UofT Libraries is getting a new library services platform in January 2021.
Learn more about the change.

Search Articles

X
Search Filters
Format Format
Subjects Subjects
Subjects Subjects
X
Sort by Item Count (A-Z)
Filter by Count
science & technology (58) 58
life sciences & biomedicine (52) 52
animals (34) 34
humans (34) 34
apoptosis (27) 27
promotes (20) 20
biochemistry & molecular biology (13) 13
mice (13) 13
cancer (12) 12
signal transduction (12) 12
cells (11) 11
cell biology (10) 10
oncology (10) 10
female (9) 9
research (9) 9
activation (8) 8
gene expression (8) 8
promote (8) 8
kinases (7) 7
pharmacology & pharmacy (7) 7
proteins (7) 7
analysis (6) 6
apoptosis - drug effects (6) 6
cell cycle (6) 6
cell line (6) 6
cell line, tumor (6) 6
health aspects (6) 6
medicine (6) 6
multidisciplinary sciences (6) 6
oxidative stress (6) 6
phosphorylation (6) 6
science & technology - other topics (6) 6
breast cancer (5) 5
cell (5) 5
cells, cultured (5) 5
cytokines (5) 5
deoxyribonucleic acid--dna (5) 5
development and progression (5) 5
drug resistance (5) 5
expression (5) 5
gene expression regulation, neoplastic (5) 5
genes (5) 5
genetic aspects (5) 5
human (5) 5
research article (5) 5
studies (5) 5
survival (5) 5
autophagy (4) 4
biology (4) 4
care and treatment (4) 4
cell death (4) 4
cell differentiation (4) 4
cell proliferation (4) 4
cell survival (4) 4
dna (4) 4
immunology (4) 4
inflammation (4) 4
life sciences (4) 4
male (4) 4
medicine, research & experimental (4) 4
metastasis (4) 4
neoplasms. tumors. oncology. including cancer and carcinogens (4) 4
original (4) 4
original article (4) 4
physiological aspects (4) 4
physiology (4) 4
proliferation (4) 4
protein (4) 4
rats (4) 4
reactive oxygen species - metabolism (4) 4
research & experimental medicine (4) 4
review (4) 4
science (4) 4
stress (4) 4
adult (3) 3
akt (3) 3
amino acid sequence (3) 3
angiogenesis (3) 3
antineoplastic agents - therapeutic use (3) 3
apoptosis - genetics (3) 3
apoptosis - physiology (3) 3
binding (3) 3
biotechnology & applied microbiology (3) 3
caspase (3) 3
caspase 3 - metabolism (3) 3
cell growth (3) 3
cell-death (3) 3
cytology (3) 3
death (3) 3
differentiation (3) 3
disease (3) 3
endothelial (3) 3
enzymes (3) 3
extracellular matrix (3) 3
gene (3) 3
gene expression profiling (3) 3
gene expression regulation (3) 3
growth (3) 3
hematology (3) 3
immune system (3) 3
more...
Language Language
Publication Date Publication Date
Click on a bar to filter by decade
Slide to change publication date range


Biological & pharmaceutical bulletin, ISSN 0918-6158, 2011, Volume 34, Issue 6, pp. 831 - 838
Journal Article
Journal Article
Blood, ISSN 0006-4971, 2015, Volume 125, Issue 23, pp. 3598 - 3608
Journal Article
European cells & materials, ISSN 1473-2262, 2015, Volume 30, pp. 200 - 209
... enzymes, which promote chondrocyte apoptosis and degrade cartilage to potentiate PTOA development... 
CDK9 | Cartilage | Flavopiridol | Inflammatory cytokines | Chondrocytes | Cell & Tissue Engineering | Engineering | Materials Science | Life Sciences & Biomedicine | Technology | Engineering, Biomedical | Materials Science, Biomaterials | Orthopedics | Science & Technology | Cell Biology | Chondrocytes - pathology | Inflammation - pathology | Apoptosis - drug effects | Extracellular Matrix - drug effects | RNA, Messenger - genetics | Extracellular Matrix - metabolism | Stress, Mechanical | Apoptosis - genetics | Cyclin-Dependent Kinase 9 - antagonists & inhibitors | RNA, Messenger - metabolism | Cartilage, Articular - pathology | Chondrocytes - drug effects | Animals | Cartilage, Articular - metabolism | Cattle | Inflammation - genetics | Cyclin-Dependent Kinase 9 - metabolism | Protein Kinase Inhibitors - pharmacology | Cartilage, Articular - drug effects | Chondrocytes - metabolism | Index Medicus | chondrocytes | inflammatory cytokines | cartilage | to the subsequent induction of chondrocyte apoptosis and cartilage matrix deterioration. Thus | we determined the effects of CDK9 inhibition in suppressing the injury response in mechanically-injured cartilage explants. Bovine cartilage explants were injured by a single compressive load of 30 % strain at 100 %/s | we measured the mRNA expression of pro-inflammatory cytokines | and chondrocyte viability and apoptosis by TUNEL staining. For long-term outcome | and by determining the mechanical properties with instantaneous and relaxation moduli. Our data showed CDK9 inhibitor markedly reduced injury-induced inflammatory cytokine and catabolic gene expression. CDK9 inhibitor also attenuated chondrocyte apoptosis and reduced cartilage matrix degradation. Lastly | and apoptotic genes by RT-PCR | and then treated with the CDK9 inhibitor Flavopiridol. To assess acute injury responses | catabolic enzymes | acute injury responses | cartilage matrix degradation was assessed by soluble glycosaminoglycan release | the mechanical properties of the injured explants were preserved by CDK9 inhibitor. Our results provide a temporal profile connecting the chain of events from mechanical impact | and thus it is an attractive target for limiting the injury response. Here | which promote chondrocyte apoptosis and degrade cartilage to potentiate PTOA development. Recent studies show that the rate-limiting step for transcriptional activation of injury response genes is controlled by cyclin-dependent kinase 9 (CDK9)
Journal Article
Frontiers in immunology, ISSN 1664-3224, 07/2019, Volume 10, pp. 1530 - 1530
Journal Article