X
Search Filters
Format Format
Subjects Subjects
Subjects Subjects
X
Sort by Item Count (A-Z)
Filter by Count
humans (9317) 9317
animals (8413) 8413
protein-serine-threonine kinases - metabolism (7922) 7922
protein-serine-threonine kinases - antagonists & inhibitors (6976) 6976
phosphorylation (4735) 4735
mice (4316) 4316
biochemistry & molecular biology (3409) 3409
protein-serine-threonine kinases - genetics (3289) 3289
enzyme inhibitors - pharmacology (3031) 3031
cell biology (3022) 3022
signal transduction (2704) 2704
male (2474) 2474
apoptosis (2334) 2334
rats (2303) 2303
cell line, tumor (2197) 2197
oncology (2173) 2173
proto-oncogene proteins - metabolism (2130) 2130
cells, cultured (2128) 2128
female (2079) 2079
activation (2043) 2043
proto-oncogene proteins c-akt (1970) 1970
cell line (1920) 1920
expression (1900) 1900
signal transduction - drug effects (1651) 1651
cancer (1631) 1631
protein kinase inhibitors - pharmacology (1612) 1612
protein-serine-threonine kinases (1593) 1593
apoptosis - drug effects (1471) 1471
proteins (1444) 1444
phosphorylation - drug effects (1321) 1321
kinases (1254) 1254
enzyme activation (1225) 1225
protein-serine-threonine kinases - physiology (1200) 1200
phosphatidylinositol 3-kinases - metabolism (1188) 1188
research (1164) 1164
tumor cells, cultured (1158) 1158
phosphatidylinositol 3-kinases - antagonists & inhibitors (1132) 1132
cell cycle proteins - metabolism (1073) 1073
proto-oncogene proteins - antagonists & inhibitors (1053) 1053
protein-kinase (1049) 1049
intracellular signaling peptides and proteins (1033) 1033
cells (1026) 1026
antineoplastic agents - pharmacology (1021) 1021
dose-response relationship, drug (1017) 1017
transfection (992) 992
signal transduction - physiology (982) 982
cell cycle proteins - antagonists & inhibitors (940) 940
blotting, western (932) 932
protein binding (925) 925
rho-associated kinases (920) 920
inhibition (898) 898
enzyme activation - drug effects (894) 894
mutation (892) 892
mitogen-activated protein kinases - metabolism (878) 878
pharmacology & pharmacy (864) 864
molecular sequence data (854) 854
gene expression (844) 844
cell cycle (829) 829
kinase (823) 823
dna-binding proteins - metabolism (813) 813
protein (809) 809
cell proliferation - drug effects (804) 804
amino acid sequence (798) 798
pyridines - pharmacology (788) 788
multidisciplinary sciences (786) 786
gene-expression (779) 779
physiological aspects (772) 772
growth (749) 749
research article (736) 736
hela cells (733) 733
pathway (715) 715
rats, sprague-dawley (714) 714
analysis (710) 710
mice, inbred c57bl (705) 705
intracellular signaling peptides and proteins - metabolism (696) 696
protein-serine-threonine kinases - chemistry (694) 694
rna interference (693) 693
protein kinases (692) 692
protein-tyrosine kinases - antagonists & inhibitors (683) 683
aurora kinases (682) 682
cell survival - drug effects (673) 673
protein-tyrosine kinases - metabolism (672) 672
chemistry, medicinal (669) 669
time factors (659) 659
in-vivo (651) 651
morpholines - pharmacology (643) 643
nf-kappa b - metabolism (643) 643
intracellular signaling peptides and proteins - antagonists & inhibitors (638) 638
protein kinases - metabolism (634) 634
akt (633) 633
mice, knockout (621) 621
physiology (618) 618
cell proliferation (617) 617
structure-activity relationship (617) 617
protein kinase inhibitors - chemistry (608) 608
cell cycle proteins - genetics (606) 606
neurosciences (598) 598
identification (597) 597
phosphatidylinositol 3-kinase (594) 594
rna, messenger - metabolism (588) 588
more...
Language Language
Language Language
X
Sort by Item Count (A-Z)
Filter by Count
English (14295) 14295
Japanese (106) 106
Chinese (32) 32
French (28) 28
German (12) 12
Russian (6) 6
Dutch (4) 4
Czech (2) 2
Hungarian (2) 2
Norwegian (2) 2
Portuguese (2) 2
Italian (1) 1
Polish (1) 1
Spanish (1) 1
Swedish (1) 1
Ukrainian (1) 1
more...
Publication Date Publication Date
Click on a bar to filter by decade
Slide to change publication date range


Nature reviews. Cancer, ISSN 1474-1768, 2017, Volume 17, Issue 2, pp. 93 - 115
.... Proliferation depends on progression through four distinct phases of the cell cycle G0/G1, S, G2 and M which is regulated by several cyclin-dependent kinases (CDKs... 
