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Found 34611 matches. Displaying 121-130
Wong ET, Liao GP, Chang JC, Xu P, Li YM, Greengard P
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GSAP modulates gamma-secretase specificity by inducing conformational change in PS1

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2019 MAR 26; 116(13):6385-6390
The mechanism by which gamma-secretase activating protein (GSAP) regulates gamma-secretase activity has not yet been elucidated. Here, we show that knockout of GSAP in cultured cells directly reduces gamma-secretase activity for A beta production, but not for Notch1 cleavage, suggesting that GSAP may induce a conformational change contributing to the specificity of gamma-secretase. Furthermore, using an active-site-directed photoprobe with double cross-linking moieties, we demonstrate that GSAP modifies the orientation and/or distance of the PS1 N-terminal fragment and the PS1 C-terminal fragment, a region containing the active site of gamma-secretase. This work offers insight into how GSAP regulates gamma-secretase specificity.
Bonito-Oliva A, Schedin-Weiss S, Younesi SS, Tiiman A, Adura C, Paknejad N, Brendel M, Romin Y, Parchem RJ, Graff C, Vukojevic V, Tjernberg LO, Terenius L, Winblad B, Sakmar TP, Graham WV
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Conformation-specific antibodies against multiple amyloid protofibril species from a single amyloid immunogen

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 2019 MAR; 23(3):2103-2114
We engineered and employed a chaperone-like amyloid-binding protein Nucleobindin 1 (NUCB1) to stabilize human islet amyloid polypeptide (hIAPP) protofibrils for use as immunogen in mice. We obtained multiple monoclonal antibody (mAb) clones that were reactive against hIAPP protofibrils. A secondary screen was carried out to identify clones that cross-reacted with amyloid beta-peptide (A beta 42) protofibrils, but not with A beta 40 monomers. These mAbs were further characterized in several in vitro assays, in immunohistological studies of a mouse model of Alzheimer's disease (AD) and in AD patient brain tissue. We show that mAbs obtained by immunizing mice with the NUCB1-hIAPP complex cross-react with A beta 42, specifically targeting protofibrils and inhibiting their further aggregation. In line with conformation-specific binding, the mAbs appear to react with an intracellular antigen in diseased tissue, but not with amyloid plaques. We hypothesize that the mAbs we describe here recognize a secondary or quaternary structural epitope that is common to multiple amyloid protofibrils. In summary, we report a method to create mAbs that are conformation-sensitive and sequence-independent and can target more than one type of protofibril species.
Ahn HJ, Baker SK, Norris EH, Strickland S
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Inflaming the Brain

NEURON 2019 MAR 20; 101(6):991-993
Exactly how cerebrovascular alterations contribute to Alzheimer's disease (AD) is still unknown. Merlini et al. (2019) show that blood-derived fibrinogen leads to dendritic spine elimination and cognitive deficit via microglial CD11b/CD18. Fibrinogen may be a significant contributor to AD pathogenesis.
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Ruggles T, Savin A, Smith N, Smith WH, Woods N
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Search for t(t)over-barH production in the H -> b(b)over-bar decay channel with leptonic t(t)over-bar decays in proton-proton collisions at root s=13 TeV

JOURNAL OF HIGH ENERGY PHYSICS 2019 MAR 5; ?(3):? Article 026
A search is presented for the associated production of a standard model Higgs boson with a top quark-antiquark pair (ttH), in which the Higgs boson decays into a b quark-antiquark pair, in proton-proton collisions at a centre-of-mass energy =13 TeV. The data correspond to an integrated luminosity of 35.9 fb(-1) recorded with the CMS detector at the CERN LHC. Candidate ttH events are selected that contain either one or two electrons or muons from the t decays and are categorised according to the number of jets. Multivariate techniques are employed to further classify the events and eventually discriminate between signal and background. The results are characterised by an observed tH signal strength relative to the standard model cross section, = sigma/sigma(SM), under the assumption of a Higgs boson mass of 125 GeV. A combined fit of multivariate discriminant distributions in all categories results in an observed (expected) upper limit on of 1.5 (0.9) at 95% confidence level, and a best fit value of 0.72 +/- 0.24(stat) +/- 0.38(syst), corresponding to an observed (expected) signal significance of 1.6 (2.2) standard deviations above the background-only hypothesis.
Sheline YI, Liston C, McEwen BS
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Parsing the Hippocampus in Depression: Chronic Stress, Hippocampal Volume, and Major Depressive Disorder

