Редактирование: NECTIN2 (раздел)

==Publications==

{{medline-entry
|title=Genetics of Human Longevity From Incomplete Data: New Findings From the Long Life Family Study.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30299504
|abstract=The special design of the Long Life Family Study provides a unique opportunity to investigate the genetics of human longevity by analyzing data on exceptional lifespans in families. In this article, we performed two series of genome wide association studies of human longevity which differed with respect to whether missing lifespan data were predicted or not predicted. We showed that the use of predicted lifespan is most beneficial when the follow-up period is relatively short. In addition to detection of strong associations of SNPs in [[APOE]], [[TOMM40]], [[NECTIN2]], and [[APOC1]] genes with longevity, we also detected a strong new association with longevity of rs1927465, located between the [[CYP26A1]] and [[MYOF]] genes on chromosome 10. The association was confirmed using data from the Health and Retirement Study. We discuss the biological relevance of the detected SNPs to human longevity.
|mesh-terms=* Aged
* Aged, 80 and over
* Apolipoprotein C-I
* Apolipoproteins E
* Calcium-Binding Proteins
* Chromosomes, Human, Pair 10
* Chromosomes, Human, Pair 19
* Denmark
* Female
* Gene Frequency
* Genome-Wide Association Study
* Humans
* Logistic Models
* Longevity
* Longitudinal Studies
* Male
* Membrane Proteins
* Membrane Transport Proteins
* Muscle Proteins
* Nectins
* Pedigree
* Polymorphism, Single Nucleotide
* Retinoic Acid 4-Hydroxylase
* United States

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6175028
}}
{{medline-entry
|title=Apolipoprotein E region molecular signatures of Alzheimer's disease.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29797398
|abstract=Although the [[APOE]] region is the strongest genetic risk factor for Alzheimer's diseases (ADs), its pathogenic role remains poorly understood. Elucidating genetic predisposition to ADs, a subset of age-related diseases characteristic for postreproductive period, is hampered by the undefined role of evolution in establishing molecular mechanisms of such diseases. This uncertainty is inevitable source of natural-selection-free genetic heterogeneity in predisposition to ADs. We performed first large-scale analysis of linkage disequilibrium (LD) structures characterized by 30 polymorphisms from five genes in the [[APOE]] 19q13.3 region (BCAM, [[NECTIN2]], [[TOMM40]], [[APOE]], and APOC1) in 2,673 AD-affected and 16,246 unaffected individuals from five cohorts. Consistent with the undefined role of evolution in age-related diseases, we found that these structures, being highly heterogeneous, are significantly different in subjects with and without ADs. The pattern of the difference represents molecular signature of AD comprised of single nucleotide polymorphisms (SNPs) from all five genes in the [[APOE]] region. Significant differences in LD in subjects with and without ADs indicate SNPs from different genes likely involved in AD pathogenesis. Significant and highly heterogeneous molecular signatures of ADs provide unprecedented insight into complex polygenetic predisposition to ADs in the [[APOE]] region. These findings are more consistent with a complex haplotype than with a single genetic variant origin of ADs in this region.
|mesh-terms=* Alzheimer Disease
* Apolipoproteins E
* Cohort Studies
* Genotype
* Humans
* Polymorphism, Single Nucleotide
|keywords=* APOE polymorphism
* Alzheimer's disease
* age-related phenotypes
* aging
* health span
* lifespan
* neurodegenerative disorders
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6052488
}}