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Related Concept Videos

Comparing Copy Number Variations and SNPs02:26

Comparing Copy Number Variations and SNPs

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Sequencing of the human genome has opened up several best-kept secrets of the genome. Scientists have identified thousands of genome variations that exist within a population. These variations can be a single nucleotide or a larger chromosomal variation.
Copy number variations or CNVs are the structural variations that cover more than 1kb of DNA sequence. The single nucleotide polymorphism (SNP), on the other hand, is a single nucleotide change or a point mutation that is found in more than 1%...
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A single nucleotide polymorphism or SNP is a single nucleotide variation at a specific genomic position in a large population. It is the most prevalent type of sequence variation found in the human genome. Point mutations that occur in more than 1% of the population qualify as SNPs. These are present once every 1000 nucleotides on an average in the human genome. Replacement of a purine with another purine (A/G) or a pyrimidine with another pyrimidine (C/T) is known as a transition. In contrast,...
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Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
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The genomes of eukaryotes are punctuated by long stretches of sequence which do not code for proteins or RNAs. Although some of these regions do contain crucial regulatory sequences, the vast majority of this DNA serves no known function. Typically, these regions of the genome are the ones in which the fastest change, in evolutionary terms, is observed, because there is typically little to no selection pressure acting on these regions to preserve their sequences.
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Leaky Scanning02:28

Leaky Scanning

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During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA.  Marilyn Kozak discovered that the sequence RCCAUGG (where R...
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Related Experiment Video

Updated: Jan 7, 2026

Targeted Next-generation Sequencing and Bioinformatics Pipeline to Evaluate Genetic Determinants of Constitutional Disease
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Computational analysis of Non-synonymous SNP effects on human PLVAP gene structure and function.

Mehnaj Khatoon1, Yamini Sri Sekar1, Swati Rani1

  • 1ICAR- National Institute of Veterinary Epidemiology and Disease Informatics, Bengaluru, 560 064, Karnataka, India.

Journal of Applied Genetics
|December 22, 2025
PubMed
Summary

Investigating plasmalemma vesicle-associated protein (PLVAP) gene variants reveals how Japanese Encephalitis Virus (JEV) enters the brain. Specific mutations impact viral entry, offering insights for diagnostics and antiviral therapies.

Keywords:
JEVMolecular dockingNon-synonymous SNPs (nsSNPs)PLVAPProtein stability

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Determining the Likelihood of Variant Pathogenicity Using Amino Acid-level Signal-to-Noise Analysis of Genetic Variation
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Area of Science:

  • Genomics and Bioinformatics
  • Virology
  • Molecular Biology

Background:

  • Plasmalemma vesicle-associated protein (PLVAP) is crucial for blood-brain barrier (BBB) integrity and serves as a receptor for Japanese Encephalitis Virus (JEV).
  • Understanding how genetic variations in PLVAP affect JEV neuroinvasion is vital for disease prevention and treatment.

Purpose of the Study:

  • To computationally analyze the functional impact of non-synonymous single-nucleotide polymorphisms (nsSNPs) in the PLVAP gene on JEV-host interactions.
  • To identify specific PLVAP variants that influence JEV binding and entry into the central nervous system.

Main Methods:

  • Retrieved and analyzed 11,883 SNPs from NCBI dbSNP, identifying 403 unique nsSNPs.
  • Performed protein stability, disorder, conservation, and molecular docking analyses to assess variant impact.
  • Prioritized five critical nsSNPs (R26H, I35T, E175G, V44G, I39S) based on their predicted effects.

Main Results:

  • Identified 43 nsSNPs significantly destabilizing PLVAP structure and 29 deleterious nsSNPs.
  • Five critical variants demonstrated pronounced destabilizing effects and altered PLVAP-JEV binding interactions.
  • Mutations were predicted to modify JEV entry efficiency and host susceptibility.

Conclusions:

  • PLVAP variants can influence JEV neuroinvasion, suggesting their potential as biomarkers for risk stratification.
  • Findings support therapeutic strategies targeting PLVAP-JEV interactions for antiviral drug discovery.
  • The computational approach can be extended to other flavivirus-host interactions for personalized medicine.