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1.
Arch Iran Med ; 19(2): 101-9, 2016 Feb.
Article in English | MEDLINE | ID: mdl-26838080

ABSTRACT

BACKGROUND: Alzheimer and Parkinson diseases (AD and PD) are the two most important neurodegenerative disorders. This paper aims to determine the possible molecular linkage between these two common neurodegenerative diseases by a combination of computational investigations. METHODS: According to our aim, common sets of identified proteins from the KEGG database were further analyzed based on Gene Ontology (GO) annotation and sequence similarities by the agglomerative hierarchical clustering.  Proteins possessing same characteristics were categorized based on biological features in distinct clusters using the R programming software. In addition to this, by the use of DAVID Program and PPI network analysis, more insight can be achieved. RESULTS: The results of this study indicated that 23 proteins are common between these two diseases. Their ontology evaluations by application of clustering methods showed that proteins belonging to a specific cluster indicate discrete properties that are different from other clusters. Furthermore, PPI network analysis confirms that the proteins with similarity ontology and sequence are also in close relationship. CONCLUSION: In conclusion, assessment of protein features supported the idea that mitochondria are the main malfunction compartment in AD and PD. Some of these common properties are apoptosis and mitochondria oxidation pathways that can be used for drug targeting. Moreover, examination of other neurodegenerative diseases can be helpful for comprehensive understanding of the origin of these diseases.


Subject(s)
Alzheimer Disease/metabolism , Parkinson Disease/metabolism , Proteins/metabolism , Alzheimer Disease/genetics , Computational Biology , Gene Ontology , Humans , Parkinson Disease/genetics , Protein Interaction Maps , Proteins/genetics
2.
Iran J Allergy Asthma Immunol ; 13(6): 428-32, 2014 Dec.
Article in English | MEDLINE | ID: mdl-25148801

ABSTRACT

Mannose-binding lectin (MBL) is a Ca⁺² -dependent collagenous lectin, that is produced by liver and mediates innate immune responses by opsonization of pathogens. The serum level of MBL varies widely among healthy individuals, ranging from 0.05 µg/ml (or lower) to over 5 µg/ml, mainly depending on genetic variation. This study has examined promoter and exon 1 of mbl2 genotype among 117 Iranian healthy blood donors. MBL Single Nucleotide Polymorphisms (SNPs) were genotyped using polymerase chain reaction (PCR), and serum levels of MBL were quantified using a double-antibody enzyme linked immunosorbent assay (ELISA). Results of this study showed that there are two promoter polymorphisms at -550 (H/L variants) and -221 (Y/X variants) positions, and three polymorphisms in exon 1 at codon 52 (D Allele), 54 (B Allele), and 57 (C Allele) in this population. B allele was significantly correlated with the lowest serum MBL level. Our results also showed that the most frequent genotype was HYA/LXA, and the genotype that associated with the highest serum level of MBL was HYA/HYA. The genotype that causes lowest MBL production in Iranian population was LYB/LXA. These results showed some differences compared to that of the other populations. To verify the originality of these differences we may need to extend the study to a larger samples of respective populations; meanwhile the importance of a new mutation, nucleotide 101 of MBL2 exon1, reported in the current study should be taken in considerations in terms of its possible pathobiological effects in following studies.


Subject(s)
Mannose-Binding Lectin/blood , Mannose-Binding Lectin/genetics , Polymorphism, Single Nucleotide , Adult , Genotype , Humans , Iran , Promoter Regions, Genetic
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