BIOLOGICAL PSYCHIATRY 2019 MAR 15; 85(6):436-438
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Ruggles T, Savin A, Smith N, Smith WH, Woods N
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Search for top quark partners with charge 5/3 in the same-sign dilepton and single-lepton final states in proton-proton collisions at root s=13 TeV

JOURNAL OF HIGH ENERGY PHYSICS 2019 MAR 14; ?(3):? Article 082
A search for the pair production of heavy fermionic partners of the top quark with charge 5/3 (X-5/3) is performed in proton-proton collisions at a center-of-mass energy of 13 TeV with the CMS detector at the CERN LHC. The data sample analyzed corresponds to an integrated luminosity of 35.9 fb(-1). The X-5/3 quark is assumed always to decay into a top quark and a W boson. Both the right-handed and left-handed X-5/3 couplings to the W boson are considered. Final states with either a pair of same-sign leptons or a single lepton are studied. No significant excess of events is observed above the expected standard model background. Lower limits at 95% confidence level on the X-5/3 quark mass are set at 1.33 and 1.30 TeV respectively for the case of right-handed and left-handed couplings to W bosons in a combination of the same-sign dilepton and single-lepton final states.
Brunner PM, Israel A, Leonard A, Pavel AB, Kim HJ, Zhang N, Czarnowicki T, Patel K, Murphrey M, Ramsey K, Rangel S, Zebda R, Soundararajan V, Zheng XZ, Estrada YD, Xu H, Krueger JG, Paller AS, Guttman-Yassky E
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Distinct transcriptomic profiles of early-onset atopic dermatitis in blood and skin of pediatric patients

ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY 2019 MAR; 122(3):318-330.e3
Background: Atopic dermatitis (AD) predominantly affects young children, but our understanding of AD pathogenesis is based on skin and blood samples from long-standing adult AD. Genomic biopsy profiling from early pediatric AD showed significant Th2 and Th17/Th22-skewing, without the characteristic adult Th1 up-regulation. Because obtaining pediatric biopsies is difficult, blood gene expression profiling may provide a surrogate for the pediatric skin signature. Objective: To define the blood profile and associated biomarkers of early moderate-to-severe pediatric AD. Methods: We compared microarrays and reverse transcription polymerase chain reaction (RT-PCR) of blood cells from 28 AD children (<5 years and within 6 months of disease onset) to healthy control blood cells. Differentially expressed genes (DEGs) in blood (fold change [FCH] > 1.2 and false discovery rate [FDR] < 0.05) were then compared with skin DEGs. Results: Eosinophil and Th2 markers (IL5RA, IL1RL1/ST2, HRH4, CCR3, SIGLEC8, PRSS33, CLC from gene arrays; IL13/IL4/CCL22 from RT-PCR) were up-regulated in early pediatric AD blood, whereas IFNG/Th1 was decreased. Th1 markers were negatively correlated with clinical severity (EASI, pruritus, transepidermal water loss [TEWL]), whereas Th2/Th17-induced interleukin (IL)-19 was positively correlated with SCORAD. Although a few RT-PCR-defined immune markers (IL-13/CCL22) were increased in blood, as previously also reported for skin, minimal overlap based on gene array DEGs was seen. Conclusion: The whole blood signature of early moderate-to-severe pediatric AD blood cells show predominantly a Th2/eosinophil profile; however, markers largely differ from the skin profile. Given their complementarity, pooling of biomarkers from blood and skin may improve profiling and predictions, providing insight regarding disease course, allergic comorbidity development, and response to systemic medications. (C) 2018 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
Zheng QF, Omans ND, Leicher R, Osunsade A, Agustinus AS, Finkin-Groner E, D'Ambrosio H, Liu B, Chandarlapaty S, Liu SX, David Y
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Reversible histone glycation is associated with disease-related changes in chromatin architecture

