, Volume 123, Issue 25, pp. 3943 - 3950
The interferon-gamma (IFN gamma)/signal transducer and activator of transcription 1 (Stat1) pathway shows higher activity in patients with essential... 
CELLS | POLYCYTHEMIA-VERA | MYELOID NEOPLASMS | MUTATION | TYROSINE KINASE JAK2 | MYELOPROLIFERATIVE NEOPLASMS | DISORDERS | ESSENTIAL THROMBOCYTHEMIA | HEMATOLOGY | WORLD-HEALTH-ORGANIZATION | TRANSGENIC MICE | Humans | Polycythemia Vera - blood | Male | Polycythemia Vera - genetics | Bone Marrow Neoplasms - genetics | Thrombocythemia, Essential - genetics | Bone Marrow Transplantation - methods | Polycythemia Vera - metabolism | Thrombopoiesis - genetics | STAT1 Transcription Factor - metabolism | Flow Cytometry | Janus Kinase 2 - metabolism | Female | Disease Models, Animal | Erythropoiesis - genetics | Mice, Inbred C57BL | Janus Kinase 2 - genetics | Mice, Transgenic | Hematopoietic Stem Cells - metabolism | Bone Marrow Neoplasms - blood | Reverse Transcriptase Polymerase Chain Reaction | STAT1 Transcription Factor - genetics | Thrombocythemia, Essential - blood | Blotting, Western | Mice, Knockout | Animals | Bone Marrow Neoplasms - metabolism | Hematopoietic Stem Cells - cytology | Mice | Mutation | Interferon-gamma - blood | Thrombocythemia, Essential - metabolism
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9. Full Text Aging of Bone Marrow Microenvironment Promotes Myeloid Bias of Hematopoietic Progenitors and Is a Target in Age-Related Myeloproliferative Neoplasms
by Ho, Ya-Hsuan and del Toro, Raquel and Rivera-Torres, José and Rak, Justyna and Korn, Claudia and García-García, Andrés and Kubovcakova, Lucia and Macías, David and Arranz, Lorena and González-Gómez, Cristina and Wittner, Monika and Nienhold, Ronny and Waller, Amie K and Foster, Holly R and Lopez-Otin, Carlos and Johnson, Randall S and Nerlov, Claus and Vainchenker, William and Ghevaert, Cedric and Louache, Fawzia and Skoda, Radek C and Andrés, Vicente and Mendez-Ferrer, Simon
Blood, ISSN 0006-4971, 11/2018, Volume 132, Issue Supplement 1, pp. 3842 - 3842
Abstract Background: BM HSC accumulate during aging but are functionally impaired; however, it remains debated whether this aging results from HSC-intrinsic... 
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10. Full Text Differential effects of hydroxyurea and INC424 on mutant allele burden and myeloproliferative phenotype in a JAK2-V617F polycythemia vera mouse model
by Kubovcakova, Lucia and Lundberg, Pontus and Grisouard, Jean and Hao-Shen, Hui and Romanet, Vincent and Andraos, Rita and Murakami, Masato and Dirnhofer, Stephan and Wagner, Kay-Uwe and Radimerski, Thomas and Skoda, Radek C
Blood, ISSN 0006-4971, 02/2013, Volume 121, Issue 7, pp. 1188 - 1199
To establish a preclinical animal model for testing drugs with potential effects on myeloproliferative neoplasms (MPNs), we first performed a detailed... 
