scholarly journals MicroRNA-21 induces stemness by downregulating transforming growth factor beta receptor 2 (TGF R2) in colon cancer cells

2011 ◽  
Vol 33 (1) ◽  
pp. 68-76 ◽  
Author(s):  
Y. Yu ◽  
S. S. Kanwar ◽  
B. B. Patel ◽  
P.-S. Oh ◽  
J. Nautiyal ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Growth Factor ◽  
Cancer Cells ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Colon Cancer Cells ◽  
Beta Receptor ◽  
Growth Factor Beta

Osteoinductive effect of soluble transforming growth factor beta receptor 3 on human osteoblast lineage

2021 ◽  
Author(s):  
Angelica Mastandrea Amanso ◽  
Archana Kamalakar ◽  
Sara Bitarafan ◽  
Shelly Abramowicz ◽  
Hicham Drissi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Human Osteoblast ◽  
Beta Receptor ◽  
Growth Factor Beta ◽  
Osteoblast Lineage

Structure and Polymorphism Analysis of Transforming Growth Factor Beta Receptor 1 (TGFBR1) in Pigs

2005 ◽  
Vol 43 (9-10) ◽  
pp. 491-500 ◽  
Author(s):  
Shin-ichi Shimanuki ◽  
Ayumi Mikawa ◽  
Yuko Miyake ◽  
Noriyuki Hamasima ◽  
Satoshi Mikawa ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Polymorphism Analysis ◽  
Beta Receptor ◽  
Growth Factor Beta

scholarly journals Novel Transforming Growth Factor-Beta Receptor 1 Antagonists through a Pharmacophore-Based Virtual Screening Approach

Molecules ◽  
2018 ◽  
Vol 23 (11) ◽  
pp. 2824 ◽  
Author(s):  
Junhao Jiang ◽  
Hui Zhou ◽  
Qihua Jiang ◽  
Lili Sun ◽  
Ping Deng
Keyword(s):  
Growth Factor ◽  
Virtual Screening ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Malignant Tumors ◽  
Pharmacophore Model ◽  
New Drugs ◽  
Beta Receptor ◽  
Potential Activity ◽  
Growth Factor Beta

As new drugs for the treatment of malignant tumors, transforming growth factor-beta receptor 1 (TGFβR1) antagonists have attracted wide attention. Based on the crystal structure of TGFβR1-BMS22 complex, the pharmacophore model A02 with two hydrogen bond acceptors (HBAs) and four hydrophobic (HYD) properties was constructed. From the common features of active ligands reported in the literature, pharmacophore model B10 was also generated, which has two aromatic ring centers (RAs) and two HYD properties. The two models have high sensitivity and specificity to the training set, and they are highly consistent in spatial structure. Combining the two pharmacophore models, two novel skeleton structures with potential activity were selected by virtual screening from the DruglikeDiverse, MiniMaybridge, and ZINC Drug-Like databases. Four compounds (YXY01–YXY04) with potential anti-TGFβR1 activity were designed based on the new skeleton structures. In combination with Lipinski’s rules; absorption, distribution, metabolism, excretion, and toxicity (ADMET); and, toxicological properties predicted in the study, YXY01-03 with the novel skeleton, good drug-like properties, and potential activity were finally discovered and may have higher safety relative to BMS22, which may be valuable for further research.

scholarly journals Captopril reverses high-glucose-induced growth effects on LLC-PK1 cells partly by decreasing transforming growth factor-beta receptor protein expressions.

1996 ◽  
Vol 7 (8) ◽  
pp. 1207-1215 ◽  
Author(s):  
J Y Guh ◽  
M L Yang ◽  
Y L Yang ◽  
C C Chang ◽  
L Y Chuang
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
High Glucose ◽  
Transforming Growth Factor ◽  
Receptor Protein ◽  
Tgf Beta ◽  
Beta Receptor ◽  
Protein Expressions ◽  
Beta Receptors ◽  
Growth Factor Beta

Transforming growth factor beta (TGF-beta) may be important in the pathogenesis of diabetic nephropathy, and captopril is effective in treating this disorder. However, the mechanisms of this therapeutic effect as related to TGF-beta and its receptors are not known. Thus, the effects of captopril on cellular growth, TGF-beta 1, and TGF-beta receptors were studied in LLC-PK1 cells cultured in normal (11 mM) or high glucose (27.5 mM). This study found that glucose dose-dependently inhibited cellular mitogenesis while inducing hypertrophy in these cells at 72 h of culture, concomitantly with enhanced TGF-beta 1 messenger RNA (mRNA) and TGF-beta receptor Types I and II protein expressions. Captopril dose-dependently (0.1 to 10 mM) increased cellular mitogenesis and inhibited hypertrophy in these cells. Moreover, captopril also decreased TGF-beta receptor Types I and II protein expressions dose-dependently. However, TGF-beta 1 mRNA was not affected by captopril. It was concluded that high glucose decreased cellular mitogenesis while increasing hypertrophy concomitantly with increased TGF-beta 1 mRNA and TGF-beta receptors in LLC-PK1 cells. Captopril can reverse high-glucose-induced growth effects by decreasing TGF-beta receptor protein expressions.

Sign in / Sign up

Export Citation Format

Share Document