Data for: The PERK/Nrf2 pathway mediates endoplasmic reticulum stress-induced injury by upregulating endoplasmic reticulophagy in H9c2 cardiomyoblasts
| Main Author: | Liu, Xiuhua |
|---|---|
| Format: | Dataset |
| Terbitan: |
Mendeley
, 2019
|
| Subjects: | |
| Online Access: |
https:/data.mendeley.com/datasets/dxv5bfjz8s |
| ctrlnum |
0.17632-dxv5bfjz8s.1 |
|---|---|
| fullrecord |
<?xml version="1.0"?>
<dc><creator>Liu, Xiuhua</creator><title>Data for: The PERK/Nrf2 pathway mediates endoplasmic reticulum stress-induced injury by upregulating endoplasmic reticulophagy in H9c2 cardiomyoblasts</title><publisher>Mendeley</publisher><description>ERS caused ER-phagy with a decrease in cell viability and an increase in cell death in H9c2 cardiomyoblasts.(A) Live/Dead staining of H9c2 cardiomyoblasts was performed using a LIVE/DEAD® Viability/Cytotoxicity Kit (bar=40 μm, n=3). TG- or TM-treated H9c2 cardiomyoblasts were incubated with calcein-AM (green) and EthD-1 (red) for 10 min, and the fluorescence was visualized using a confocal microscope. Green fluorescence indicates live cells, while red fluorescence indicates dead cells. (E) Ultrastructural lesions in the ER caused by TG or TM and the occurrence of ER-phagy were observed via transmission electron microscopy (bar=500 nm). (F) Representative confocal microscopy images corresponding to analysis of ER-phagy for TG- or TM-treated H9c2 cardiomyoblasts and showing colocalization of autophagosomes with ER-fragments (bar=15 μm; n=3). LC3B was labeled with Texas Red, while calreticulin was labeled with Alexa Fluor 488. </description><subject>Autophagy</subject><subject>Endoplasmic Reticulum Stress</subject><type>Other:Dataset</type><identifier>10.17632/dxv5bfjz8s.1</identifier><rights>Attribution-NonCommercial 3.0 Unported</rights><rights>https://creativecommons.org/licenses/by-nc/3.0</rights><relation>https:/data.mendeley.com/datasets/dxv5bfjz8s</relation><date>2019-10-17T15:29:53Z</date><recordID>0.17632-dxv5bfjz8s.1</recordID></dc>
|
| format |
Other:Dataset Other |
| author |
Liu, Xiuhua |
| title |
Data for: The PERK/Nrf2 pathway mediates endoplasmic reticulum stress-induced injury by upregulating endoplasmic reticulophagy in H9c2 cardiomyoblasts |
| publisher |
Mendeley |
| publishDate |
2019 |
| topic |
Autophagy Endoplasmic Reticulum Stress |
| url |
https:/data.mendeley.com/datasets/dxv5bfjz8s |
| contents |
ERS caused ER-phagy with a decrease in cell viability and an increase in cell death in H9c2 cardiomyoblasts.(A) Live/Dead staining of H9c2 cardiomyoblasts was performed using a LIVE/DEAD® Viability/Cytotoxicity Kit (bar=40 μm, n=3). TG- or TM-treated H9c2 cardiomyoblasts were incubated with calcein-AM (green) and EthD-1 (red) for 10 min, and the fluorescence was visualized using a confocal microscope. Green fluorescence indicates live cells, while red fluorescence indicates dead cells. (E) Ultrastructural lesions in the ER caused by TG or TM and the occurrence of ER-phagy were observed via transmission electron microscopy (bar=500 nm). (F) Representative confocal microscopy images corresponding to analysis of ER-phagy for TG- or TM-treated H9c2 cardiomyoblasts and showing colocalization of autophagosomes with ER-fragments (bar=15 μm; n=3). LC3B was labeled with Texas Red, while calreticulin was labeled with Alexa Fluor 488. |
| id |
IOS7969.0.17632-dxv5bfjz8s.1 |
| institution |
Universitas Islam Indragiri |
| affiliation |
onesearch.perpusnas.go.id |
| institution_id |
804 |
| institution_type |
library:university library |
| library |
Teknologi Pangan UNISI |
| library_id |
2816 |
| collection |
Artikel mulono |
| repository_id |
7969 |
| city |
INDRAGIRI HILIR |
| province |
RIAU |
| shared_to_ipusnas_str |
1 |
| repoId |
IOS7969 |
| first_indexed |
2020-04-08T08:23:40Z |
| last_indexed |
2020-04-08T08:23:40Z |
| recordtype |
dc |
| _version_ |
1686587567225438208 |
| score |
17.538404 |