MYELOFIBROSIS | BONE-MARROW | IN-VIVO | TYROSINE KINASE JAK2 | DISORDERS | ESSENTIAL THROMBOCYTHEMIA | INHIBITOR | HEMATOLOGY | EXPRESSION | HEMATOPOIETIC STEM | TRANSGENIC MICE | Hydroxyurea - pharmacology | Polycythemia Vera - genetics | Hematopoiesis - drug effects | Janus Kinase 2 - deficiency | Polycythemia Vera - metabolism | STAT5 Transcription Factor - metabolism | Bone Marrow Transplantation | Female | Polycythemia Vera - pathology | Janus Kinase 2 - antagonists & inhibitors | Disease Models, Animal | Pyrazoles - pharmacology | Mice, Inbred C57BL | Janus Kinase 2 - genetics | Hematopoiesis - genetics | Mice, Transgenic | Mice, Knockout | Phenotype | Animals | Signal Transduction - drug effects | Alleles | Polycythemia Vera - drug therapy | Mice | Mutation | Amino Acid Substitution
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11. Full Text Loss of Ezh2 synergizes with JAK2-V617F in initiating myeloproliferative neoplasms and promoting myelofibrosis
by Shimizu, Takafumi and Kubovcakova, Lucia and Nienhold, Ronny and Zmajkovic, Jakub and Meyer, Sara C and Hao-Shen, Hui and Geier, Florian and Dirnhofer, Stephan and Guglielmelli, Paola and Vannucchi, Alessandro M and Feenstra, Jelena D Milosevic and Kralovics, Robert and Orkin, Stuart H and Skoda, Radek C
The Journal of experimental medicine, 07/2016, Volume 213, Issue 8, p. 1479
Myeloproliferative neoplasm (MPN) patients frequently show co-occurrence of JAK2-V617F and mutations in epigenetic regulator genes, including EZH2 In this... 
Janus Kinase 2 - genetics | Hematologic Neoplasms - pathology | Myeloproliferative Disorders - pathology | Enhancer of Zeste Homolog 2 Protein - deficiency | Mutation, Missense | Myeloproliferative Disorders - genetics | Animals | Mice, Mutant Strains | Tumor Suppressor Proteins - deficiency | Janus Kinase 2 - metabolism | Myeloproliferative Disorders - metabolism | Hematologic Neoplasms - genetics | Mice | Hematologic Neoplasms - metabolism | Amino Acid Substitution
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12. Full Text JAK2V617F and Loss of Ezh2 in Hematopoietic Cells Contribute Synergistically to Myeloproliferative Neoplasm Initiation Potential, and Accelerate Progression of Disease
by Shimizu, Takafumi and Hao-Shen, Hui and Kubovcakova, Lucia and Lundberg, Pontus and Dirnhofer, Stephan and Orkin, Stuart H and Grisouard, Jean and Shimizu, Yukiko and Pianta, Annalisa and Szczerba, Barbara and Nienhold, Ronny and Skoda, Radek C
Blood, ISSN 0006-4971, 12/2014, Volume 124, Issue 21, pp. 158 - 158
Abstract Background ;The gain-of-function JAK2 mutation, JAK2V617F, is the most common molecular abnormality in myeloproliferative neoplasms (MPNs) and appears... 
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13. Full Text Myeloproliferative neoplasms can be initiated from a single hematopoietic stem cell expressingJAK2-V617F
by Lundberg, Pontus and Takizawa, Hitoshi and Kubovcakova, Lucia and Guo, Guoji and Hao-Shen, Hui and Dirnhofer, Stephan and Orkin, Stuart H and Manz, Markus G and Skoda, Radek C
The Journal of Experimental Medicine, ISSN 0022-1007, 10/2014, Volume 211, Issue 11, pp. 2213 - 2230
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14. Full Text Muscarinic receptors are affected by corticotropin-releasing hormone and c-fos gene disruptions
: Is there a mutual connection to adrenoceptors?
by Nováková, Martina and Benes, Jan and Kubovčákova, Lucia and Kvetňanský, Richard and Mysliveček, Jaromír
Journal of Molecular Neuroscience, ISSN 0895-8696, 2/2006, Volume 30, Issue 1, pp. 69 - 70
In the last decade, progress in gene disruption technology has allowed the study of the effects of the single-gene knockout (KO) on different molecules... 
