Renormalization of Polyakov loops in fundamental and higher representations

We compare two renormalization procedures, one based on the short distance behavior of heavy quark-antiquark free energies and the other by using bare Polyakov loops at different temporal extent of the lattice and find that both prescriptions are equivalent, resulting in renormalization constants that depend on the bare coupling. Furthermore these renormalization constants show Casimir scaling for higher representations of the Polyakov loops. The analysis of Polyakov loops in different representations of the color SU(3) group indicates that a simple perturbative inspired relation in terms of the quadratic Casimir operator is realized to a good approximation at temperatures T \gsim T_c for renormalized as well as bare loops. In contrast to a vanishing Polyakov loop in representations with non-zero triality in the confined phase, the adjoint loops are small but non-zero even for temperatures below the critical one. The adjoint quark-antiquark pairs exhibit screening. This behavior can be related to the binding energy of gluelump states.Comment: 7 pages, 11 figures. Presented at 25th International Symposium on Lattice Field Theory, Regensburg, Germany, 30 Jul - 4 Aug 200

Color Screening and Quark-Quark Interactions in Finite Temperature QCD

We analyze the screening of static diquark sources in 2-flavor QCD and compare results with the screening of static quark-antiquark pairs. We show that a two quark system in a fixed color representations is screened at short distances like a single quark source in the same color representation whereas at large distances the two quarks are screened independently. At high temperatures we observe that the relative strength of the interaction in diquark and quark-antiquark systems, respectively, obeys Casimir scaling. We use this result to examine the possible existence of heavy quark-quark bound states in the high temperature phase of QCD. We find support for the existence of $bb$ states up to about $2T_c$ while $cc$ states are unlikely to be formed above $T_c$.Comment: 8 pages, 6 figure

Evidence for aggregation of protein kinase CK2 in the cell: a novel strategy for studying CK2 holoenzyme interaction by BRET2

Protein kinase CK2 is a ubiquitous pro-survival kinase whose substrate targets are involved in various cellular processes. Crystal structure analysis confirmed constitutive activity of the kinase, yet CK2 activity regulation in the cell is still obscure. In-vitro studies suggest autoinhibitory aggregation of the hetero-tetrameric CK2 holoenzyme as a basis for CK2 regulation. In this study, we applied bioluminescent resonance energy transfer (BRET) technology to investigate CK2 holoenzyme aggregation in living cells. We designed a BRET2 pair consisting of the fusion proteins CK2 alpha-Rluc8 and CK2 alpha-GFP(2). This BRET2 sensor reported specific interaction of CK2 holoenzyme complexes. Furthermore, the BRET2 sensor was applied to study modulators of CK2 aggregation. We found that CK2 aggregation is not static and can be influenced by the CK2-binding protein alpha subunit of the heterotrimeric G-protein that stimulates adenylyl cyclase (G(alpha s)) and the polycationic compound polylysine. G(alpha s), but not the CK2 substrate beta-arrestin2, decreased the BRET2 signal by up to 50 %. Likewise polylysine, but not the CK2 inhibitor DRB, decreased the signal in a dose-dependent manner up to 50 %. For the first time, we present direct experimental evidence for CK2 holoenzyme aggregates in the cell. Our data suggest that CK2 activity may be controlled by holoenzyme aggregation, to our knowledge a novel mechanism for protein kinase regulation. Moreover, the BRET2 sensor used in our study is a novel tool for studying CK2 regulation by aggregation and pharmacological screening for novel allosteric CK2 effectors

Epigenetic Repression of Androgen Receptor Transcription in Mutation-Negative Androgen Insensitivity Syndrome (AIS Type II)

Context: Inactivating mutations within the AR gene are present in only ~40% of individuals with clinically and hormonally diagnosed androgen insensitivity syndrome (AIS). Previous studies revealed the existence of an AR gene mutation-negative group of patients with AIS who have compromised androgen receptor (AR) function (AIS type II). Objective: To investigate whether AIS type II can be due to epigenetic repression of AR transcription. Design: Quantification of AR mRNA and AR proximal promoter CpG methylation levels in genital skin-derived fibroblasts (GFs) derived from patients with AIS type II and control individuals. Setting: University hospital endocrine research laboratory. Patients: GFs from control individuals (n = 11) and patients with AIS type II (n = 14). Main Outcome Measure(s): Measurement of AR mRNA and AR promoter CpG methylation as well as activity of AR proximal promoter in vitro. Results: Fifty-seven percent of individuals with AIS type II (n = 8) showed a reduced AR mRNA expression in their GFs. A significant inverse correlation was shown between AR mRNA abundance and methylation at two consecutive CpGs within the proximal AR promoter. Methylation of a 158-bp-long region containing these CpGs was sufficient to severely reduce reporter gene expression. This region was bound by the runt related transcription factor 1 (RUNX1). Ectopic expression of RUNX1 in HEK293T cells was able to inhibit reporter gene expression through this region. Conclusions: Aberrant CpGs methylation within the proximal AR promoter plays an important role in the control of AR gene expression and may result in AIS type II. We suggest that transcriptional modifiers, such as RUNX1, could play roles therein offering new perspectives for understanding androgen-mediated endocrine diseases

Epigenetic Repression of Androgen Receptor Transcription in Mutation-Negative Androgen Insensitivity Syndrome (AIS Type II)

Context: Inactivating mutations within the AR gene are present in only ~40% of individuals with clinically and hormonally diagnosed androgen insensitivity syndrome (AIS). Previous studies revealed the existence of an AR gene mutation-negative group of patients with AIS who have compromised androgen receptor (AR) function (AIS type II). Objective: To investigate whether AIS type II can be due to epigenetic repression of AR transcription. Design: Quantification of AR mRNA and AR proximal promoter CpG methylation levels in genital skin-derived fibroblasts (GFs) derived from patients with AIS type II and control individuals. Setting: University hospital endocrine research laboratory. Patients: GFs from control individuals (n = 11) and patients with AIS type II (n = 14). Main Outcome Measure(s): Measurement of AR mRNA and AR promoter CpG methylation as well as activity of AR proximal promoter in vitro. Results: Fifty-seven percent of individuals with AIS type II (n = 8) showed a reduced AR mRNA expression in their GFs. A significant inverse correlation was shown between AR mRNA abundance and methylation at two consecutive CpGs within the proximal AR promoter. Methylation of a 158-bp-long region containing these CpGs was sufficient to severely reduce reporter gene expression. This region was bound by the runt related transcription factor 1 (RUNX1). Ectopic expression of RUNX1 in HEK293T cells was able to inhibit reporter gene expression through this region. Conclusions: Aberrant CpGs methylation within the proximal AR promoter plays an important role in the control of AR gene expression and may result in AIS type II. We suggest that transcriptional modifiers, such as RUNX1, could play roles therein offering new perspectives for understanding androgen-mediated endocrine diseases