Evidence map›Paper›PMID 19225881›Full record

ArticleNeurochemical research2009

Increased phosphorylation of Ets-like transcription factor-1 in neurons of hypoxic preconditioned mice.

Jun Jiang, Weiwei Yang, Ping Huang, Xiangning Bu, Nan Zhang, Junfa Li

Abstract read
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In one paragraph

Article in Neurochemical research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 26% of its field
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

3 citing papers in PubMed, 13 citations in OpenAlex.

  1. Alpha-synuclein oligomerization increases its effect on promoting NMDA receptor internalization.International journal of clinical and experimental pathology · 2019
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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

6 authors at 1 institution in 1 country.

Jun JiangDepartment of Neurobiology and Beijing Institute for Neuroscience, Capital Medical University, #10 You An Men Wai Xi Tou Tiao, 100069 Beijing, China.
Weiwei Yang
Ping Huang
Xiangning Bu
Nan Zhang
Junfa Li
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ets-like transcription factor-1 (Elk-1) is a target of mitogen activated protein kinase (MAPK) which has been reported to play a key role in the induction of tolerance to ischemic and hypoxic injury, but little is known about the role of Elk-1 in the development of cerebral hypoxic preconditioning (HPC). In this study, we found that Elk-1 phosphorylation at Ser383 (p-Ser383 Elk-1), not protein expression, increased significantly (P < 0.05) in both hippocampus and frontal cortex of mice after repetitive auto-hypoxia exposures from 1 to 6 times (H1-H6, n = 6 for each group) when compared to that of the normoxic control group (H0, n = 6). The enhanced p-Ser383 Elk-1 was also found in the nuclear extract of H3 mice brain. Similarly, increased p-Ser383 Elk-1 was observed by immunostaining in the hippocampus and frontal cortex of mice from H3 and H6 groups. In addition, we found that the increased p-Ser383 Elk-1 co-localized with a neuron-specific protein, neurogranin, in the brain of H3 mice by using double immunofluorescence labeling. These results suggested that the enhanced neuron-specific phosphorylation of Elk-1 at Ser383 is involved in cerebral HPC of mice.

Indexed as

AnimalsBlotting, WesternCerebral CortexElectrophoresis, Polyacrylamide Gelets-Domain Protein Elk-1Fluorescent Antibody TechniqueHippocampusHypoxiaImmunohistochemistryMaleMiceMice, Inbred BALB CNeurograninNeuronsPhosphorylationets-Domain Protein Elk-1Neurogranin

Identifiers

PMID19225881
OpenAlexW2104755157

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.