X
Search Filters
Format Format
Format Format
X
Sort by Item Count (A-Z)
Filter by Count
Journal Article (3466) 3466
Publication (439) 439
Book Chapter (14) 14
Book Review (14) 14
Newsletter (11) 11
Book / eBook (8) 8
Conference Proceeding (6) 6
Magazine Article (3) 3
Dissertation (2) 2
more...
Subjects Subjects
Subjects Subjects
X
Sort by Item Count (A-Z)
Filter by Count
humans (2764) 2764
male (1343) 1343
female (1277) 1277
index medicus (1252) 1252
animals (1069) 1069
hematology (987) 987
polycythemia-vera (940) 940
middle aged (830) 830
adult (811) 811
polycythemia (668) 668
mice (653) 653
mutation (650) 650
aged (641) 641
essential thrombocythemia (522) 522
janus kinase 2 - genetics (503) 503
myeloproliferative disorders (412) 412
oncology (411) 411
janus kinase 2 - metabolism (361) 361
polycythemia - blood (361) 361
polycythemia - metabolism (336) 336
hematocrit (335) 335
polycythemia - etiology (335) 335
tyrosine kinase jak2 (334) 334
erythropoiesis (328) 328
polycythemia vera (309) 309
polycythemia vera - blood (292) 292
erythropoietin (271) 271
polycythemia vera - genetics (271) 271
aged, 80 and over (256) 256
myeloproliferative disorders - genetics (255) 255
iron - metabolism (250) 250
polycythemia vera - metabolism (249) 249
signal transduction (241) 241
erythrocytes - metabolism (238) 238
myelofibrosis (234) 234
polycythemia - genetics (232) 232
hemic and lymphatic diseases (229) 229
rats (229) 229
myeloproliferative neoplasms (219) 219
erythropoietin - metabolism (212) 212
research (212) 212
expression (209) 209
jak2 (207) 207
hypoxia (203) 203
leukemia (199) 199
adolescent (193) 193
genetic aspects (187) 187
abridged index medicus (186) 186
cell biology (185) 185
biochemistry & molecular biology (184) 184
medicine, research & experimental (180) 180
hemoglobins - metabolism (178) 178
myeloproliferative disorders - metabolism (178) 178
polycythemia vera - pathology (173) 173
article (167) 167
polycythemia - physiopathology (165) 165
iron isotopes (163) 163
janus kinase 2 - antagonists & inhibitors (157) 157
erythrocytosis (156) 156
bone marrow - metabolism (154) 154
cancer (153) 153
erythropoietin - blood (152) 152
erythropoietin - biosynthesis (151) 151
tumors (151) 151
thrombocythemia, essential - genetics (148) 148
janus kinase 2 (147) 147
myeloid metaplasia (145) 145
diagnosis (142) 142
phosphorylation (142) 142
anemia (141) 141
disease (141) 141
erythropoietin - pharmacology (141) 141
analysis (139) 139
myeloproliferative disorders - pathology (137) 137
risk factors (137) 137
polycythemia - complications (136) 136
cells, cultured (135) 135
cells (134) 134
time factors (134) 134
blood (133) 133
primary myelofibrosis - genetics (133) 133
gene expression (132) 132
primary myelofibrosis (129) 129
medicine, general & internal (127) 127
activation (124) 124
physiological aspects (124) 124
thrombosis (124) 124
chronic disease (123) 123
polycythemia vera - complications (123) 123
oxygen - metabolism (122) 122
erythropoiesis - drug effects (121) 121
amino acid substitution (119) 119
case-control studies (119) 119
polycythemia vera - diagnosis (118) 118
bone marrow (116) 116
bone marrow cells (115) 115
polycythemia vera - drug therapy (114) 114
care and treatment (113) 113
child (113) 113
hematopoietic stem cells - metabolism (113) 113
more...