INVESTIGATIONAL AURORA KINASE | PHASE-II TRIAL | POLO-LIKE-KINASE | EARLY EMBRYONIC-DEVELOPMENT | DINACICLIB SCH 727965 | ADVANCED SOLID TUMORS | ONCOLOGY | PREVENTS TUMOR-GROWTH | VOLASERTIB BI 6727 | DEPENDENT KINASE INHIBITOR | SMALL-MOLECULE INHIBITOR | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Humans | Checkpoint Kinase 1 - physiology | Aurora Kinase A - antagonists & inhibitors | Cyclin-Dependent Kinase 2 - physiology | Cell Cycle Proteins - antagonists & inhibitors | Protein-Tyrosine Kinases - physiology | Aurora Kinase A - physiology | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Proto-Oncogene Proteins - antagonists & inhibitors | Signal Transduction | Protein-Serine-Threonine Kinases - physiology | Checkpoint Kinase 1 - antagonists & inhibitors | Clinical Trials as Topic | Neoplasms - drug therapy | Animals | Cyclin-Dependent Kinase 4 - physiology | Nuclear Proteins - antagonists & inhibitors | Proto-Oncogene Proteins - physiology | Cyclin-Dependent Kinase 2 - antagonists & inhibitors | Cyclin-Dependent Kinase 6 - physiology | Nuclear Proteins - physiology | Cell Cycle Proteins - physiology | Protein-Tyrosine Kinases - antagonists & inhibitors | Proteins | Care and treatment | Usage | MicroRNA | Cell cycle | Research | Cancer
Journal Article
Cell death and differentiation, ISSN 1476-5403, 2014, Volume 21, Issue 10, pp. 1511 - 1521
Necroptosis is a form of programmed cell death that depends on the activation of receptor interacting protein kinase-1 (RIPK1) and RIPK3 by receptors such as... 
APOPTOSIS | RIPOPTOSOME | MLKL | MACROPHAGES | DOWNSTREAM | BIOCHEMISTRY & MOLECULAR BIOLOGY | MIXED LINEAGE KINASE | PROGRAMMED NECROSIS | DOMAIN-LIKE | CLEAVAGE | CELL-DEATH | CELL BIOLOGY | Protein Kinases - metabolism | Protein Structure, Tertiary | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Tumor Necrosis Factor-alpha - metabolism | Cell Line | Phosphorylation | Protein Kinases - genetics | Cell Survival | Humans | Protein Multimerization | Receptors, Tumor Necrosis Factor, Type I | Caspase 8 - metabolism | Imidazoles - pharmacology | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Necrosis - physiopathology | RNA Interference | Indoles - pharmacology | RNA, Small Interfering | Apoptosis - physiology | Enzyme Activation | Receptor-Interacting Protein Serine-Threonine Kinases - antagonists & inhibitors | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Receptor-Interacting Protein Serine-Threonine Kinases/genetics | Protein Kinases/genetics | Receptor-Interacting Protein Serine-Threonine Kinases/antagonists & inhibitors | Caspase 8/metabolism | Receptor-Interacting Protein Serine-Threonine Kinases/metabolism | Tumor Necrosis Factor-alpha/antagonists & inhibitors | Indoles/pharmacology | Life Sciences | Tumor Necrosis Factor-alpha/metabolism | Imidazoles/pharmacology | Immunology | Apoptosis/physiology | Protein Kinases/metabolism | Necrosis/physiopathology | Original Paper
Journal Article
Cancer cell, ISSN 1535-6108, 2010, Volume 17, Issue 6, pp. 547 - 559
In mice, Lkb1 deletion and activation of Kras G12D results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these... 