NATURE COMMUNICATIONS 2019 MAR 20; 10(?):? Article 1289
Cellular proteins continuously undergo non-enzymatic covalent modifications (NECMs) that accumulate under normal physiological conditions and are stimulated by changes in the cellular microenvironment. Glycation, the hallmark of diabetes, is a prevalent NECM associated with an array of pathologies. Histone proteins are particularly susceptible to NECMs due to their long half-lives and nucleophilic disordered tails that undergo extensive regulatory modifications; however, histone NECMs remain poorly understood. Here we perform a detailed analysis of histone glycation in vitro and in vivo and find it has global ramifications on histone enzymatic PTMs, the assembly and stability of nucleosomes, and chromatin architecture. Importantly, we identify a physiologic regulation mechanism, the enzyme DJ-1, which functions as a potent histone deglycase. Finally, we detect intense histone glycation and DJ-1 overexpression in breast cancer tumors. Collectively, our results suggest an additional mechanism for cellular metabolic damage through epigenetic perturbation, with implications in pathogenesis.
Oyarzabal A, Marin-Valencia I
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Synaptic energy metabolism and neuronal excitability, in sickness and health

JOURNAL OF INHERITED METABOLIC DISEASE 2019 MAR; 42(2):220-236
Most of the energy produced in the brain is dedicated to supporting synaptic transmission. Glucose is the main fuel, providing energy and carbon skeletons to the cells that execute and support synaptic function: neurons and astrocytes, respectively. It is unclear, however, how glucose is provided to and used by these cells under different levels of synaptic activity. It is even more unclear how diseases that impair glucose uptake and oxidation in the brain alter metabolism in neurons and astrocytes, disrupt synaptic activity, and cause neurological dysfunction, of which seizures are one of the most common clinical manifestations. Poor mechanistic understanding of diseases involving synaptic energy metabolism has prevented the expansion of therapeutic options, which, in most cases, are limited to symptomatic treatments. To shed light on the intersections between metabolism, synaptic transmission, and neuronal excitability, we briefly review current knowledge of compartmentalized metabolism in neurons and astrocytes, the biochemical pathways that fuel synaptic transmission at resting and active states, and the mechanisms by which disorders of brain glucose metabolism disrupt neuronal excitability and synaptic function and cause neurological disease in the form of epilepsy.
Spence JS, He RN, Hoffmann HH, Das T, Thinon E, Rice CM, Peng T, Chandran K, Hang HC
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IFITM3 directly engages and shuttles incoming virus particles to lysosomes

NATURE CHEMICAL BIOLOGY 2019 MAR; 15(3):259-268
Interferon-induced transmembrane proteins (IFITMs 1, 2 and 3) have emerged as important innate immune effectors that prevent diverse virus infections in vertebrates. However, the cellular mechanisms and live-cell imaging of these small membrane proteins have been challenging to evaluate during viral entry of mammalian cells. Using CRISPR-Cas9-mediated IFITM-mutant cell lines, we demonstrate that human IFITM1, IFITM2 and IFITM3 act cooperatively and function in a dose-dependent fashion in interferon-stimulated cells. Through site-specific fluorophore tagging and live-cell imaging studies, we show that IFITM3 is on endocytic vesicles that fuse with incoming virus particles and enhances the trafficking of this pathogenic cargo to lysosomes. IFITM3 trafficking is specific to restricted viruses, requires S-palmitoylation and is abrogated with loss-of-function mutants. The site-specific protein labeling and live-cell imaging approaches described here should facilitate the functional analysis of host factors involved in pathogen restriction as well as their mechanisms of regulation.