Library Location Library Location
Language Language
Language Language
X
Sort by Item Count (A-Z)
Filter by Count
English (3229) 3229
German (62) 62
Russian (61) 61
Japanese (37) 37
French (33) 33
Polish (22) 22
Italian (17) 17
Chinese (13) 13
Spanish (13) 13
Hungarian (7) 7
Korean (3) 3
Portuguese (3) 3
Turkish (3) 3
Czech (2) 2
Norwegian (2) 2
Ukrainian (2) 2
Afrikaans (1) 1
Danish (1) 1
Dutch (1) 1
Finnish (1) 1
Romanian (1) 1
Serbian (1) 1
Slovak (1) 1
more...
Publication Date Publication Date
Click on a bar to filter by decade
Slide to change publication date range


Journal of Biological Chemistry, ISSN 0021-9258, 12/2012, Volume 287, Issue 50, pp. 42352 - 42360
Interferons (IFNs) have important antiviral and antineoplastic properties, but the precise mechanisms required for generation of these responses remain to be... 
KINASE PATHWAY | ACTIVATION | ANTAGONIST | I INTERFERONS | PHOSPHORYLATION | MAP KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | GROWTH | GENES | GENERATION | CELLS RESPOND | Humans | Hematopoietic Stem Cells - pathology | Polycythemia Vera - genetics | Intracellular Signaling Peptides and Proteins - metabolism | Phosphoproteins - metabolism | Embryo, Mammalian - metabolism | MAP Kinase Signaling System | Polycythemia Vera - metabolism | U937 Cells | Interferon Type I - metabolism | Membrane Proteins - metabolism | Receptor, Interferon alpha-beta - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Polycythemia Vera - pathology | Intracellular Signaling Peptides and Proteins - genetics | Fibroblasts - metabolism | Receptor, Interferon alpha-beta - metabolism | Embryo, Mammalian - pathology | Membrane Proteins - genetics | p38 Mitogen-Activated Protein Kinases - genetics | Hematopoietic Stem Cells - metabolism | Phosphoproteins - genetics | Fibroblasts - pathology | Nerve Tissue Proteins - genetics | Mice, Knockout | Nerve Tissue Proteins - metabolism | Adaptor Proteins, Signal Transducing | Animals | Interferon Type I - genetics | Mice | MAP Kinases (MAPKs) | Signal Transduction | Cytokines | Cytokine | Cytokine Action | Innate Immunity | Antiviral Agents | Interferon | Polycythemia Vera | Protein Degradation
Journal Article
FASEB Journal, ISSN 0892-6638, 02/2012, Volume 26, Issue 2, pp. 894 - 906
The JAK2 mutation V617F is detectable in a majority of patients with Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs). Enforced expression... 
Microenvironment | Cytokines | Fibrosis | Cancer | COLLAGEN PRODUCTION | POLYCYTHEMIA-VERA | BIOCHEMISTRY & MOLECULAR BIOLOGY | PRIMARY MYELOFIBROSIS | HEMATOPOIETIC PROGENITORS | CELL BIOLOGY | microenvironment | SIGNAL-TRANSDUCTION | CD34(+) CELLS | M RECEPTOR | MOUSE MODEL | BIOLOGY | TYROSINE KINASE JAK2 | cancer | cytokines | fibrosis | CELL-LINE | Humans | Neovascularization, Pathologic | Polycythemia Vera - genetics | Thrombocythemia, Essential - pathology | Myeloproliferative Disorders - pathology | Phosphatidylinositol 3-Kinases - metabolism | Mutation, Missense | Primary Myelofibrosis - pathology | RNA, Messenger - metabolism | Thrombocythemia, Essential - genetics | Myeloproliferative Disorders - genetics | Case-Control Studies | Gene Knockdown Techniques | Polycythemia Vera - metabolism | STAT5 Transcription Factor - metabolism | Base Sequence | Bone Marrow - metabolism | Janus Kinase 2 - metabolism | Myeloproliferative Disorders - metabolism | Oncostatin M - metabolism | Polycythemia Vera - pathology | Janus Kinase 2 - antagonists & inhibitors | Primary Myelofibrosis - metabolism | Cell Line | RNA, Messenger - genetics | Janus Kinase 2 - genetics | Mutant Proteins - genetics | Mutant Proteins - metabolism | Oncostatin M - blood | Primary Myelofibrosis - genetics | Animals | Bone Marrow - pathology | Mice | Cytokines - biosynthesis | Oncostatin M - genetics | Thrombocythemia, Essential - metabolism | Amino Acid Substitution
Journal Article
Leukemia, ISSN 0887-6924, 2007, Volume 21, Issue 8, pp. 1658 - 1668
JAK2V617F and MPLW515L/K represent recently identified mutations in myeloproliferative disorders (MPD) that cause dysregulated JAK-STAT signaling, which is... 
