TY - JOUR

T1 - Candidate SNP-markers of rheumatoid arthritis that can significantly alter the affinity of the TATA-binding protein for human gene promoters

AU - Chadaeva, I. V.

AU - Rasskazov, D. A.

AU - Sharypova, E. B.

AU - Drachkova, I. A.

AU - Oshchepkova, E. A.

AU - Savinkova, L. K.

AU - Ponomarenko, P. M.

AU - Ponomarenko, M. P.

AU - Kolchanov, N. A.

AU - Kozlov, V. A.

PY - 2019/8/1

Y1 - 2019/8/1

N2 - Rheumatoid polyarthritis (RA) is an autoimmune disease with autoantibodies, including antibodies to citrullant antigens and proinflammatory cytokines, such as TNF-a and IL-6, which are involved in the induction of chronic synovitis, bone erosion, followed by deformity. Immunopathogenesis is based on the mechanisms of the breakdown of immune tolerance to its own antigens, which is characterized by an increase in the activity of T-effector cells, causing RA symptomatology. At the same time, against the background of such increased activity of effector lymphocytes, a decrease in the activity of a number of regulatory cells, including regulatory T-cells (Treg) and myeloid suppressor cells, is recorded. There is reason to say that it is the change in the activity of suppressor cells that is the leading element in RA pathogenesis. That is why only periods of weakening (remission) of RA are spoken of. According to the more powerful female immune system compared to the male one, the risk of developing RA in women is thrice as high, this risk decreases during breastfeeding and grows during pregnancy as well as after menopause in proportion to the level of sex hormones. It is believed that 50 % of the risk of developing RA depends on the conditions and lifestyle, while the remaining 50 % is dependent on genetic predisposition. That is why, RA fits the main idea of postgenomic predictive-preventive personalized medicine that is to give a chance to those who would like to reduce his/her risk of diseases by bringing his/her conditions and lifestyle in line with the data on his/her genome sequenced. This is very important, since doctors consider RA as one of the most frequent causes of disability. Using the Web service SNP_TATA_Z-tester (http://beehive.bionet.nsc.ru/cgi-bin/mgs/tatascan_fox/start.pl), 227 variants of single nucleotide polymorphism (SNP) of the human gene promoters were studied. As a result, 43 candidate SNP markers for RA that can alter the affinity of the TATA-binding protein (TBP) for the promoters of these genes were predicted.

AB - Rheumatoid polyarthritis (RA) is an autoimmune disease with autoantibodies, including antibodies to citrullant antigens and proinflammatory cytokines, such as TNF-a and IL-6, which are involved in the induction of chronic synovitis, bone erosion, followed by deformity. Immunopathogenesis is based on the mechanisms of the breakdown of immune tolerance to its own antigens, which is characterized by an increase in the activity of T-effector cells, causing RA symptomatology. At the same time, against the background of such increased activity of effector lymphocytes, a decrease in the activity of a number of regulatory cells, including regulatory T-cells (Treg) and myeloid suppressor cells, is recorded. There is reason to say that it is the change in the activity of suppressor cells that is the leading element in RA pathogenesis. That is why only periods of weakening (remission) of RA are spoken of. According to the more powerful female immune system compared to the male one, the risk of developing RA in women is thrice as high, this risk decreases during breastfeeding and grows during pregnancy as well as after menopause in proportion to the level of sex hormones. It is believed that 50 % of the risk of developing RA depends on the conditions and lifestyle, while the remaining 50 % is dependent on genetic predisposition. That is why, RA fits the main idea of postgenomic predictive-preventive personalized medicine that is to give a chance to those who would like to reduce his/her risk of diseases by bringing his/her conditions and lifestyle in line with the data on his/her genome sequenced. This is very important, since doctors consider RA as one of the most frequent causes of disability. Using the Web service SNP_TATA_Z-tester (http://beehive.bionet.nsc.ru/cgi-bin/mgs/tatascan_fox/start.pl), 227 variants of single nucleotide polymorphism (SNP) of the human gene promoters were studied. As a result, 43 candidate SNP markers for RA that can alter the affinity of the TATA-binding protein (TBP) for the promoters of these genes were predicted.

KW - Gene

KW - Gene expression

KW - Promoter

KW - Rheumatoid polyarthritis (RA)

KW - Significant change

KW - Single nucleotide polymorphism (SNP)

KW - SNP-marker

KW - TATA binding protein (TBP)

KW - TBP-binding site (TATA box)

KW - TBP-promoter affinity

KW - NITRIC-OXIDE SYNTHASE

KW - rheumatoid polyarthritis (RA)

KW - LECTIN

KW - promoter

KW - BOX POLYMORPHISMS

KW - gene

KW - RISK

KW - POLYMERASE-II TRANSCRIPTION

KW - DEFICIENCY

KW - HUMAN HEREDITARY-DISEASES

KW - significant change

KW - single nucleotide polymorphism (SNP)

KW - DNA

KW - PATIENT

KW - EXPRESSION

KW - gene expression

UR - http://www.scopus.com/inward/record.url?scp=85081964876&partnerID=8YFLogxK

U2 - 10.18699/VJ19.586

DO - 10.18699/VJ19.586

M3 - Article

AN - SCOPUS:85081964876

VL - 23

SP - 1047

EP - 1058

JO - Вавиловский журнал генетики и селекции

JF - Вавиловский журнал генетики и селекции

SN - 2500-0462

IS - 8

ER -