Initiation Factors

Пономаренко, М. П.; Савинкова, Л. К.; Колчанов, Н. А.

doi:10.1016/b978-0-12-374984-0.00798-1

Cited by 4 publications

(2 citation statements)

References 20 publications

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“…For the present study, it was helpful that an intermediate position between these extremes belongs to SNPs in the DNA sites binding to the TATA-binding protein (TBP); these SNPs constitute ~10% of all the known regulatory SNP markers relevant to medicine, whereas TBP is only one of 2600 known DNA-binding proteins in humans [ 31 ]. The above-mentioned special place of such SNPs can be mostly explained by the necessity of a TBP-binding site within the [−70; −20] region of the promoter for any mRNA [ 32 ] because RNA polymerase II binds to the anchoring complex TBP-promoter, and this event triggers assembly of the transcription preinitiation complex for this mRNA [ 33 ]. These results were obtained in studies on unviability of TBP -null animals [ 34 ] or animals harboring a knockdown [ 35 ] of the TBP gene.…”

Section: Introductionmentioning

confidence: 99%

How to Use SNP_TATA_Comparator to Find a Significant Change in Gene Expression Caused by the Regulatory SNP of This Gene’s Promoter via a Change in Affinity of the TATA-Binding Protein for This Promoter

Пономаренко

Рассказов

Arkova

et al. 2015

BioMed Research International

118

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The use of biomedical SNP markers of diseases can improve effectiveness of treatment. Genotyping of patients with subsequent searching for SNPs more frequent than in norm is the only commonly accepted method for identification of SNP markers within the framework of translational research. The bioinformatics applications aimed at millions of unannotated SNPs of the “1000 Genomes” can make this search for SNP markers more focused and less expensive. We used our Web service involving Fisher's Z-score for candidate SNP markers to find a significant change in a gene's expression. Here we analyzed the change caused by SNPs in the gene's promoter via a change in affinity of the TATA-binding protein for this promoter. We provide examples and discuss how to use this bioinformatics application in the course of practical analysis of unannotated SNPs from the “1000 Genomes” project. Using known biomedical SNP markers, we identified 17 novel candidate SNP markers nearby: rs549858786 (rheumatoid arthritis); rs72661131 (cardiovascular events in rheumatoid arthritis); rs562962093 (stroke); rs563558831 (cyclophosphamide bioactivation); rs55878706 (malaria resistance, leukopenia), rs572527200 (asthma, systemic sclerosis, and psoriasis), rs371045754 (hemophilia B), rs587745372 (cardiovascular events); rs372329931, rs200209906, rs367732974, and rs549591993 (all four: cancer); rs17231520 and rs569033466 (both: atherosclerosis); rs63750953, rs281864525, and rs34166473 (all three: malaria resistance, thalassemia).

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Section: Introductionmentioning

confidence: 99%

How to Use SNP_TATA_Comparator to Find a Significant Change in Gene Expression Caused by the Regulatory SNP of This Gene’s Promoter via a Change in Affinity of the TATA-Binding Protein for This Promoter

Пономаренко

Рассказов

Arkova

et al. 2015

BioMed Research International

118

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“…On the other hand, the effects of SNPs that are located in regulatory regions of genes [ 38 , 70 ] are still difficult to predict in silico [ 71 ]. Most studies in this field deal with regulatory SNPs in binding sites of TATA-binding protein (TBP) in the region [-70; -20] upstream of the transcription start of various mRNAs encoded in the human genome [ 72 , 73 ] (assembly of the preinitiation complex starts with binding of RNA polymerase to the anchoring TBP/DNA complex [ 74 , 75 ]). For this reason, model animals with a null-mutation [ 76 ] or a knockdown of TBP [ 77 ] are always inviable.…”

Section: Introductionmentioning

confidence: 99%

Obesity-related known and candidate SNP markers can significantly change affinity of TATA-binding protein for human gene promoters

et al. 2015

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BackgroundObesity affects quality of life and life expectancy and is associated with cardiovascular disorders, cancer, diabetes, reproductive disorders in women, prostate diseases in men, and congenital anomalies in children. The use of single nucleotide polymorphism (SNP) markers of diseases and drug responses (i.e., significant differences of personal genomes of patients from the reference human genome) can help physicians to improve treatment. Clinical research can validate SNP markers via genotyping of patients and demonstration that SNP alleles are significantly more frequent in patients than in healthy people. The search for biomedical SNP markers of interest can be accelerated by computer-based analysis of hundreds of millions of SNPs in the 1000 Genomes project because of selection of the most meaningful candidate SNP markers and elimination of neutral SNPs.ResultsWe cross-validated the output of two computer-based methods: DNA sequence analysis using Web service SNP_TATA_Comparator and keyword search for articles on comorbidities of obesity. Near the sites binding to TATA-binding protein (TBP) in human gene promoters, we found 22 obesity-related candidate SNP markers, including rs10895068 (male breast cancer in obesity); rs35036378 (reduced risk of obesity after ovariectomy); rs201739205 (reduced risk of obesity-related cancers due to weight loss by diet/exercise in obese postmenopausal women); rs183433761 (obesity resistance during a high-fat diet); rs367732974 and rs549591993 (both: cardiovascular complications in obese patients with type 2 diabetes mellitus); rs200487063 and rs34104384 (both: obesity-caused hypertension); rs35518301, rs72661131, and rs562962093 (all: obesity); and rs397509430, rs33980857, rs34598529, rs33931746, rs33981098, rs34500389, rs63750953, rs281864525, rs35518301, and rs34166473 (all: chronic inflammation in comorbidities of obesity). Using an electrophoretic mobility shift assay under nonequilibrium conditions, we empirically validated the statistical significance (α < 0.00025) of the differences in TBP affinity values between the minor and ancestral alleles of 4 out of the 22 SNPs: rs200487063, rs201381696, rs34104384, and rs183433761. We also measured half-life (t1/2), Gibbs free energy change (ΔG), and the association and dissociation rate constants, ka and kd, of the TBP-DNA complex for these SNPs.ConclusionsValidation of the 22 candidate SNP markers by proper clinical protocols appears to have a strong rationale and may advance postgenomic predictive preventive personalized medicine.

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Prediction and verification of the influence of the rs367781716 SNP on the interaction of the ТАТА-binding protein with the promoter of the human АВСА9 gene

Arkova

Драчкова

Arshinova

et al. 2016

Russ J Genet Appl Res

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Initiation Factors

Cited by 4 publications

References 20 publications

How to Use SNP_TATA_Comparator to Find a Significant Change in Gene Expression Caused by the Regulatory SNP of This Gene’s Promoter via a Change in Affinity of the TATA-Binding Protein for This Promoter

How to Use SNP_TATA_Comparator to Find a Significant Change in Gene Expression Caused by the Regulatory SNP of This Gene’s Promoter via a Change in Affinity of the TATA-Binding Protein for This Promoter

Obesity-related known and candidate SNP markers can significantly change affinity of TATA-binding protein for human gene promoters

Prediction and verification of the influence of the rs367781716 SNP on the interaction of the ТАТА-binding protein with the promoter of the human АВСА9 gene

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