X
Search Filters
Format Format
Format Format
X
Sort by Item Count (A-Z)
Filter by Count
Journal Article (2096) 2096
Book Review (314) 314
Publication (272) 272
Book Chapter (19) 19
Book / eBook (5) 5
Conference Proceeding (4) 4
Reference (3) 3
Data Set (1) 1
Dissertation (1) 1
Magazine Article (1) 1
more...
Subjects Subjects
Subjects Subjects
X
Sort by Item Count (A-Z)
Filter by Count
index medicus (2036) 2036
humans (1581) 1581
animals (1112) 1112
mice (737) 737
proto-oncogene proteins c-abl - metabolism (695) 695
biochemistry & molecular biology (643) 643
phosphorylation (632) 632
cell biology (616) 616
oncology (555) 555
proto-oncogene proteins c-abl - genetics (519) 519
c-abl (392) 392
signal transduction (345) 345
tyrosine kinase (342) 342
apoptosis (318) 318
female (313) 313
imatinib mesylate (313) 313
research (311) 311
male (301) 301
cell line (298) 298
proto-oncogene proteins - genetics (298) 298
proteins (288) 288
activation (275) 275
cancer (273) 273
mutation (269) 269
molecular sequence data (261) 261
cell line, tumor (256) 256
genetics & heredity (225) 225
amino acid sequence (224) 224
bcr-abl (222) 222
chronic myelogenous leukemia (220) 220
protein binding (220) 220
benzamides (213) 213
pyrimidines - pharmacology (210) 210
hematology (208) 208
tyrosine (208) 208
proto-oncogene proteins - metabolism (207) 207
kinases (200) 200
leukemia (199) 199
protein (194) 194
gene expression (192) 192
genetic aspects (191) 191
hemic and lymphatic diseases (190) 190
proto-oncogene proteins c-abl - antagonists & inhibitors (190) 190
chronic myeloid-leukemia (189) 189
cells, cultured (188) 188
leukemia, myelogenous, chronic, bcr-abl positive - genetics (187) 187
article (185) 185
proto-oncogenes (185) 185
protein-tyrosine kinases - metabolism (181) 181
multidisciplinary sciences (180) 180
piperazines - pharmacology (180) 180
cells (176) 176
expression (175) 175
dna-damage (171) 171
physiological aspects (168) 168
base sequence (161) 161
transfection (161) 161
apoptosis - drug effects (156) 156
analysis (154) 154
fusion proteins, bcr-abl - genetics (154) 154
protein kinase inhibitors - pharmacology (147) 147
dna damage (144) 144
binding sites (143) 143
protein-tyrosine kinases - genetics (137) 137
antineoplastic agents - pharmacology (136) 136
gene expression regulation (135) 135
p53 (135) 135
middle aged (133) 133
nuclear proteins - metabolism (132) 132
tumor suppressor protein p53 - metabolism (132) 132
imatinib (131) 131
tumor cells, cultured (131) 131
dna-binding proteins - metabolism (130) 130
adult (127) 127
blotting, western (127) 127
tyrosine - metabolism (124) 124
gene (123) 123
proto-oncogene proteins c-abl - chemistry (123) 123
oncogenes (122) 122
proto-oncogene proteins c-abl - physiology (121) 121
binding (120) 120
tumors (118) 118
research article (117) 117
mice, knockout (114) 114
enzyme activation (111) 111
genes (108) 108
chronic myeloid leukemia (107) 107
cell cycle (106) 106
rats (106) 106
src homology domains (106) 106
dna-binding proteins - genetics (105) 105
health aspects (105) 105
cell proliferation (104) 104
leukemia, myelogenous, chronic, bcr-abl positive - drug therapy (103) 103
neoplasms (103) 103
growth (102) 102
transcription, genetic (102) 102
fusion proteins, bcr-abl - metabolism (101) 101
medicine (101) 101
proto-oncogene proteins c-bcr (100) 100
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


Science Translational Medicine, ISSN 1946-6234, 05/2017, Volume 9, Issue 391, p. eaaf3962
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 | Index Medicus | Phosphorylation | Abl | Dopamine | Parkinson's disease | Kinase | Parkin
Journal Article
Journal Article
Cell, ISSN 0092-8674, 2003, Volume 112, Issue 6, pp. 845 - 857
Journal Article
Journal Article
Journal Article
Cell death & disease, ISSN 2041-4889, 06/2017, Volume 8, Issue 6, pp. e2899 - e2899
We recently established c-Abl as a potent suppressor of triple-negative breast cancer (TNBC) progression through its reactivation of a p53:p21 signaling axis... 
