X
Search Filters
Format Format
Format Format
X
Sort by Item Count (A-Z)
Filter by Count
Journal Article (1175) 1175
Publication (212) 212
Book Review (10) 10
Book Chapter (7) 7
Book / eBook (4) 4
Conference Proceeding (2) 2
Data Set (1) 1
more...
Subjects Subjects
Subjects Subjects
X
Sort by Item Count (A-Z)
Filter by Count
humans (825) 825
animals (705) 705
biochemistry & molecular biology (491) 491
proto-oncogene proteins c-abl - metabolism (486) 486
phosphorylation (443) 443
mice (440) 440
index medicus (439) 439
cell biology (345) 345
c-abl (271) 271
proto-oncogene proteins c-abl - genetics (254) 254
tyrosine kinase (215) 215
cell line (214) 214
apoptosis (206) 206
signal transduction (203) 203
oncology (188) 188
activation (179) 179
proto-oncogene proteins c-abl - physiology (160) 160
molecular sequence data (159) 159
imatinib mesylate (155) 155
protein binding (153) 153
research (145) 145
amino acid sequence (142) 142
cells, cultured (142) 142
cell line, tumor (129) 129
pyrimidines - pharmacology (128) 128
hemic and lymphatic diseases (125) 125
protein (125) 125
male (124) 124
proteins (121) 121
proto-oncogene proteins c-abl - antagonists & inhibitors (118) 118
article (116) 116
bcr-abl (115) 115
dna-damage (114) 114
female (112) 112
tyrosine (112) 112
benzamides (109) 109
protein-tyrosine kinases - metabolism (109) 109
hematology (107) 107
proto-oncogene proteins - metabolism (105) 105
piperazines - pharmacology (104) 104
proto-oncogene proteins - genetics (104) 104
expression (103) 103
transfection (102) 102
cancer (98) 98
signal transduction - physiology (98) 98
cells (97) 97
tyrosine - metabolism (96) 96
genetics & heredity (95) 95
enzyme activation (94) 94
dna damage (91) 91
physiological aspects (91) 91
proto-oncogene proteins c-abl - chemistry (91) 91
src homology domains (89) 89
dna-binding proteins - metabolism (87) 87
leukemia (87) 87
chronic myelogenous leukemia (86) 86
p53 (86) 86
binding sites (83) 83
gene expression (83) 83
mutation (83) 83
nuclear proteins - metabolism (83) 83
rats (83) 83
mice, knockout (81) 81
protein kinase inhibitors - pharmacology (78) 78
apoptosis - drug effects (77) 77
protein structure, tertiary (77) 77
chronic myeloid-leukemia (76) 76
analysis (74) 74
kinases (74) 74
apoptosis - physiology (73) 73
genetic aspects (73) 73
tumor cells, cultured (73) 73
biophysics (72) 72
tumor suppressor protein p53 - metabolism (72) 72
base sequence (71) 71
gene (70) 70
growth (70) 70
multidisciplinary sciences (70) 70
binding (69) 69
abl tyrosine kinase (66) 66
imatinib (66) 66
blotting, western (64) 64
neoplasms (64) 64
research article (64) 64
cell cycle (61) 61
gene expression regulation (61) 61
abl (59) 59
oxidative stress (59) 59
protein-tyrosine kinases - genetics (59) 59
antineoplastic agents - pharmacology (58) 58
models, biological (58) 58
signal transduction - drug effects (58) 58
mice, inbred c57bl (57) 57
proto-oncogene proteins - physiology (57) 57
dna-binding proteins - genetics (56) 56
genes, abl (56) 56
tumor protein p73 (56) 56
signal-transduction (55) 55
fusion proteins, bcr-abl - genetics (54) 54
nuclear proteins - genetics (53) 53
more...
Library Location Library Location
Language Language
Publication Date Publication Date
Click on a bar to filter by decade
Slide to change publication date range


PLoS ONE, ISSN 1932-6203, 05/2014, Volume 9, Issue 5, p. e97694
Chronic myelogenous leukemia patients treated with tyrosine kinase inhibitor, Imatinib, were shown to have increased serum levels of C-peptide. Imatinib... 