CELLCYCLE | SIGNALING | INACTIVATION | SUPPRESSOR | SIGNATURES | ONCOLOGY | SRC | ADENOCARCINOMA | SENSITIVITY | MUTATIONS | LKB1/STK11 | EXPRESSION | TUMORIGENESIS | CELL BIOLOGY | Lung Neoplasms - drug therapy | Protein-Serine-Threonine Kinases - deficiency | Protein-Tyrosine Kinases - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Genomics | Humans | Lung Neoplasms - metabolism | Gene Expression Profiling | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Cell Movement - genetics | Phosphorylation - genetics | RNA Interference | Gene Expression Regulation, Neoplastic - genetics | MAP Kinase Kinase 1 - antagonists & inhibitors | Carcinoma, Non-Small-Cell Lung - metabolism | Signal Transduction - genetics | Enzyme Inhibitors - therapeutic use | Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors | Focal Adhesion Protein-Tyrosine Kinases - genetics | Focal Adhesions - genetics | Signal Transduction - drug effects | Mice, Nude | Cell Line, Tumor | Mice | TOR Serine-Threonine Kinases | src-Family Kinases - genetics | Protein-Tyrosine Kinases - antagonists & inhibitors | ras Proteins - genetics | Lung Neoplasms - pathology | Cell Transdifferentiation - genetics | Protein-Tyrosine Kinases - genetics | Neoplasm Metastasis - drug therapy | Mice, Mutant Strains | Protein-Serine-Threonine Kinases - antagonists & inhibitors | src-Family Kinases - metabolism | Female | Drug Therapy, Combination | Lung Neoplasms - genetics | Cell Adhesion - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Focal Adhesion Protein-Tyrosine Kinases - metabolism | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | src-Family Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - genetics | Proto-Oncogene Proteins - genetics | Up-Regulation - genetics | Xenograft Model Antitumor Assays | Neoplasm Metastasis - genetics | Animals | MAP Kinase Kinase 2 - antagonists & inhibitors | Protein Kinase Inhibitors - therapeutic use | Focal Adhesions - metabolism | Proteomics | Protein Kinase Inhibitors - pharmacology | Oncology, Experimental | Analysis | Lung cancer | Development and progression | Metastasis | Research | Cancer
Journal Article
Journal Article
Molecular biology of the cell, ISSN 1059-1524, 04/2011, Volume 22, Issue 8, pp. 1191 - 1206
.... Cyclin-dependent kinase 1 (Cdk1) is the primary upstream kinase that directs mitotic progression by phosphorylation of a large number of substrate proteins... 
ANAPHASE-PROMOTING COMPLEX | XENOPUS EGG EXTRACTS | PROTEIN PHOSPHATASES | CYCLE-DEPENDENT PHOSPHORYLATION | UBIQUITIN LIGASE | M-PHASE | CHROMOSOME ALIGNMENT | CELL-CYCLE | TUMOR-CELLS | SPINDLE-ASSEMBLY CHECKPOINT | CELL BIOLOGY | Cyclin-Dependent Kinases - metabolism | Gene Expression - drug effects | Xenopus Proteins - genetics | Mitosis | Protein-Tyrosine Kinases - metabolism | Humans | Phosphoprotein Phosphatases - metabolism | G2 Phase - drug effects | CDC2 Protein Kinase - metabolism | Cell Cycle Proteins - antagonists & inhibitors | Protein-Tyrosine Kinases - genetics | Cyclin B - genetics | cdc25 Phosphatases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Prometaphase - drug effects | Female | Cyclin-Dependent Kinases - antagonists & inhibitors | Phosphorylation - drug effects | cdc25 Phosphatases - metabolism | Cyclin-Dependent Kinases - genetics | Nuclear Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | CDC2 Protein Kinase - genetics | Protein Phosphatase 2 - antagonists & inhibitors | CDC2 Protein Kinase - antagonists & inhibitors | Xenopus laevis | Cell Cycle Proteins - metabolism | Protein Phosphatase 2 - genetics | Protein-Serine-Threonine Kinases - genetics | Nuclear Proteins - metabolism | Phosphoprotein Phosphatases - antagonists & inhibitors | cdc25 Phosphatases - genetics | Xenopus Proteins - antagonists & inhibitors | Membrane Proteins | Animals | Phosphoprotein Phosphatases - genetics | Nuclear Proteins - antagonists & inhibitors | Protein Phosphatase 2 - metabolism | Cyclin B - metabolism | Feedback, Physiological - drug effects | Xenopus Proteins - metabolism | Protein Kinase Inhibitors - pharmacology | S Phase - drug effects | HeLa Cells | Protein-Tyrosine Kinases - antagonists & inhibitors
Journal Article
Nature, ISSN 0028-0836, 06/2009, Volume 459, Issue 7248, pp. 852 - 856
Cells normally grow to a certain size before they enter mitosis and divide. Entry into mitosis depends on the activity of Cdk1, which is inhibited by the Wee1 kinase and activated by the Cdc25 phosphatase... 
