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He M, Subramanian R, Bangs F, Omelchenko T, Liem KF, Kapoor TM, Anderson KV
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The kinesin-4 protein Kif7 regulates mammalian Hedgehog signalling by organizing the cilium tip compartment
NATURE CELL BIOLOGY 2014 JUL; 16(7):663-+
Mammalian Hedgehog (Hh) signal transduction requires a primary cilium, a microtubule-based organelle, and the Gli-Sufu complexes that mediate Hh signalling, which are enriched at cilia tips. Kif7, a kinesin-4 family protein, is a conserved regulator of the Hh signalling pathway and a human ciliopathy protein. Here we show that Kif7 localizes to the cilium tip, the site of microtubule plus ends, where it limits cilium length and controls cilium structure. Purified recombinant Kif7 binds the plus ends of growing microtubules in vitro, where it reduces the rate of microtubule growth and increases the frequency of microtubule catastrophe. Kif7 is not required for normal intraflagellar transport or for trafficking of Hh pathway proteins into cilia. Instead, a central function of Kif7 in the mammalian Hh pathway is to control cilium architecture and to create a single cilium tip compartment, where Gli-Sufu activity can be correctly regulated.
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Campagnari C, Danielson T, Flowers K, Geffert P, George C, Golf F, Incandela J, Justus C, Kovalskyi D, Krutelyov V, Villalba RM, Mccoll N, Pavlunin V, Richman J, Rossin R, Stuart D, To W, West C, Apresyan A, Bornheim A, Bunn J, Chen Y, Di Marco E, Duarte J, Kcira D, Ma Y, Mott A, Newman HB, Pena C, Rogan C, Spiropulu M, Timciuc V, Veverka J, Wilkinson R, Xie S, Zhu RY, Azzolini V, Calamba A, Carroll R, Ferguson T, Iiyama Y, Jang DW, Paulini M, Russ J, Vogel H, Vorobiev I, Cumalat JP, Drell BR, Ford WT, Gaz A, Lopez EL, Nauenberg U, Smith JG, Stenson K, Ulmer KA, Wagner SR, Alexander J, Chatterjee A, Eggert N, Gibbons LK, Hopkins W, Khukhunaishvili A, Kreis B, Mirman N, Kaufman GN, Patterson JR, Ryd A, Salvati E, Sun W, Teo WD, Thom J, Thompson J, Tucker J, Weng Y, Winstrom L, Wittich P, Winn D, Abdullin S, Albrow M, Anderson J, Apollinari G, Bauerdick LAT, Beretvas A, Berryhill J, Bhat PC, Burkett K, Butler JN, Chetluru V, Cheung HWK, Chlebana F, Cihangir S, Elvira VD, Fisk I, Freeman J, Gao Y, Gottschalk E, Gray L, Green D, Gutsche O, Hare D, Harris RM, Hirschauer J, Hooberman B, Jindariani S, Johnson M, Joshi U, Kaadze K, Klima B, Kunori S, Kwan S, Linacre J, Lincoln D, Lipton R, Lykken J, Maeshima K, Marraffino JM, Outschoorn VIM, Maruyama S, Mason D, McBride P, Mishra K, Mrenna S, Musienko Y, Newman-Holmes C, O'Dell V, Prokofyev O, Ratnikova N, Sexton-Kennedy E, Sharma S, Spalding WJ, Spiegel L, Taylor L, Tkaczyk S, Tran NV, Uplegger L, Vaandering EW, Vidal R, Whitmore J, Wu W, Yang F, Yun JC, Acosta D, Avery P, Bourilkov D, Cheng T, Das S, De Gruttola M, Di Giovanni GP, Dobur D, Drozdetskiy A, Field RD, Fisher M, Fu Y, Furic IK, Hugon J, Kim B, Konigsberg J, Korytov A, Kropivnitskaya A, Kypreos T, Low JF, Matchev K, Milenovic P, Mitselmakher G, Muniz L, Rinkevicius A, Skhirtladze N, Snowball M, Yelton J, Zakaria M, Gaultney V, Hewamanage S, Linn S, Markowitz P, Martinez