Редактирование: NAV2

Neuron navigator 2 (EC 3.6.4.12) (Helicase APC down-regulated 1) (Pore membrane and/or filament-interacting-like protein 2) (Retinoic acid inducible in neuroblastoma 1) (Steerin-2) (Unc-53 homolog 2) (unc53H2) [HELAD1] [KIAA1419] [POMFIL2] [RAINB1] [STEERIN2]

==Publications==

{{medline-entry
|title=Genetic associations with age of menopause in familial longevity.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31188284
|abstract=We hypothesize that mechanisms associated with extended reproductive age may overlap with mechanisms for the selection of genetic variants that slow aging and decrease risk for age-related diseases. Therefore, the goal of this analysis is to search for genetic variants associated with delayed age of menopause (AOM) among women in a study of familial longevity. We performed a meta-analysis of genome-wide association studies for AOM in 1,286 women in the Long Life Family Study (LLFS) and 3,151 women in the Health and Retirement Study, and then sought replication in the Framingham Heart Study (FHS). We used Cox proportional hazard regression of AOM to account for censoring, with a robust variance estimator to adjust for within familial relations. In the meta-analysis, a single nucleotide polymorphism (SNP) previously associated with AOM reached genome-wide significance (rs16991615; HR = 0.74, P = 6.99 × 10). A total of 35 variants reached >10 level of significance and replicated in the FHS and in a 2015 large meta-analysis (ReproGen Consortium). We also identified several novel SNPs associated with AOM including rs3094005: [[MICB]], rs13196892: [[TXNDC5]] | MUTED, rs72774935: [[SSBP2]] | [[ATG10]], rs9447453: [[COL12A1]], rs114298934: [[FHL2]] | [[NCK2]], rs6467223: [[TNPO3]], rs9666274 and rs10766593: [[NAV2]], and rs7281846: [[HSPA13]]. This work indicates novel associations and replicates known associations between genetic variants and AOM. A number of these associations make sense for their roles in aging. Supplemental Digital Content 1, http://links.lww.com/MENO/A420.
|mesh-terms=* Adult
* Age Factors
* Aged
* Aging
* Cohort Studies
* Family
* Female
* Genome, Human
* Genome-Wide Association Study
* Genotype
* Humans
* Longevity
* Male
* Menopause
* Middle Aged
* Polymorphism, Single Nucleotide
* Reproduction
* Young Adult

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7008937
}}
{{medline-entry
|title=Low expression of aging-related [[[[NRXN3]]]] is associated with Alzheimer disease: A systematic review and meta-analysis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29995770
|abstract=Alzheimer disease (AD) is a common neurodegenerative disorder with distinct pathological features, with aging considered the greatest risk factor. We explored how aging contributes to increased AD risk, and determined concurrent and coordinate changes (including genetic and phenotypic modifications) commonly exhibited in both normal aging and AD. Using the Gene Expression Omnibus (GEO) database, we collected 1 healthy aging-related and 3 AD-related datasets of the hippocampal region. The normal aging dataset was divided into 3 age groups: young (20-40 years old), middle-aged (40-60 years old), and elderly (>60 years old). These datasets were used to analyze the differentially expressed genes (DEGs). The Gene Ontology (GO) terms, pathways, and function network analysis of these DEGs were analyzed. One thousand two hundred ninety-one DEGs were found to be shared in the natural aging groups and AD patients. Among the shared DEGs, [[ATP6V1E1]], [[GNG3]], [[NDUFV2]], [[GOT1]], [[USP14]], and [[NAV2]] have been previously found in both normal aging individuals and AD patients. Furthermore, using Java Enrichment of Pathways Extended to Topology (JEPETTO) analysis based on Kyoto Encyclopedia of Genes and Genomes (KEGG) database, we determined that changes in aging-related KEGG annotations may contribute to the aging-dependence of AD risk. Interestingly, [[[[NRXN3]]]], the second most commonly deregulated gene identified in the present study, is known to carry a mutation in AD patients. According to functional network analysis, [[[[NRXN3]]]] plays a critical role in synaptic functions involved in the cognitive decline associated with normal aging and AD. Our results indicate that the low expression of aging-related [[[[NRXN3]]]] may increase AD risk, though the potential mechanism requires further clarification.
|mesh-terms=* Adult
* Aged
* Aging
* Alzheimer Disease
* Down-Regulation
* Gene Expression
* Humans
* Middle Aged
* Nerve Tissue Proteins
* Polymorphism, Single Nucleotide
* Risk Factors
* Young Adult

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6076205
}}