FISSION YEAST | WEE1 | PHOSPHORYLATION | NIM1/CDR1 MITOTIC INDUCER | PROTEIN-KINASE | NEGATIVE REGULATION | MULTIDISCIPLINARY SCIENCES | GROWTH | DIVISION PLANE | DUAL-SPECIFICITY KINASE | SCHIZOSACCHAROMYCES-POMBE | Protein Kinases - metabolism | Cell Polarity | Phosphorylation | Mitosis | Protein-Tyrosine Kinases - metabolism | Cell Cycle Proteins - metabolism | Nuclear Proteins - metabolism | Protein Transport | Cell Cycle Proteins - antagonists & inhibitors | Schizosaccharomyces - metabolism | Nuclear Proteins - antagonists & inhibitors | ras-GRF1 - metabolism | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Schizosaccharomyces pombe Proteins - metabolism | Cell Cycle - physiology | G2 Phase | Protein-Serine-Threonine Kinases - metabolism | Schizosaccharomyces - cytology | Fungal Proteins - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors | Schizosaccharomyces pombe Proteins - antagonists & inhibitors | Arctic research | Cell cycle | Physiological aspects | Cell physiology | Genetic aspects | Research | Protein kinases | Proteins | Cell growth | Kinases | Molecular biology | Monitoring systems | ras-GRF1 | Protein-Serine-Threonine Kinases | Schizosaccharomyces pombe Proteins | Fungal Proteins | Cellular Biology | Nuclear Proteins | Life Sciences | Cell Cycle | Protein Kinases | Protein-Tyrosine Kinases | Cell Cycle Proteins | Schizosaccharomyces
Journal Article
American journal of physiology. Heart and circulatory physiology, ISSN 1522-1539, 2005, Volume 288, Issue 2, pp. H971 - H976
Pharmacological activation of the prosurvival kinases Akt and ERK-1/2 at reperfusion, after a period of lethal ischemia, protects the heart against ischemia-reperfusion injury... 
Myocardial infarction | Phosphatidylinositol 3-kinase-Akt | Reperfusion injury | Mitogen-activated protein kinases | MITOCHONDRIAL PERMEABILITY TRANSITION | OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | phosphatidylinositol 3-kinase-Akt | mitogen-activated protein kinases | myocardial infarction | PORE | INJURY | PERIPHERAL VASCULAR DISEASE | reperfusion injury | Phosphorylation | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Male | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Myocardial Reperfusion Injury - pathology | Myocardial Infarction - pathology | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Survival - physiology | Protein-Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins - metabolism | MAP Kinase Kinase 1 - antagonists & inhibitors | Proto-Oncogene Proteins - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Enzyme Inhibitors - pharmacology | Rats | MAP Kinase Kinase 1 - metabolism | Myocardium - pathology | MAP Kinase Kinase 2 - metabolism | Myocardial Infarction - metabolism | Rats, Sprague-Dawley | Proto-Oncogene Proteins c-akt | Myocardial Reperfusion Injury - metabolism | Myocardium - enzymology | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Ischemic Preconditioning, Myocardial | MAP Kinase Kinase 2 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - metabolism
Journal Article
Journal Article
PloS one, ISSN 1932-6203, 06/2013, Volume 8, Issue 6, p. e66796
Human protein kinases (HPKs) have profound effects on cellular responses. To better understand the role of HPKs and the signaling networks that influence influenza virus replication, a small interfering RNA (siRNA... 
A VIRUS | SIGNAL-TRANSDUCTION | ANTIVIRAL THERAPY | AVIAN INFLUENZA | PROTEIN-KINASE | MULTIDISCIPLINARY SCIENCES | IN-VIVO | CELL-CYCLE ARREST | NF-KAPPA-B | RESISTANT INFLUENZA | RESPIRATORY SYNCYTIAL VIRUS | Protein Kinases - metabolism | Up-Regulation | Protein Kinases - genetics | Influenza, Human - pathology | MicroRNAs - antagonists & inhibitors | Virus Replication - genetics | Humans | Influenza A virus - genetics | Influenza, Human - enzymology | Protein Kinases - chemistry | MicroRNAs - metabolism | RNA Interference | NIMA-Related Kinases - antagonists & inhibitors | Base Sequence | Madin Darby Canine Kidney Cells | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Viral Core Proteins - metabolism | Influenza, Human - virology | MicroRNAs - agonists | RNA, Ribosomal, 18S - metabolism | MAP Kinase Kinase Kinase 1 - antagonists & inhibitors | Protein-Serine-Threonine Kinases - metabolism | MAP Kinase Kinase Kinase 1 - metabolism | A549 Cells | Influenza A virus - physiology | RNA, Ribosomal, 18S - genetics | Protein-Serine-Threonine Kinases - genetics | Influenza A virus - isolation & purification | Phenotype | Sequence Alignment | Animals | Influenza, Human - genetics | Dogs | NIMA-Related Kinases - metabolism | NIMA-Related Kinases - genetics | MAP Kinase Kinase Kinase 1 - genetics | RNA-Binding Proteins - metabolism | Influenza viruses | MicroRNA | Health aspects | Protein kinases | Influenza | Genes | Pandemics | Transcription | Genomics | Viruses | Infections | Antagonists | Kinases | Genetic screening | Proteins | Signal transduction | Cell cycle | miRNA | siRNA | Gene expression | Ribonucleic acid--RNA | Studies | Signaling | Infectious diseases | Swine flu | MicroRNAs | Proteomics | Replication | Viral infections | Apoptosis | RNA | Ribonucleic acid
Journal Article