G, Rodriguez JL, Adams T, Askew A, Bochenek J, Chen J, Diamond B, Haas J, Hagopian S, Hagopian V, Johnson KF, Prosper H, Veeraraghavan V, Weinberg M, Baarmand MM, Dorney B, Hohlmann M, Kalakhety H, Yumiceva F, Adams MR, Apanasevich L, Bazterra VE, Betts RR, Bucinskaite I, Callner J, Cavanaugh R, Evdokimov O, Gauthier L, Gerber CE, Hofman DJ, Khalatyan S, Kurt P, Moon DH, O'Brien C, Silkworth C, Strom D, Turner P, Varelas N, Akgun U, Albayrak EA, Bilki B, Clarida W, Dilsiz K, Duru F, Merlo JP, Mermerkaya H, Mestvirishvili A, Moeller A, Nachtman J, Ogul H, Onel Y, Ozok F, Sen S, Tan P, Tiras E, Wetzel J, Yetkin T, Yi K, Barnett BA, Blumenfeld B, Bolognesi S, Gritsan AV, Hu G, Maksimovic P, Martin C, Swartz M, Whitbeck A, Baringer P, Bean A, Benelli G, Kenny RP, Murray M, Noonan D, Sanders S, Stringer R, Wood JS, Barfuss AF, Chakaberia I, Ivanov A, Khalil S, Makouski M, Maravin Y, Saini LK, Shrestha S, Svintradze I, Gronberg J, Lange D, Rebassoo F, Wright D, Baden A, Calvert B, Eno SC, Gomez JA, Hadley NJ, Kellogg RG, Kolberg T, Lu Y, Marionneau M, Mignerey AC, Pedro K, Skuja A, Temple J, Tonjes MB, Tonwar SC, Apyan A, Bauer G, Busza W, Cali IA, Chan M, Di Matteo L, Dutta V, Ceballos GG, Goncharov M, Gulhan D, Kim Y, Klute M, Lai YS, Levin A, Luckey PD, Ma T, Nahn S, Paus C, Ralph D, Roland C, Roland G, Stephans GSF, Stockli F, Sumorok K, Velicanu D, Wolf R, Wyslouch B, Yang M, Yilmaz Y, Yoon AS, Zanetti M, Zhukova V, Dahmes B, De Benedetti A, Gude A, Kao SC, Klapoetke K, Kubota Y, Mans J, Pastika N, Rusack R, Singovsky A, Tambe N, Turkewitz J, Acosta JG, Cremaldi LM, Kroeger R, Oliveros S, Perera L, Rahmat R, Sanders DA, Summers D, Avdeeva E, Bloom K, Bose S, Claes DR, Dominguez A, Suarez RG, Keller J, Kravchenko I, Lazo-Flores J, Malik S, Meier F, Snow GR, Dolen J, Godshalk A, Iashvili I, Jain S, Kharchilava A, Kumar A, Rappoccio S, Wan Z, Alverson G, Barberis E, Baumgartel D, Chasco M, Haley J, Massironi A, Nash D, Orimoto T, Trocino D, Wood D, Zhang J, Anastassov A, Hahn KA, Kubik A, Lusito L, Mucia N, Odell N, Pollack B, Pozdnyakov A, Schmitt M, Stoynev S, Sung K, Velasco M, Won S, Berry D, Brinkerhoff A, Chan KM, Hildreth M, Jessop C, Karmgard DJ, Kolb J, Lannon K, Luo W, Lynch S, Marinelli N, Morse DM, Pearson T, Planer M, Ruchti R, Slaunwhite J, Valls N, Wayne M, Wolf M, Antonelli L, Bylsma B, Durkin LS, Flowers S, Hill C, Hughes R, Kotov K, Ling TY, Puigh D, Rodenburg M, Smith G, Vuosalo C, Winer BL, Wolfe H, Wulsin HW, Berry E, Elmer P, Halyo V, Hebda P, Hegeman J, Hunt A, Jindal P, Koay SA, Lujan P, Marlow D, Medvedeva T, Mooney M, Olsen J, Piroue P, Quan X, Raval A, Saka H, Stickland D, Tully C, Werner JS, Zenz SC, Zuranski A, Brownson E, Lopez A, Mendez H, Vargas JER, Alagoz E, Benedetti D, Bolla G, Bortoletto D, De Mattia M, Everett A, Hu Z, Jones M, Jung K, Koybasi O, Kress M, Leonardo N, Pegna DL, Maroussov V, Merkel P, Miller DH, Neumeister N, Shipsey I, Silvers D, Svyatkovskiy A, Wang F, Xie W, Xu L, Yoo HD, Zablocki J, Zheng Y, Parashar N, Adair A, Akgun B, Ecklund KM, Geurts FJM, Li W, Michlin B, Padley BP, Redjimi R, Roberts J, Zabel J, Betchart B, Bodek A, Covarelli R, de Barbaro P, Demina R, Eshaq Y, Ferbel T, Garcia-Bellido A, Goldenzweig P, Han J, Harel