Eigensystem multiscale analysis for the Anderson model via the Wegner estimate

We present a new approach to the eigensystem multiscale analysis (EMSA) for random Schr\"odinger operators that relies on the Wegner estimate. The EMSA treats all energies of the finite volume operator in an energy interval at the same time, simultaneously establishing localization of all eigenfunctions with eigenvalues in the energy interval with high probability. It implies all the usual manifestations of localization (pure point spectrum with exponentially decaying eigenfunctions, dynamical localization). The new method removes the restrictive level spacing hypothesis used in the previous versions of the EMSA. The method is presented in the context of the Anderson model, allowing for single site probability distributions that are H\"older continuous of order $\alpha \in (0,1]$.Comment: arXiv admin note: substantial text overlap with arXiv:1611.02650, arXiv:1509.0852

A Simplified Min-Sum Decoding Algorithm for Non-Binary LDPC Codes

Non-binary low-density parity-check codes are robust to various channel impairments. However, based on the existing decoding algorithms, the decoder implementations are expensive because of their excessive computational complexity and memory usage. Based on the combinatorial optimization, we present an approximation method for the check node processing. The simulation results demonstrate that our scheme has small performance loss over the additive white Gaussian noise channel and independent Rayleigh fading channel. Furthermore, the proposed reduced-complexity realization provides significant savings on hardware, so it yields a good performance-complexity tradeoff and can be efficiently implemented.Comment: Partially presented in ICNC 2012, International Conference on Computing, Networking and Communications. Accepted by IEEE Transactions on Communication

The DNA Binding Properties of the Parsley bZIP Transcription Factor CPRF4a Are Regulated by Light

The common plant regulatory factors (CPRFs) from parsley are transcription factors with a basic leucine zipper motif that bind to cis-regulatory elements frequently found in promoters of light-regulated genes. Recent studies have revealed that certain CPRF proteins are regulated in response to light by changes in their expression level and in their intracellular localization. Here, we describe an additional mechanism contributing to the light-dependent regulation of CPRF proteins. We show that the DNA binding activity of the factor CPRF4a is modulated in a phosphorylation-dependent manner and that cytosolic components are involved in the regulation of this process. Moreover, we have identified a cytosolic kinase responsible for CPRF4a phosphorylation. Modification of recombinant CPRF4a by this kinase, however, is insufficient to cause a full activation of the factor, suggesting that additional modifications are required. Furthermore, we demonstrate that the DNA binding activity of the factor is modified upon light treatment. The results of additional irradiation experiments suggest that this photoresponse is controlled by different photoreceptor systems. We discuss the possible role of CPRF4a in light signal transduction as well as the emerging regulatory network controlling CPRF activities in parsley

EMSA input

Brief summary of Portland State University Enrollment Management & Student Affairs input on what they believe the PSU values statement should contain

Targeting the Ets Binding Site of the HER2/neu Promoter with Pyrrole-Imidazole Polyamides

Three DNA binding polyamides (1-3) were synthesized that bind with high affinity (Ka = 8.7·10^9 M^-1 to 1.4·10^10 M^-1) to two 7-base pair sequences overlapping the Ets DNA binding site (EBS; GAGGAA) within the regulatory region of the HER2/neu proximal promoter. As measured by electrophoretic mobility shift assay, polyamides binding to flanking elements upstream (1) or downstream (2 and 3) of the EBS were one to two orders of magnitude more effective than the natural product distamycin at inhibiting formation of complexes between the purified EBS protein, epithelial restricted with serine box (ESX), and the HER2/neu promoter probe. One polyamide, 2, completely blocked Ets-DNA complex formation at 10 nM ligand concentration, whereas formation of activator protein-2-DNA complexes was unaffected at the activator protein-2 binding site immediately upstream of the HER2/neu EBS, even at 100 nM ligand concentration. At equilibrium, polyamide 1 was equally effective at inhibiting Ets/DNA binding when added before or after in vitro formation of protein-promoter complexes, demonstrating its utility to disrupt endogenous Ets-mediated HER2/neu preinitiation complexes. Polyamide 2, the most potent inhibitor of Ets-DNA complex formation by electrophoretic mobility shift assay, was also the most effective inhibitor of HER2/neu promoter-driven transcription measured in a cell-free system using nuclear extract from an ESX- and HER2/neu-overexpressing human breast cancer cell line, SKBR-3