INACTIVATION | CELLS | ACTIVATION | TGF-BETA | METASTASIS | MPS1 | PHOSPHORYLATION | TYROSINE KINASE | GROWTH | RECEPTOR | CELL BIOLOGY | Apoptosis - drug effects | Protein-Tyrosine Kinases - metabolism | Humans | Multiprotein Complexes - genetics | Triple Negative Breast Neoplasms - drug therapy | Tumor Suppressor Protein p53 - genetics | Protein-Tyrosine Kinases - genetics | MCF-7 Cells | Imatinib Mesylate - adverse effects | Imatinib Mesylate - administration & dosage | Triple Negative Breast Neoplasms - pathology | Cell Cycle Proteins - genetics | Female | Cytoplasm - genetics | Gene Expression Regulation, Neoplastic - drug effects | Protein-Serine-Threonine Kinases - metabolism | 14-3-3 Proteins - genetics | Proto-Oncogene Proteins c-abl - genetics | Cell Cycle Proteins - metabolism | Mutant Proteins - genetics | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Mutant Proteins - metabolism | Drug Resistance, Neoplasm - genetics | Triple Negative Breast Neoplasms - genetics | Protein Binding | Proto-Oncogene Proteins c-abl - metabolism | Cell Proliferation - drug effects | Adaptor proteins | Oxidative stress | GTP-binding protein | Imatinib | Senescence | p53 Protein | Breast cancer | Kinases | Gene expression | Nuclei | 14-3-3 protein | Antitumor agents | Organoids | Protein kinase | Mutation | Localization | Cytoplasm | Index Medicus | Original
Journal Article
Journal Article
Cancer Cell, ISSN 1535-6108, 2009, Volume 16, Issue 5, pp. 401 - 412
Inhibition of BCR-ABL by imatinib induces durable responses in many patients with chronic myeloid leukemia (CML), but resistance attributable to kinase domain... 
CHEMBIO | HUMDISEASE | CHRONIC MYELOGENOUS LEUKEMIA | DASATINIB BMS-354825 | MESYLATE | CML | ONCOLOGY | KINASE DOMAIN MUTATIONS | AMN107 | IMATINIB RESISTANCE | NILOTINIB | Proto-Oncogene Proteins c-abl - antagonists & inhibitors | Humans | Imidazoles - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Crystallography, X-Ray | Pyridazines - pharmacology | Protein Kinase Inhibitors - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Antineoplastic Agents - pharmacology | Fusion Proteins, bcr-abl - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Proto-Oncogene Proteins c-abl - genetics | Cell Growth Processes - drug effects | Proto-Oncogene Proteins c-abl - chemistry | Models, Molecular | Imidazoles - pharmacology | Antineoplastic Agents - chemistry | Mice, SCID | Pyridazines - chemistry | Fusion Proteins, bcr-abl - genetics | Animals | Signal Transduction - drug effects | Fusion Proteins, bcr-abl - antagonists & inhibitors | Cell Line, Tumor | Proto-Oncogene Proteins c-abl - metabolism | Mice | Protein Kinase Inhibitors - pharmacology | Fusion Proteins, bcr-abl - metabolism | Chronic myeloid leukemia | BCR protein | Imatinib | Mutagenesis | Abl protein | Mutation | Fusion protein | Tumors | Index Medicus | imatinib resistance | dasatinib | nilotinib | compound mutation
Journal Article