Neurology | Neurosciences | Biomedicine | NEUROSCIENCES | BIOCHEMISTRY & MOLECULAR BIOLOGY | Corticotropin-Releasing Hormone - physiology | Animals | Corticotropin-Releasing Hormone - deficiency | Genes, fos | Restraint, Physical | Corticotropin-Releasing Hormone - genetics | Mice | Receptors, Adrenergic - physiology | Mice, Knockout | Receptors, Muscarinic - physiology | Stress, Psychological - physiopathology | ACTH | Physiological aspects | Hormones
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15. Full Text Ruxolitinib-induced defects in DNA repair cause sensitivity to PARP inhibitors in myeloproliferative neoplasms
by Nieborowska-Skorska, Margaret and Maifrede, Silvia and Dasgupta, Yashodhara and Sullivan, Katherine and Flis, Sylwia and Le, Bac Viet and Solecka, Martyna and Belyaeva, Elizaveta A and Kubovcakova, Lucia and Nawrocki, Morgan and Kirschner, Martin and Zhao, Huaqing and Prchal, Josef T and Piwocka, Katarzyna and Moliterno, Alison R and Wasik, Mariusz and Koschmieder, Steffen and Green, Anthony Richard and Skoda, Radek C and Skorski, Tomasz
ISSN 0006-4971, 2017
Cell Line | Phthalazines | Myeloproliferative Disorders | Piperazines | Pyrazoles | Humans | Receptors, Thrombopoietin | Poly(ADP-ribose) Polymerase Inhibitors | Neoplasms | Drug Synergism | Janus Kinase 2 | Calreticulin | Animals | Heterografts | DNA Repair | Mice | Tumor Cells, Cultured
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16. Full Text JAK2-V617F Expressing Stem Cells Display a Competitive Advantage At Low Limiting Dilution and Are Capable of Initiating MPN Phenotype
by Lundberg, Pontus and Kubovcakova, Lucia and Takizawa, Hitoshi and Hao-Shen, Hui and Manz, Markus G and Skoda, Radek C
Blood, ISSN 0006-4971, 11/2011, Volume 118, Issue 21, pp. 615 - 615
Abstract Abstract 615 JAK2-V617F is the most common genetic alteration in myeloproliferative neoplasms (MPN). Forced expression of JAK2-V617F in animal models... 
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17. Full Text Ethanol consumption increases rat stress hormones and adrenomedullary gene expression
by Patterson-Buckendahl, Patricia and Kubovcakova, Lucia and Krizanova, Olga and Pohorecky, Larissa A and Kvetnansky, Richard
Alcohol, ISSN 0741-8329, 2005, Volume 37, Issue 3, pp. 157 - 166
Numerous reports document altered drinking behavior following acute stressors but few describe physiological responses to acute stress of chronic ethanol... 
Epinephrine | Norepinephrine | Corticosterone | Prolactin | Catecholamine enzyme mRNA | norepinephrine | prolactin | TYROSINE-HYDROXYLASE | PHENYLETHANOLAMINE-N-METHYLTRANSFERASE | REPEATED IMMOBILIZATION STRESS | epinephrine | PLASMA-CATECHOLAMINES | SUBSTANCE ABUSE | ALCOHOL-CONSUMPTION | BLOOD-PRESSURE | MESSENGER-RNA | PHARMACOLOGY & PHARMACY | TOXICOLOGY | BIOSYNTHETIC-ENZYMES | corticosterone | catecholamine enzyme mRNA | PITUITARY-ADRENAL AXIS | Arousal - genetics | Gene Expression Regulation - genetics | Stress, Psychological - blood | RNA, Messenger - genetics | Rats | Male | Alcohol Drinking - adverse effects | Rats, Sprague-Dawley | Arousal - drug effects | Gene Expression Regulation - drug effects | Prolactin - blood | Tyrosine 3-Monooxygenase - genetics | Arousal - physiology | Norepinephrine - blood | Alcohol Drinking - blood | Animals | Dopamine beta-Hydroxylase - genetics | Epinephrine - blood | Adrenal Medulla - physiopathology | Adrenal Medulla - drug effects | Corticosterone - blood | Stress, Psychological - complications | Phenylethanolamine N-Methyltransferase - genetics | Tyrosine | Enzymes | Messenger RNA | Alcohol, Denatured | Genetic research | Physiological aspects | Alcohol | Peptide hormones | Gene expression | Human subjects | Consumption | Plasma | Hypotheses | Ethanol | Diet | Rodents | Alcoholism | Hormones | Experiments | Stress | Food
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