The cellular protein nucleolin preferentially binds long-looped G-quadruplex nucleic acids

open5noBACKGROUND: G-quadruplexes (G4s) are four-stranded nucleic acid structures that form in G-rich sequences. Nucleolin (NCL) is a cellular protein reported for its functions upon G4 recognition, such as induction of neurodegenerative diseases, tumor and virus mechanisms activation. We here aimed at defining NCL/G4 binding determinants. METHODS: Electrophoresis mobility shift assay was used to detect NCL/G4 binding; circular dichroism to assess G4 folding, topology and stability; dimethylsulfate footprinting to detect G bases involved in G4 folding. RESULTS: The purified full-length human NCL was initially tested on telomeric G4 target sequences to allow for modulation of loop, conformation, length, G-tract number, stability. G4s in promoter regions with more complex sequences were next employed. We found that NCL binding to G4s heavily relies on G4 loop length, independently of the conformation and oligonucleotide/loop sequence. Low stability G4s are preferred. When alternative G4 conformations are possible, those with longer loops are preferred upon binding to NCL, even if G-tracts need to be spared from G4 folding. CONCLUSIONS: Our data provide insight into how G4s and the associated proteins may control the ON/OFF molecular switch to several pathological processes, including neurodegeneration, tumor and virus activation. Understanding these regulatory determinants is the first step towards the development of targeted therapies. GENERAL SIGNIFICANCE: The indication that NCL binding preferentially stimulates and induces folding of G4s containing long loops suggests NCL ability to modify the overall structure and steric hindrance of the involved nucleic acid regions. This protein-induced modification of the G4 structure may represent a cellular mechanosensor mechanism to molecular signaling and disease pathogenesis.openLago, Sara; Tosoni, Elena; Nadai, Matteo; Palumbo, Manlio; Richter, Sara NLago, Sara; Tosoni, Elena; Nadai, Matteo; Palumbo, Manlio; Richter, Sar

Inhibition of oncogenic transcription factor REL by the natural product derivative calafianin monomer 101 induces proliferation arrest and apoptosis in human B-lymphoma cell lines

Increased activity of transcription factor NF-κB has been implicated in many B-cell lymphomas. We investigated effects of synthetic compound calafianin monomer (CM101) on biochemical and biological properties of NF-κB. In human 293 cells, CM101 selectively inhibited DNA binding by overexpressed NF-κB subunits REL (human c-Rel) and p65 as compared to NF-κB p50, and inhibition of REL and p65 DNA binding by CM101 required a conserved cysteine residue. CM101 also inhibited DNA binding by REL in human B-lymphoma cell lines, and the sensitivity of several B-lymphoma cell lines to CM101-induced proliferation arrest and apoptosis correlated with levels of cellular and nuclear REL. CM101 treatment induced both phosphorylation and decreased expression of anti-apoptotic protein Bcl-XL, a REL target gene product, in sensitive B-lymphoma cell lines. Ectopic expression of Bcl-XL protected SUDHL-2 B-lymphoma cells against CM101-induced apoptosis, and overexpression of a transforming mutant of REL decreased the sensitivity of BJAB B-lymphoma cells to CM101-induced apoptosis. Lipopolysaccharide-induced activation of NF-κB signaling upstream components occurred in RAW264.7 macrophages at CM101 concentrations that blocked NF-κB DNA binding. Direct inhibitors of REL may be useful for treating B-cell lymphomas in which REL is active, and may inhibit B-lymphoma cell growth at doses that do not affect some immune-related responses in normal cells.R01 GM094551 - NIGMS NIH HHS; P50 GM067041 - NIGMS NIH HHS; GM094551 - NIGMS NIH HHS; R24 GM111625 - NIGMS NIH HHS; GM067041 - NIGMS NIH HH

Sequential induction of NF-κB/Rel family proteins during B-cell terminal differentiation

The NF-kappa B/Rel family of at least five transcription factor polypeptides is thought to function both as a developmental regulator in B cells and as a rapid response system in all cells. To examine this notion in more detail, we determined the protein contents of both the inducible and constitutive NF-kappa B/Rel activities in a pre-B-cell line, 70Z/3, and a mature B-cell line, WEHI 231. NF-kappa B p50/p65 is the major inducible nuclear complex after lipopolysaccharide or phorbol myristate acetate treatment of 70Z/3 cells. The constitutive and inducible complexes in WEHI 231 cells are mainly composed of p50 and Rel. The constitutive or induced activities are all sensitive to I kappa B-alpha, but this inhibitor is very short-lived in WEHI 231 cells, suggesting that the balance between synthesis and degradation of I kappa B-alpha determines whether a particular cell lineage has constitutive activity. A patterned expression of the NF-kappa B/Rel activator proteins emerges from an analysis of other B-lineage cell lines and splenic B cells: mainly p50 and p65 in pre-B (and non-B) cells, a predominance of Rel and p50 in mature B cells, and expression of p52 and RelB in plasmacytoma lines. This ordered pattern of regulators may reflect the requirement for expression of different genes during terminal B-cell differentiation because different combinations of NF-kappa B/Rel family members preferentially activate distinct kappa B sites in reporter constructs