Редактирование: RAD51B

DNA repair protein RAD51 homolog 2 (R51H2) (RAD51 homolog B) (Rad51B) (RAD51-like protein 1) [RAD51L1] [REC2]

==Publications==

{{medline-entry
|title=Increased age-adjusted hazard of death associated with a common single nucleotide polymorphism of the human [[RAD52]] gene in a cardiovascular cohort.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29024686
|abstract=Aging may be characterized as the progressive increase of the risk of death caused by a decrease of almost all bodily functions. While a great number of model organism studies have established the role of DNA double strand breaks (DSBs) as one of the main causes of aging, few studies have examined whether common polymorphisms in human DSB repair genes influence aging and mortality. More importantly, to the best of our knowledge, no longitudinal study has thus far examined the link between polymorphisms in DSB repair and the risk of death. This longitudinal study thus analyses whether four common polymorphisms (rs2155209, rs7963551, rs17105278, rs2735383) in four selected DSB repair genes (MRE11A, [[RAD52]], [[RAD51B]], NBS1) influence the hazard of age-adjusted death in a cohort of patients with typical symptoms of ischemic heart disease. The results have shown that rs7963551 G/T heterozygotes exhibit a significantly increased hazard of death when compared with the combined GG and TT homozygotes (HR=1.42, 95% CI: 1.06-1.91, p=0.018). This study indicates that the SNP affecting efficiency of DSB repair may influence aging in humans.
|mesh-terms=* Aged
* Cardiovascular Diseases
* Cohort Studies
* DNA Breaks, Double-Stranded
* DNA Damage
* DNA Repair
* DNA-Binding Proteins
* Female
* Genetic Predisposition to Disease
* Genotype
* Heterozygote
* Humans
* Longitudinal Studies
* Male
* Middle Aged
* Multivariate Analysis
* Mutation
* Polymorphism, Single Nucleotide
* Proportional Hazards Models
* Rad52 DNA Repair and Recombination Protein
* Risk
|keywords=* Aging
* DNA damage
* DNA damage response
* Double strand breaks
* Longitudinal study
* RAD52
|full-text-url=https://sci-hub.do/10.1016/j.mad.2017.10.003
}}
{{medline-entry
|title=[What's new in dermatological research?].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23522705
|abstract=Dermatological research is more and more productive and its level higher and higher. Choosing the most significant articles is difficult. Mast cell plays a role in the initiation of inflammation and therefore in poorer healing. Keratinocytes derive from stem cells and progenitors, which are independent. They can be activated directly by heat through sensory proteins at their surface. The cutaneous nervous system has an organization similar to that of the most complex sensory organs. In psoriasis, denervation induces a significant plaque regression. The cerebral integration of skin appearance modulates the skin reactivity to histamine. Pruritus is linked to specific receptors in the skin, which give specific projections into the brain and are histamine-dependent or not. Atopic dermatitis may be linked to the nonspecific activation of Th2 immune system, particularly to abnormalities of the skin barrier. Skin bacteria, but not intestinal, modulate the formation of skin immunity. Raf kinases are well known in melanoma and play an important role in physiological conditions: they are not essential to the initial development of the melanocyte lineage but to maintain it. In culture, melanocytes can be dedifferentiated in melanoblasts. Sunburns are consecutive to the activation of [[TLR3]] by UVB. ANRIL gene is involved in the polymorphism of neurofibromatosis 1 and gene [[RAD51B]] is linked to the risk of male breast cancer. MCV infection is linked to sites with sialic acid. Aging objectified by telomere shortening is accelerated by stress.
|mesh-terms=* Aging
* Biomarkers, Tumor
* Biomedical Research
* Breast Neoplasms, Male
* DNA-Binding Proteins
* Denervation
* Dermatitis, Atopic
* Dermatology
* Humans
* Male
* Melanoma
* Neurofibromatosis 1
* Polymorphism, Genetic
* Pruritus
* Psoriasis
* Skin Diseases
* Skin Neoplasms
* Sunburn
* Telomere Shortening
* Th2 Cells
* Toll-Like Receptor 3
* raf Kinases

|full-text-url=https://sci-hub.do/10.1016/S0151-9638(12)70133-3
}}