Evidence map›Paper›PMID 39636430›Full record

ReviewMolecular and cellular biochemistry2025

Autophagy-related gene BECN1 single nucleotide polymorphisms in diseases.

Sargeet Kaur, Jitendraa Vashistt, Ajay Kumar, Jyoti Parkash, Harish Changotra

Erratum issuedAbstract readReview
PubMed Publisher
In one paragraph

Review in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Sargeet Kaur *Department of Biotechnology and Bioinformatics, Jaypee University of Information Technology, Waknaghat, Solan, Himachal Pradesh, 173 234, India.ORCID http://orcid.org/0000-0001-5868-3084
Jitendraa VashisttDepartment of Biotechnology and Bioinformatics, Jaypee University of Information Technology, Waknaghat, Solan, Himachal Pradesh, 173 234, India.ORCID http://orcid.org/0000-0002-8702-3170
Ajay KumarTranslational Health Science and Technology Institute (THSTI), Faridabad, Haryana, 121001, India.ORCID http://orcid.org/0000-0001-9914-7421
Jyoti ParkashDepartment of Zoology, School of Basic and Applied Sciences, Central University of Punjab, Bathinda, 151 001, India.ORCID http://orcid.org/0000-0002-6399-700X
Harish Changotra *Department of Molecular Biology and Biochemistry, Guru Nanak Dev University, Amritsar, Punjab, 143 005, India. hchangotra@yahoo.com.ORCID http://orcid.org/0000-0002-1465-5257

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a cytoprotective process that operates within a cell to maintain cellular homeostasis. An array of multiple proteins is involved to mediate this conserved cellular process. Among these, Beclin 1 protein encoded by BECN1 gene plays a crucial role during the initiation of autophagy. It acts as a molecular platform onto which multiple proteins interact to mediate autophagy initiation. The functioning of such proteins has reportedly been influenced by the molecular markers such as Single Nucleotide Polymorphisms (SNPs) present within the encoding gene. The SNPs within the autophagy gene have been known to influence the functioning of autophagy proteins which further is involved in various diseases. Studies have reported that the SNPs within the BECN1 are involved in various diseases. This report outlines the findings of all the existing research on the role of SNPs within BECN1.

Indexed as

AutophagyBeclin-1Polymorphism, Single NucleotideAnimalsHumansBeclin-1BECN1 protein, humanAutophagyBeclin 1Intronic variantsRegulatory variantsSingle nucleotide polymorphisms

Identifiers

PMID39636430

What OpenQuestion holds

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Registered trials

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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.