GENE | MULTIDISCIPLINARY SCIENCES | AMELIORATION | SENSITIVITY | MESYLATE GLEEVEC | MAFA | GASTROINTESTINAL STROMAL TUMORS | NKX6.1 | BINDING | CHRONIC MYELOID-LEUKEMIA | PDX-1 | Glucose Transporter Type 2 - genetics | Proto-Oncogene Proteins c-abl - antagonists & inhibitors | Homeodomain Proteins - metabolism | Insulin - biosynthesis | Glucose Transporter Type 2 - metabolism | Proto-Oncogene Proteins c-abl - physiology | Benzamides - pharmacology | Insulin - genetics | Cell Line | Proto-Oncogene Proteins c-abl - genetics | Gene Expression Regulation | Pyrimidines - pharmacology | Transcription Factors - genetics | Imatinib Mesylate | Piperazines - pharmacology | Homeodomain Proteins - genetics | Transcription Factors - metabolism | Animals | Insulin-Secreting Cells - drug effects | Leukemia, Myeloid - metabolism | Glucose - metabolism | Trans-Activators - metabolism | Mice | Protein Kinase Inhibitors - pharmacology | Peptide Biosynthesis - drug effects | RNA, Small Interfering - metabolism | Laboratories | Leukemia | Insulinoma | Glucose | Kinases | Homeobox | Immunology | Rodents | Inhibition | Pancreas | Protein-tyrosine kinase | Glucose transporter | Tyrosine | Imatinib | Myeloid leukemia | Therapeutic applications | Diabetes mellitus | siRNA | Chronic myeloid leukemia | Metabolism | Gene expression | Nkx2.2 protein | Insulin | Medicine | Serum levels | Pathology | Inhibitors | Diabetes | Transporter | Binding sites | Endocrinology
Journal Article
Diabetologia, ISSN 0012-186X, 6/2013, Volume 56, Issue 6, pp. 1327 - 1338
It is not clear how small tyrosine kinase inhibitors, such as imatinib mesilate, protect against diabetes and beta cell death. The aim of this study was to... 
EndoC-βH1 cells | Medicine & Public Health | Human Physiology | Cell death | PIP 3 signalling | SHIP2 | Metabolic Diseases | Internal Medicine | c-Abl | Imatinib mesilate | Insulin-producing cells | PIP | signalling | PHOSPHORYLATION | SENSITIVITY | PTEN | RECEPTOR | EndoC-beta H1 cells | TYROSINE KINASE INHIBITORS | GLUCOSE | 3,4,5-TRISPHOSPHATE | ENDOCRINOLOGY & METABOLISM | MESYLATE GLEEVEC | OSCILLATIONS | PIP3 signalling | Cell Survival - drug effects | Green Fluorescent Proteins - metabolism | Phosphorylation | Phosphatidylinositol Phosphates - metabolism | Humans | Cells, Cultured | PTEN Phosphohydrolase - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Pyrimidines - pharmacology | Imatinib Mesylate | Piperazines - pharmacology | Insulin - metabolism | Pyrroles - pharmacology | Signal Transduction - drug effects | Time Factors | HEK293 Cells | Protein Binding | Proto-Oncogene Proteins c-abl - metabolism | Indoles - pharmacology | Benzamides - pharmacology | Protein Kinase Inhibitors - pharmacology | Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases | Phosphoric Monoester Hydrolases - metabolism | Cell Membrane - drug effects | Antimitotic agents | Enzymes | Inositol | Pancreatic beta cells | Phosphatases | Analysis | Phospholipids | Diabetes | Antineoplastic agents | Gene expression | Insulin | Cells | Cell and Molecular Biology | Basic Medicine | Medical and Health Sciences | Medicin och hälsovetenskap | Cell- och molekylärbiologi | Medicinska och farmaceutiska grundvetenskaper
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 01/2011, Volume 31, Issue 1, pp. 157 - 163
Mutations in parkin, an E3 ubiquitin ligase, are the most common cause of autosomal-recessive Parkinson's disease (PD). Here, we show that the stress-signaling... 
