Protective Effect of Deferricoprogen Isolated from Monascus purpureus NTU 568 on Citrinin-Induced Apoptosis in HEK-293 Cells

2012 ◽  
Vol 60 (32) ◽  
pp. 7880-7885 ◽  
Author(s):  
Li-Chuan Hsu ◽  
Ya-Wen Hsu ◽  
Yu-Han Liang ◽  
Zhi-Hu Lin ◽  
Yao-Haur Kuo ◽  
...  
Keyword(s):  
Protective Effect ◽  
Monascus Purpureus ◽  
Hek 293 ◽  
Hek 293 Cells ◽  
293 Cells ◽  
Induced Apoptosis

scholarly journals Protective effect of ginsenoside Rk1, a major rare saponin from black ginseng, on cisplatin‐induced nephrotoxicity in HEK ‐293 cells

2020 ◽  
Vol 36 (9) ◽  
pp. 732-740 ◽  
Author(s):  
Jun‐Nan Hu ◽  
Xing‐Yue Xu ◽  
Shuang Jiang ◽  
Ying Liu ◽  
Zhi Liu ◽  
...  
Keyword(s):  
Protective Effect ◽  
Hek 293 ◽  
Hek 293 Cells ◽  
293 Cells ◽  
Black Ginseng

Golgi-SNARE GS28 potentiates cisplatin-induced apoptosis by forming GS28–MDM2–p53 complexes and by preventing the ubiquitination and degradation of p53

2012 ◽  
Vol 444 (2) ◽  
pp. 303-314 ◽  
Author(s):  
Nian-Kang Sun ◽  
Shang-Lang Huang ◽  
Kun-Yi Chien ◽  
Chuck C.-K. Chao
Keyword(s):  
P53 Protein ◽  
Ectopic Expression ◽  
Hek 293 ◽  
Hek 293 Cells ◽  
Protein Receptor ◽  
293 Cells ◽  
Cisplatin Sensitivity ◽  
The Stability ◽  
Induced Apoptosis ◽  
Protein Attachment

In the present study, we observed that the Golgi-SNARE (soluble N-ethylmaleimide-sensitive fusion protein-attachment protein receptor) GS28 forms a complex with p53 in HEK (human embryonic kidney)-293 cells. Given that p53 represents a tumour suppressor that affects the sensitivity of cancer cells to various chemotherapeutic drugs, we examined whether GS28 may influence the level of sensitivity to the DNA-damaging drug cisplatin. Indeed, knockdown of GS28 using short-hairpin RNA (shGS28) induced resistance to cisplatin in HEK-293 cells. On the other hand, overexpression of GS28 sensitized HEK-293 cells to cisplatin, whereas no sensitization effect was noted for the mitotic spindle-damaging drugs vincristine and taxol. Accordingly, we observed that knockdown of GS28 reduced the accumulation of p53 and its pro-apoptotic target Bax. Conversely, GS28 overexpression induced the accumulation of p53 and Bax as well as the pro-apoptotic phosphorylation of p53 on Ser46. Further experiments showed that these cellular responses could be abrogated by the p53 inhibitor PFT-α (pifithrin-α), indicating that GS28 may affect the stability and activity of p53. The modulatory effects of GS28 on cisplatin sensitivity and p53 stability were absent in lung cancer H1299 cells which are p53-null. As expected, ectopic expression of p53 in H1299 cells restored the modulatory effects of GS28 on sensitivity to cisplatin. In addition, GS28 was found to form a complex with the p53 E3 ligase MDM2 (murine double minute 2) in H1299 cells. Furthermore, the ubiquitination of p53 was reduced by overexpression of GS28 in cells, confirming that GS28 enhances the stability of the p53 protein. Taken together, these results suggest that GS28 may potentiate cells to DNA-damage-induced apoptosis by inhibiting the ubiquitination and degradation of p53.

scholarly journals Individual and combined use of ginsenoside F2 and cyanidin-3-O-glucoside attenuates H2O2-induced apoptosis in HEK-293 cells via the NF-κB pathway

RSC Advances ◽  
2017 ◽  
Vol 7 (66) ◽  
pp. 41713-41722 ◽  
Author(s):  
Di Liu ◽  
Ying Wang ◽  
Shuang Ma ◽  
Hongyu Sun ◽  
Wenyan Shi ◽  
...  
Keyword(s):  
Hek 293 ◽  
Hek 293 Cells ◽  
293 Cells ◽  
Combined Use ◽  
Induced Apoptosis

Ginsenoside F2 and cyanidin-3-O-glucoside synergistically inhibited H2O2-induced apoptosis in HEK-293 cells through mitochondria-mediated apoptotic and NF-κB pathways.