MYELOFIBROSIS | JAK2(V617F) | POLYCYTHEMIA-VERA | ESSENTIAL THROMBOCYTHEMIA | JAK2V617F | myeloproliferative disorder | mutation | kinase inhibitor | MEGAKARYOBLASTIC LEUKEMIA | ACTIVATING MUTATION | ONCOLOGY | V617F | ACUTE LYMPHOBLASTIC-LEUKEMIA | JAK2 | HEMATOLOGY | MYELOID METAPLASIA | fms-Like Tyrosine Kinase 3 - antagonists & inhibitors | Apoptosis - drug effects | Humans | STAT Transcription Factors - metabolism | Polycythemia Vera - genetics | Myeloproliferative Disorders - genetics | Janus Kinase 3 - antagonists & inhibitors | Polycythemia Vera - metabolism | fms-Like Tyrosine Kinase 3 - genetics | Janus Kinase 2 - metabolism | Myeloproliferative Disorders - metabolism | Colony-Forming Units Assay | Phosphorylation - drug effects | Janus Kinase 3 - metabolism | Janus Kinase 2 - antagonists & inhibitors | Primary Myelofibrosis - metabolism | Primary Myelofibrosis - drug therapy | Thrombopoietin - metabolism | Enzyme Inhibitors - pharmacology | Janus Kinase 2 - genetics | Myeloproliferative Disorders - drug therapy | Pyrimidines - pharmacology | Mice, SCID | Mutation - genetics | Sulfonamides - pharmacology | Receptors, Thrombopoietin - metabolism | Receptors, Thrombopoietin - antagonists & inhibitors | fms-Like Tyrosine Kinase 3 - metabolism | Receptors, Thrombopoietin - genetics | Primary Myelofibrosis - genetics | Animals | Janus Kinase 3 - genetics | Stem Cells - drug effects | Polycythemia Vera - drug therapy | Cell Proliferation - drug effects | Mice | Cell Cycle - drug effects | Antibody diversity | Chemical inhibitors | Genetic aspects | Research | Health aspects | Myeloproliferative disorders
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 02/2019, Volume 129, Issue 2, pp. 442 - 451
The field of hereditary kidney cancer has begun to mature following the identification of several germline syndromes that define genetic and molecular features... 
