Evidence map›Paper›PMID 27417725›Full record

ArticleDoklady. Biochemistry and biophysics2016

The role of STAT transcription factors in apoptosis regulation of hypothalamic neurons in aging in HER-2/neu transgenic mice and wild-type FVB/N mice.

E D Bazhanova, V N Anisimov

Abstract read
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Article in Doklady. Biochemistry and biophysics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 27% 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

2 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
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

2 authors at 2 institutions in 1 country.

E D BazhanovaSechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, pr. Morisa Toreza 44, St. Petersburg, 194223, Russia. bazhanovae@mail.ru.
V N AnisimovPetrov Research Institute of Oncology, ul. Leningradskaya 68, pos. Pesochnyi-2, St. Petersburg, 189646, Russia.
Institute of Evolutionary Physiology and Biochemistry · RUInstitute of Oncology NN Petrov · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

For the firsts time, the involvement of the STAT pathway in the regulation of neuronal apoptosis in physiological aging and in old mice overexpressing the HER-2/neu oncogene was studied. We showed that suppression of STAT3, STAT5, and STAT6 and overexpression of the proapoptotic factor STAT1, which provides p53-mediated apoptosis, are the causes for increasing the number of apoptotic neurons in physiological aging. HER-2 tyrosine kinase receptor overexpression promotes neuronal survival through activation of STAT-signaling pathway with simultaneous suppression of the proapoptotic factor STAT1.

Indexed as

AgingAnalysis of VarianceAnimalsApoptosisBlotting, WesternCaspase 3Cell SurvivalErb-b2 Receptor Tyrosine KinasesFemaleGene ExpressionHypothalamusIn Situ Nick-End LabelingMice, TransgenicNeuronsSTAT Transcription FactorsTumor Suppressor Protein p53Casp3 protein, mouseCaspase 3Erbb2 protein, mouseErb-b2 Receptor Tyrosine KinasesSTAT Transcription FactorsTumor Suppressor Protein p53

Identifiers

PMID27417725
OpenAlexW2461918711

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.