Type 2 IP3 receptors are involved in uranyl acetate induced apoptosis in HEK 293 cells

Toxicology ◽  
2009 ◽  
Vol 262 (1) ◽  
pp. 73-79 ◽  
Author(s):  
Juraj Kopacek ◽  
Karol Ondrias ◽  
Barbora Sedlakova ◽  
Jana Tomaskova ◽  
Lucia Zahradnikova ◽  
...  
Keyword(s):  
Uranyl Acetate ◽  
Ip3 Receptors ◽  
Hek 293 ◽  
Hek 293 Cells ◽  
293 Cells ◽  
Induced Apoptosis

scholarly journals Characteristics and requirements of basal autophagy in HEK 293 cells

Autophagy ◽  
2013 ◽  
Vol 9 (9) ◽  
pp. 1407-1417 ◽  
Author(s):  
Patience Musiwaro ◽  
Matthew Smith ◽  
Maria Manifava ◽  
Simon A. Walker ◽  
Nicholas T. Ktistakis
Keyword(s):  
Hek 293 ◽  
Hek 293 Cells ◽  
293 Cells

Halothane Inhibition of Recombinant Cardiac L-type Ca2+ Channels Expressed in HEK-293 Cells

2005 ◽  
Vol 103 (6) ◽  
pp. 1156-1166 ◽  
Author(s):  
Kevin J. Gingrich ◽  
Son Tran ◽  
Igor M. Nikonorov ◽  
Thomas J. Blanck
Keyword(s):  
Charge Transfer ◽  
Calcium Channels ◽  
Dependent Manner ◽  
Current Time ◽  
Hek 293 ◽  
Hek 293 Cells ◽  
293 Cells ◽  
Dependent Inactivation ◽  
Voltage Dependent

Background Volatile anesthetics depress cardiac contractility, which involves inhibition of cardiac L-type calcium channels. To explore the role of voltage-dependent inactivation, the authors analyzed halothane effects on recombinant cardiac L-type calcium channels (alpha1Cbeta2a and alpha1Cbeta2aalpha2/delta1), which differ by the alpha2/delta1 subunit and consequently voltage-dependent inactivation. Methods HEK-293 cells were transiently cotransfected with complementary DNAs encoding alpha1C tagged with green fluorescent protein and beta2a, with and without alpha2/delta1. Halothane effects on macroscopic barium currents were recorded using patch clamp methodology from cells expressing alpha1Cbeta2a and alpha1Cbeta2aalpha2/delta1 as identified by fluorescence microscopy. Results Halothane inhibited peak current (I(peak)) and enhanced apparent inactivation (reported by end pulse current amplitude of 300-ms depolarizations [I300]) in a concentration-dependent manner in both channel types. alpha2/delta1 coexpression shifted relations leftward as reported by the 50% inhibitory concentration of I(peak) and I300/I(peak)for alpha1Cbeta2a (1.8 and 14.5 mm, respectively) and alpha1Cbeta2aalpha2/delta1 (0.74 and 1.36 mm, respectively). Halothane reduced transmembrane charge transfer primarily through I(peak) depression and not by enhancement of macroscopic inactivation for both channels. Conclusions The results indicate that phenotypic features arising from alpha2/delta1 coexpression play a key role in halothane inhibition of cardiac L-type calcium channels. These features included marked effects on I(peak) inhibition, which is the principal determinant of charge transfer reductions. I(peak) depression arises primarily from transitions to nonactivatable states at resting membrane potentials. The findings point to the importance of halothane interactions with states present at resting membrane potential and discount the role of inactivation apparent in current time courses in determining transmembrane charge transfer.

Micropatterned surfaces of PDMS as growth templates for HEK 293 cells

2007 ◽  
Vol 9 (4) ◽  
pp. 475-485 ◽  
Author(s):  
R. M. Johann ◽  
Ch. Baiotto ◽  
Ph. Renaud
Keyword(s):  
Hek 293 ◽  
Hek 293 Cells ◽  
293 Cells

Calcium Induces Expression of Cytoplasmic Gelsolin in SH-SY5Y and HEK-293 Cells

2010 ◽  
Vol 35 (7) ◽  
pp. 1075-1082 ◽  
Author(s):  
Lina Ji ◽  
Abha Chauhan ◽  
Ved Chauhan
Keyword(s):  
Hek 293 ◽  
Hek 293 Cells ◽  
293 Cells ◽  
Cytoplasmic Gelsolin
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