MEDICINE, RESEARCH & EXPERIMENTAL | POSITRON-EMISSION-TOMOGRAPHY | INDUCIBLE FACTOR (HIF)-1-ALPHA | HIPPEL-LINDAU-DISEASE | TUMOR-SUPPRESSOR PROTEIN | FUMARATE-HYDRATASE | CHUVASH POLYCYTHEMIA | TRANSCRIPTIONAL REGULATION | RENAL-CELL CARCINOMA | ENDOTHELIAL GROWTH-FACTOR | REDUCTIVE CARBOXYLATION | Kidney Neoplasms - genetics | Neoplastic Syndromes, Hereditary - pathology | Humans | Genetic Diseases, Inborn - genetics | Leiomyomatosis - metabolism | Kidney Neoplasms - metabolism | Genetic Diseases, Inborn - pathology | Genetic Diseases, Inborn - therapy | Neoplastic Syndromes, Hereditary - metabolism | Neovascularization, Pathologic - pathology | Leiomyomatosis - therapy | Leiomyomatosis - pathology | Carcinoma, Renal Cell | Genetic Diseases, Inborn - metabolism | Neoplastic Syndromes, Hereditary - genetics | Von Hippel-Lindau Tumor Suppressor Protein - genetics | Von Hippel-Lindau Tumor Suppressor Protein - metabolism | Kidney Neoplasms - therapy | Neovascularization, Pathologic - therapy | Models, Biological | Neoplastic Syndromes, Hereditary - therapy | Kidney Neoplasms - pathology | Neovascularization, Pathologic - genetics | Neovascularization, Pathologic - metabolism | Mutation | Cell Hypoxia - genetics | Leiomyomatosis - genetics | Physiological aspects | Care and treatment | Genetic aspects | Research | Gene mutations | Kidney cancer | Enzymes | Transcription factors | Medical imaging | Metastasis | Metabolism | Defects | Proteins | Angiogenesis | Ultrasonic imaging | Glycolysis | Biomarkers | Tumor suppressor genes | Hypoxia | VHL protein | Tumorigenesis | Neoplasia | Vascular endothelial growth factor | Clear cell-type renal cell carcinoma | Glutamine | Tumors
Journal Article
Journal of Experimental Medicine, ISSN 0022-1007, 2016, Volume 213, Issue 2, pp. 273 - 290
Journal Article
Journal of Molecular Medicine, ISSN 0946-2716, 1/2013, Volume 91, Issue 1, pp. 59 - 67
In Chuvash polycythemia, a homozygous 598C>T mutation in the von Hippel–Lindau gene (VHL) leads to an R200W substitution in VHL protein, impaired degradation... 
Human Genetics | Hypoxia-inducible factors | Biomedicine | Glycolysis | Internal Medicine | Molecular Medicine | VHL | Glucose | Insulin | Gluconeogenesis | MEDICINE, RESEARCH & EXPERIMENTAL | HYPOXIA-INDUCIBLE FACTOR | CELLS | PROMOTES GLYCOGEN ACCUMULATION | THROMBOSIS | ERYTHROPOIESIS | DEFICIENCY | GENETICS & HEREDITY | MICE | OXYGEN HOMEOSTASIS | EXPRESSION | Glucose Transport Proteins, Facilitative - metabolism | Polycythemia - genetics | Glucose-6-Phosphatase - genetics | Glycated Hemoglobin A - metabolism | Humans | Middle Aged | Polycythemia - blood | Male | Muscle, Skeletal - metabolism | Pyruvate Dehydrogenase Complex - genetics | Insulin - blood | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Adult | Female | Von Hippel-Lindau Tumor Suppressor Protein - genetics | Glucose Transport Proteins, Facilitative - genetics | Von Hippel-Lindau Tumor Suppressor Protein - metabolism | Pyruvate Dehydrogenase Complex - metabolism | Signal Transduction | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Liver - metabolism | Gene Expression Regulation | Genotype | Glucose-6-Phosphatase - metabolism | Homozygote | Hypoxia - blood | Hypoxia - genetics | Animals | Alleles | Hypoxia - physiopathology | Mice | Polycythemia - physiopathology | Mutation | Blood Glucose - metabolism | Glucose metabolism | Transcription factors | Polycythemia | Physiological aspects | Development and progression | Genetic aspects | Research | High altitude | Hypoxia-inducible factor 1 | Transcription | Liver | Genes | Inactivation | Degradation | Rodents | Hemoglobin | Skeleton | Glucose transporter | Enzymes | Fasting | Deactivation | Diabetes mellitus | Glycerol | Pharmacology | Hypoglycemia | Gene expression | Metabolism | Patients | Citric acid | Skeletal muscle | Homozygotes | Hippel-Lindau gene | Hypoxia | Neoplasia | glucose | hypoxia inducible factors | insulin | gluconeogenesis | glycolysis
Journal Article
Journal Article
Journal Article