Evidence map›Paper›PMID 37511907›Full record

ArticleLife (Basel, Switzerland)2023

Discovering Deleterious Single Nucleotide Polymorphisms of Human AKT1 Oncogene: An In Silico Study.

Ruojun Zhang, Nahid Akhtar, Atif Khurshid Wani, Khalid Raza, Vikas Kaushik

Open access · goldAbstract read
In one paragraph

Article in Life (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Cancer-associated TRF1 mutations alter PARP1 interaction dynamics: an in silico study.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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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

5 authors at 3 institutions in 2 countries.

Ruojun ZhangSchool of Life Sciences and Technology, Tongji University, Shanghai 200092, China.
Nahid AkhtarSchool of Bioengineering and Biosciences, Lovely Professional University, Phagwara 144411, India.ORCID 0000-0002-8286-3736
Atif Khurshid WaniSchool of Bioengineering and Biosciences, Lovely Professional University, Phagwara 144411, India.
Khalid RazaDepartment of Computer Science, Jamia Millia Islamia, New Delhi 110025, India.ORCID 0000-0002-3646-6828
Vikas KaushikSchool of Bioengineering and Biosciences, Lovely Professional University, Phagwara 144411, India.ORCID 0000-0003-2349-1220
Lovely Professional University · INJamia Millia Islamia · INTongji University · CN

Funding

Jamia Millia Islamia JMI/DCS/2022-23
6 · The paper itself

Abstract

backgroundAKT1 is a serine/threonine kinase necessary for the mediation of apoptosis, angiogenesis, metabolism, and cell proliferation in both normal and cancerous cells. The mutations in the AKT1 gene have been associated with different types of cancer. Further, the AKT1 gene mutations are also reported to be associated with other diseases such as Proteus syndrome and Cowden syndromes. Hence, this study aims to identify the deleterious AKT1 missense SNPs and predict their effect on the function and structure of the AKT1 protein using various computational tools.

methodsExtensive in silico approaches were applied to identify deleterious SNPs of the human AKT1 gene and assessment of their impact on the function and structure of the AKT1 protein. The association of these highly deleterious missense SNPs with different forms of cancers was also analyzed. The in silico approach can help in reducing the cost and time required to identify SNPs associated with diseases.

resultsIn this study, 12 highly deleterious SNPs were identified which could affect the structure and function of the AKT1 protein. Out of the 12, four SNPs-namely, G157R, G159V, G336D, and H265Y-were predicted to be located at highly conserved residues. G157R could affect the ligand binding to the AKT1 protein. Another highly deleterious SNP, R273Q, was predicted to be associated with liver cancer.

conclusionsThis study can be useful for pharmacogenomics, molecular diagnosis of diseases, and developing inhibitors of the AKT1 oncogene.

Indexed as

AKT1kinaseoncogeneSNPs

Identifiers

PMID37511907
PMCPMC10381612
OpenAlexW4383818032

What OpenQuestion holds

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LicenceCC BY
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.