Evidence map›Paper›PMID 33539011›Full record

ArticleAdvances in experimental medicine and biology2021

Aging and Protein Kinases.

Ayse Basak Engin, Atilla Engin

Abstract read
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In one paragraph

Article in Advances in experimental medicine and biology, 2021. 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 21% 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, 3 citations in OpenAlex.

  1. Article
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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

2 authors at 1 institution in 1 country.

Ayse Basak EnginDepartment of Toxicology, Faculty of Pharmacy, Gazi University, Ankara, Turkey. abengin@gmail.com.
Atilla EnginDepartment of General Surgery, Faculty of Medicine, Gazi University, Ankara, Turkey.
Gazi University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, aging has been tried to be explained with large numbers of theories, but none of them can elucidate the changes occurring in the aging process alone. A unified theory encompassing the mechanisms of genetic factors and repair systems in aging is becoming increasingly required. Almost 37 protein kinases contribute to all processes of aging and senescence. Furthermore, these kinases not only regulate the large number of metabolic pathways related to aging processes, but also control these pathways through 12 checkpoints. Thus, in this chapter, the metabolic targets of protein kinases signal transduction pathways were discussed in terms of the aging perspective under five headings, which are the indispensable stages of the aging process. Although the most popular classical aging theories have been stated as DNA damage theory, mitochondrial theory, free radical theory, and telomere theory, it was concluded that the aging process is controlled by protein kinases regardless of the different theories.

Indexed as

DNA DamageProtein KinasesAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsDNA RepairSignal TransductionAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsProtein KinasesAtaxia- and Rad3-related (ATR)Ataxia-telangiectasia mutated (ATM)Base excision repair (BER)DNA damageDNA damage response (DDR)DNA-dependent protein kinase, catalytic subunit (DNA-PKcs)Insulin-like growth factor signaling (IIS)Mammalian target of rapamycin complex 1 (mTORC1)Nucleotide excision repair (NER)Polo-like kinase-1 (PLK1)

Identifiers

PMID33539011
OpenAlexW3127468439

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.