Evidence map›Paper›PMID 21735102›Full record

ArticleMolecular biology reports2012

Glutaredoxin 2a, a mitochondrial isoform, plays a protective role in a human cell line under serum deprivation.

Su-Jung Kim, Hyun-Joo Jung, Hojin Choi, Chang-Jin Lim

Abstract read
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In one paragraph

Article in Molecular biology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Su-Jung KimDepartment of Biochemistry, College of Natural Sciences, Kangwon National University, 192-1 Hyoja-2-dong, Chuncheon, 200-701, Korea.
Hyun-Joo Jung
Hojin Choi
Chang-Jin Lim

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The roles of mitochondrial glutaredoxin (Grx2a) under serum deprivation were assessed using the human stable HepG2 cell lines overexpressing or down-regulating Grx2a. The Grx2a-overexpressing stable cells displayed enhanced proliferation, decreased reactive oxygen species (ROS) and caspase-3 activity levels, and increased total GSH level, compared to the vector control cells. These characteristics of the overexpressing stable cells were reversed by down-regulating Grx2a in the same cell line. In the limited serum conditions, the Grx2a-overexpressing stable pcDNA3.0/HA-Grx2a cells exhibited higher cellular viabilities and total GSH level, and showed much lower enhancement in ROS and caspase-3 activity levels than the vector control pcDNA3.0/HA cells. However, the Grx2a-down-regulating stable cells gave rise to diminished cellular viabilities and further decreased total GSH level, and contained significantly higher ROS and caspase-3 activity levels, under serum deprivation than the vector control cells. These results suggest that Grx2a plays proliferative and anti-apoptotic roles under serum deprivation.

Indexed as

Adaptation, PhysiologicalCadmiumCulture Media, Serum-FreeDown-RegulationGlutaredoxinsHep G2 CellsHumansMitochondriaProtective AgentsProtein IsoformsRNA, MessengerUp-RegulationCadmiumCulture Media, Serum-FreeGLRX2 protein, humanGlutaredoxinsProtective AgentsProtein IsoformsRNA, Messenger

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.