PATHOGENESIS | S-NITROSYLATION | PROTECTIVE FUNCTION | SUBSTRATE | NEURODEGENERATION | PROTEIN LIGASE | MUTATIONS | STRESS | NEUROSCIENCES | UBIQUITIN LIGASE ACTIVITY | CELL-DEATH | Free Radical Scavengers - pharmacology | Phosphorylation - physiology | Peptide Elongation Factors - metabolism | Humans | Oxidative Stress - physiology | Male | Piperazines - toxicity | Green Fluorescent Proteins - genetics | Metalloporphyrins - pharmacology | Case-Control Studies | Brain - metabolism | Pyrimidines - toxicity | Transfection - methods | Ubiquitination - drug effects | Tumor Suppressor Proteins - genetics | Statistics, Nonparametric | MPTP Poisoning - pathology | Phosphorylation - drug effects | Peptide Elongation Factors - genetics | Disease Models, Animal | Polyethylene Glycols - pharmacology | Cell Line | Proto-Oncogene Proteins c-abl - genetics | Tumor Suppressor Proteins - metabolism | Drug Administration Schedule | Immunoprecipitation - methods | Mice, Inbred C57BL | RNA, Small Interfering - pharmacology | Dopamine - pharmacology | Ubiquitin-Protein Ligases - metabolism | Gene Expression Regulation - physiology | MPTP Poisoning - drug therapy | Imatinib Mesylate | Brain - drug effects | Gene Expression Regulation - drug effects | Tyrosine - metabolism | Animals | MPTP Poisoning - metabolism | Acetylcysteine - pharmacology | Brain - pathology | Protein Kinase Inhibitors - toxicity | Proto-Oncogene Proteins c-abl - metabolism | Mice | Benzamides | Oxidative Stress - drug effects | MPTP Poisoning - chemically induced | Ubiquitin-Protein Ligases - genetics | Brief Communications
Journal Article
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 11/2014, Volume 111, Issue 46, pp. 16365 - 16370
Adipocyte differentiation, or adipogenesis, is a complex and highly regulated process. A recent proteomic analysis has predicted that the nonreceptor tyrosine... 
Proteins | Phosphorylation | HEK293 cells | Plasmids | Cell lines | Ligands | Gene expression regulation | Adipocytes | Lipogenesis | Regulator genes | C-Abl | Differentiation | Pro12Ala polymorphism | PPAR gamma | Adipogenesis | differentiation | ACTIVATED RECEPTOR-GAMMA | IMPROVED INSULIN SENSITIVITY | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | DNA-DAMAGE | c-Abl | GROWTH-FACTOR RECEPTOR | IN-VITRO | adipogenesis | PPAR-GAMMA-2 | TERMINAL DIFFERENTIATION | CML PATIENTS | NIH 3T3 Cells | Proto-Oncogene Proteins c-abl - antagonists & inhibitors | Species Specificity | Adipogenesis - drug effects | Humans | Adipocytes - drug effects | Mutation, Missense | Proto-Oncogene Proteins c-abl - physiology | Adipogenesis - physiology | HEK293 Cells | Transcription, Genetic | Benzamides - pharmacology | Protein Stability | PPAR gamma - genetics | Protein Structure, Tertiary | Proto-Oncogene Proteins c-abl - chemistry | Pyrimidines - pharmacology | 3T3-L1 Cells | Imatinib Mesylate | Phosphotyrosine - chemistry | Piperazines - pharmacology | Proline - chemistry | Protein Interaction Mapping | Sequence Homology, Amino Acid | Point Mutation | PPAR gamma - physiology | Animals | Protein Isoforms - biosynthesis | Adipocytes - metabolism | Protein Binding | Mice | Polymorphism, Single Nucleotide | Protein Kinase Inhibitors - pharmacology | Protein Processing, Post-Translational | PPAR gamma - chemistry | Protein Isoforms - genetics | Tyrosine | Protein research | Cell research | Research | Cell differentiation | Health aspects | Phosphotransferases | Biological Sciences
Journal Article
Journal Article
Journal Article