Quark-gluon vertex in general kinematics

The original publication can be found at www.springerlink.com Submitted to Cornell University’s online archive www.arXiv.org in 2007 by Jon-Ivar Skullerud. Post-print sourced from www.arxiv.org.We compute the quark–gluon vertex in quenched lattice QCD in the Landau gauge, using an off-shell mean-field O(a)-improved fermion action. The Dirac-vector part of the vertex is computed for arbitrary kinematics. We find a substantial infrared enhancement of the interaction strength regardless of the kinematics.Ayse Kizilersu, Derek B. Leinweber, Jon-Ivar Skullerud and Anthony G. William

Human promoter CTAG1A and modified constructs.

<p>(<b>a</b>) The 535 base pair long promoter region of human gene CTAG1A is rich in CpGs and exhibits α-scores higher than the genomic distribution with pronounced peaks. Shown are the composite α_k-scores (top), the individual α_k-scores for different sizes of <i>k</i> in the middle graph (colour coded, blue = negative, red/orange = positive), and CpGs in yellow (bottom). The three strongest regions are marked by red bars. (<b>b</b>) In-vitro activity of the original CTAG1A promoter (hCTAG1A Promoter), the three strongest α-score regions deleted (hCTAG1A delta), the three strongest α-score regions replaced with sequences from the genomic concatomer (hCTAG1A replace), and the three strongest α-score regions replaced with sequences from the promoter-like concatomer (hCTAG1A UP). Also shown are results without any promoter (Negative CO) and the SV40 core promoter (SV40 Promoter AVG).</p

<i>In-vitro</i> promoter activity driven by artificial constructs.

<p>Artificial constructs ArS110, ArS300, ArS201 and ArS232 exhibit strong promoter activity driving a reporter gene (firefly luciferase, internally normalized by renilla luciferase) in mammalian cell lines: (<b>a</b>) CHO/hamster, (<b>b</b>) P19/mouse, (<b>c</b>) VERO/monkey, (<b>d</b>) HEK293/human, but not in (<b>e</b>) the insect cell line Sf9/army worm. Also shown are the negative control (−) and the SV40 core promoter activity (+). (<b>f</b>) TATA-boxes 1 (left) and 2 (right) were deleted from construct ArS232: deletion of TATA-box 1 only (dT1) results in lack of activity, deletion of TATA-box 2 (dT2) does not change expression levels, while deletion of both (dT1&2) results in slightly increased expression levels.</p

Calculation of the binding constants <i>k</i>_on, <i>k</i>_off, and <i>K_D</i> for the TFIIB binding assays.

<p>Calculation of the binding constants <i>k</i>_on, <i>k</i>_off, and <i>K_D</i> for the TFIIB binding assays.</p

Binding affinity of artificial promoter constructs to the transcription factors TFIIB and TBP.

<p>The binding expressed as Δnm on the y-axis was monitored in real time as sec (x-axis), using the ForteBio Octet QK instrument. Binding was conducted in four phases: (i) loading of biotinylated DNA fragments to the streptavidin biosensor tip, (ii) washing in Kinetics Buffer, (iii) association of the transcription factor and (iii) dissociation of the transcription factor. (<b>a</b>) The promoter constructs ArS110, ArS201, ArS232 and ArS300 show similar binding affinities to the TFIIB protein. (<b>b</b>) The promoter constructs ArS232, ArS232 dT1, ArS232 dT2 and ArS232 dT12 exhibit sequence-specific binding to the TBP protein. ArS232 dT12 lacking two TATA-Boxes shows the lowest binding affinity compared to the other constructs. (<b>c</b>) TFIIB binding vs. a negative control, for which we chose a 85 bp long sequence from inside the coding region of the luciferase gene (pGL3-Basic Promoter Promega: 1314 bp–1399 bp).</p

List of significantly associated haplotypes.

<p>List of significantly associated haplotypes.</p

Differentially expressed genes by the risk alleles at 29 Mb and 33 Mb play important role in T-cell immunity.

<p>A. The risk allele at the 29 Mb at homozygous state has a clear cis-regulation effect on the expression levels of <i>TRPC6</i>, <i>KIAA1377</i>, and <i>ANGPTL5</i>, three of the most proximal genes. <i>BIRC3</i>, which is also proximal to the 29 Mb risk locus, had a significant p-value, however the FDR value was slightly above the threshold of 0.05. The risk allele at 29 Mb was also associated with a regulatory effect on genes near the 33 Mb locus and a change in the expression of <i>PIK3R6</i> significantly. B. A large network of molecules that play a major role in activation of T-lymphocyte and other immune cells (IPA category: cell-to-cell signaling and interaction, hematological system development and function). This network includes 15 molecules of which expressions are significantly altered in individuals carrying at least one copy of the shared risk allele at the 33 Mb locus. The outcomes of such expression changes are significantly linked to decrease in T-cell activation.</p

Top 10 differentially expressed genes by the risk haplotype at each locus.

<p>Top 10 differentially expressed genes by the risk haplotype at each locus.</p

Two neighboring loci on chromosome 5 are independently associated with disease risk.

<p>A. The top SNP of the first peak (29 Mb) is in high LD with nearby variants and shows no evidence of linkage to the top SNPs in the second peak (33 Mb). B. The 29 Mb peak is comprised of two haplotype blocks, and C. the risk haplotypes for the 29 Mb peak are rather common in the population. Similarly, D. the second peak also shows no linkage with the first peak in the combined analysis, whereas E. analysis of only B-cell lymphoma shows SNPs in strong LD within the second peak and in moderate LD with SNPs in the first peak. The top SNPs in the combined analysis and B-cell-lymphoma-only analysis are independent, and F. make up separate haplotypes at the second locus. G. Both risk haplotypes at the second locus are rare. Color-coding of SNPs in A, D, E, reflects their r² value relative the top SNP of that region, ranging from grey (not in LD) to red (strong LD).</p