PMID- 38420094
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240301
IS  - 2168-8184 (Print)
IS  - 2168-8184 (Electronic)
IS  - 2168-8184 (Linking)
VI  - 16
IP  - 1
DP  - 2024 Jan
TI  - Computational Exploration of Single-Nucleotide Polymorphisms in the Human hRAS 
      Gene: Implications and Insights.
PG  - e53119
LID - 10.7759/cureus.53119 [doi]
LID - e53119
AB  - Background A group of genes called oncogenes includes the Harvey rat sarcoma 
      virus (hRAS) gene. Along with hRAS, Kirsten rat sarcoma viral oncogene homolog 
      (kRAS) and neuroblastoma RAS viral oncogene homolog (nRAS) genes belong to the 
      Rat sarcoma (Ras) family of oncogenes. These three genes result in Rho guanosine 
      triphosphate hydrolases (GTPases) as their protein product. Instructions for 
      producing the protein hRAS, which is mainly involved in controlling cell 
      division, are provided by the hRAS gene. The hRAS protein transfers signals from 
      outside through a process called signal transduction. Because the hRAS protein is 
      a GTPase, it changes the chemical guanosine-5'-triphosphate (GTP) into guanosine 
      diphosphate (GDP). GTP and GDP molecules operate as switches to turn on and off 
      the hRAS. This study aimed to anticipate the structure and stability of the 
      protein resulting from missense single-nucleotide polymorphisms (SNPs) in the 
      human hRAS genes. Methodology To investigate the possible negative effects 
      associated with these SNPs, bioinformatic analysis is typically essential. The 
      following tools were employed for forecasting harmful SNPs: Scale-Invariant 
      Feature Transform (SIFT), Protein Analysis Through Evolutionary Relationships 
      (PANTHER), non-synonymous SNP by Protein Variation Effect Analyzer (PROVEAN), and 
      non-synonymous SNP by Single Nucleotide Polymorphism Annotation Platform (SNAP). 
      Results The present study identified a total of 11 SNPs using the SIFT approach, 
      which were shown to have functional significance. Only two of these 11 SNPs were 
      determined to be tolerable, whereas nine were shown to be detrimental. Among the 
      11 SNPs analyzed, seven (Q61H, Q99H, K117R, A121D, A146V, R169W, R169Q) were 
      classified as possibly damaging,and four (G13V, Q22K, Q61K, Q13V) were 
      categorized as probably benign according to the predictions made by PANTHER 
      tools. Therefore, the seven SNPs were identified as high-risk SNPs. Conclusions 
      Given that SNPs have the potential to be candidates for cellular alterations 
      brought on by mutations that are associated with cancer, this study provides 
      vital information about how SNPs might be utilized as a diagnostic marker for 
      cancer.
CI  - Copyright (c) 2024, Dakshitha et al.
FAU - Dakshitha, Sankar
AU  - Dakshitha S
AD  - Physiology, Saveetha Dental College and Hospitals, Saveetha Institute of Medical 
      and Technical Sciences, Saveetha University, Chennai, IND.
FAU - Priya Dharshini, Boopathi
AU  - Priya Dharshini B
AD  - Physiology, Saveetha Dental College and Hospitals, Saveetha Institute of Medical 
      and Technical Sciences, Saveetha University, Chennai, IND.
FAU - Suresh, Vasugi
AU  - Suresh V
AD  - Physiology, Saveetha Dental College and Hospitals, Saveetha Institute of Medical 
      and Technical Sciences, Saveetha University, Chennai, IND.
FAU - Dilipan, Elangovan
AU  - Dilipan E
AD  - Physiology, Saveetha Dental College and Hospitals, Saveetha Institute of Medical 
      and Technical Sciences, Saveetha University, Chennai, IND.
LA  - eng
PT  - Journal Article
DEP - 20240128
PL  - United States
TA  - Cureus
JT  - Cureus
JID - 101596737
PMC - PMC10899094
OTO - NOTNLM
OT  - amino acid
OT  - bioinformatic tools
OT  - computational biology
OT  - hras gene
OT  - single-nucleotide polymorphism (snp)
COIS- The authors have declared that no competing interests exist.
EDAT- 2024/02/29 06:43
MHDA- 2024/02/29 06:44
PMCR- 2024/01/28
CRDT- 2024/02/29 04:06
PHST- 2023/12/11 00:00 [received]
PHST- 2024/01/28 00:00 [accepted]
PHST- 2024/02/29 06:44 [medline]
PHST- 2024/02/29 06:43 [pubmed]
PHST- 2024/02/29 04:06 [entrez]
PHST- 2024/01/28 00:00 [pmc-release]
AID - 10.7759/cureus.53119 [doi]
PST - epublish
SO  - Cureus. 2024 Jan 28;16(1):e53119. doi: 10.7759/cureus.53119. eCollection 2024 
      Jan.