Редактирование: F11R

Junctional adhesion molecule A precursor (JAM-A) (Junctional adhesion molecule 1) (JAM-1) (Platelet F11 receptor) (Platelet adhesion molecule 1) (PAM-1) (CD321 antigen) [JAM1] [JCAM] [UNQ264/PRO301]

==Publications==

{{medline-entry
|title=[Adhesion molecule JAM-A, its function and mechanism of epigenetic regulation].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28509452
|abstract=The article represents evidence about structures, properties and functions of adhesion molecule JAM-A/1 belonging to JAM subfamily. This protein plays an important role in epithelial tight junction formation and immune function. Current article focuses on the role of JAM-A protein in pathogenesis associated to ageing: atherosclerosis, apoplexy, thrombosis, hypertension, ophthalmological pathology. We propose short peptides Lys-Glu, Lys-Glu-Asp, and Ala-Glu-Asp-Gly could influence on [[F11R]] gene expression that leads to recovery of JAM-A synthesis in cells.
|mesh-terms=* Aging
* Cell Adhesion Molecules
* Epigenesis, Genetic
* Gene Expression
* Humans
* Oligopeptides
* Protective Factors
* Receptors, Cell Surface
|keywords=* JAM-A
* age-related pathology
* epigenetics
* short peptides

}}
{{medline-entry
|title=[[USF1]] gene variants, cardiovascular risk, and mortality in European Americans: analysis of two US cohort studies.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/17885212
|abstract=A common haplotype of the upstream transcription factor 1 gene ([[USF1]]) has been associated with decreased susceptibility to familial combined hyperlipidemia (FCHL) and, paradoxically, with increased risk of cardiovascular disease (CVD) and all-cause mortality. We assessed associations between [[USF1]] tagSNPs, CVD risk factors, and aging-related phenotypes using data from 2 large population-based cohorts, Coronary Artery Risk Development in Young Adults (CARDIA) and the Cardiovascular Health Study (CHS), comprising younger and older adults, respectively. In CARDIA, each additional copy of the FCHL low-risk allele was associated with 2.4 mg/dL lower levels of LDL cholesterol (P=0.01) and decreased risk of subclinical atherosclerosis as assessed by coronary artery calcium (odds ratio 0.79; 95%CI 0.63 to 0.98). Whereas there was little association between [[USF1]] genotype and metabolic or CVD traits in older adults from CHS, the [[USF1]] low-risk dyslipidemia allele was associated with higher plasma C-reactive protein and interleukin (IL)-6 levels and with increased risk of mortality, particularly attributable to noncardiovascular causes. There appears to be a complex and possibly age-dependent relationship between [[USF1]] genotype, atherosclerosis phenotypes, and CVD risk. [[USF1]] may influence mortality through pathways distinct from atherosclerosis. Alternatively, linkage disequilibrium with neighboring polymorphisms in other genes such as [[F11R]] may be responsible for the observed [[USF1]] genotype-phenotype associations in older adults.
|mesh-terms=* Adult
* Age Factors
* Aged
* Aged, 80 and over
* Aging
* Blood Glucose
* C-Reactive Protein
* Calcium
* Cardiovascular Diseases
* Carotid Artery, Common
* Cohort Studies
* Coronary Artery Disease
* Coronary Vessels
* European Continental Ancestry Group
* Female
* Follow-Up Studies
* Genetic Predisposition to Disease
* Humans
* Hyperlipidemia, Familial Combined
* Insulin
* Interleukin-6
* Linkage Disequilibrium
* Lipids
* Male
* Odds Ratio
* Phenotype
* Polymorphism, Single Nucleotide
* Prospective Studies
* Risk Assessment
* Risk Factors
* Time Factors
* United States
* Upstream Stimulatory Factors

|full-text-url=https://sci-hub.do/10.1161/ATVBAHA.107.154559
}}