A, Miner DC, Petrillo G, Vishnevskiy D, Zielinski M, Bhatti A, Ciesielski R, Demortier L, Goulianos K, Lungu G, Malik S, Mesropian C, Arora S, Barker A, Chou JP, Contreras-Campana C, Contreras-Campana E, Duggan D, Ferencek D, Gershtein Y, Gray R, Halkiadakis E, Hidas D, Lath A, Panwalkar S, Park M, Patel R, Rekovic V, Robles J, Salur S, Schnetzer S, Seitz C, Somalwar S, Stone R, Thomas S, Thomassen P, Walker M, Rose K, Spanier S, Yang ZC, York A, Bouhali O, Eusebi R, Flanagan W, Gilmore J, Kamon T, Khotilovich V, Montalvo R, Osipenkov I, Pakhotin Y, Perloff A, Roe J, Safonov A, Sakuma T, Suarez I, Tatarinov A, Toback D, Akchurin N, Cowden C, Damgov J, Dragoiu C, Dudero PR, Kovitanggoon K, Lee SW, Libeiro T, Volobouev I, Appelt E, Delannoy AG, Greene S, Gurrola A, Johns W, Maguire C, Mao Y, Melo A, Sharma M, Sheldon P, Snook B, Tuo S, Velkovska J, Arenton MW, Boutle S, Cox B, Francis B, Goodell J, Hirosky R, Ledovskoy A, Lin C, Neu C, Wood J, Gollapinni S, Harr R, Karchin PE, Don CKK, Lamichhane P, Sakharov A, Belknap DA, Borrello L, Carlsmith D, Cepeda M, Dasu S, Duric S, Friis E, Grothe M, Hall-Wilton R, Herndon M, Herve A, Klabbers P, Klukas J, Lanaro A, Loveless R, Mohapatra A, Ojalvo I, Perry T, Pierro GA, Polese G, Ross I, Sarangi T, Savin A, Smith WH, Swanson J
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Measurement of the production cross section for a W boson and two b jets in pp collisions at root s=7 TeV
PHYSICS LETTERS B 2014 JUL 30; 735(?):204-225
The production cross section for a Wboson and two b jets is measured using proton-proton collisions at v root s = 7 TeV in a data sample collected with the CMS experiment at the LHC corresponding to an integrated luminosity of 5.0 fb(-1). The W + bbevents are selected in the W..decay mode by requiring a muon with transverse momentum pT> 25GeVand pseudorapidity |eta| < 2.1, and exactly two b-tagged jets with pT> 25GeVand |eta| < 2.4. The measured W + bbproduction cross section in the fiducial region, calculated at the level of final-state particles, is s(pp. W + bb) xB(W..) = 0.53 +/- 0.05 (stat.) +/- 0.09 (syst.) +/- 0.06 (theo.) 0.01 (lum.) pb, in agreement with the standard model prediction. In addition, kinematic distributions of the W + bbsystem are in agreement with the predictions of a simulation usingMadGraphandpythia. (C) 2014 The Authors. Published by Elsevier B. V.
Steele JW, Brautigam H, Short JA, Sowa A, Shi MX, Yadav A, Weaver CM, Westaway D, Fraser PE, St George-Hyslop PH, Gandy S, Hof PR, Dickstein DL
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Early Fear Memory Defects Are Associated With Altered Synaptic Plasticity and Molecular Architecture in the TgCRND8 Alzheimer's Disease Mouse Model
JOURNAL OF COMPARATIVE NEUROLOGY 2014 JUL 1; 522(10):2319-2335
Alzheimer's disease (AD) is a complex and slowly progressing dementing disorder that results in neuronal and synaptic loss, deposition in brain of aberrantly folded proteins, and impairment of spatial and episodic memory. Most studies of mouse models of AD have employed analyses of cognitive status and assessment of amyloid burden, gliosis, and molecular pathology during disease progression. Here we sought to understand the behavioral, cellular, ultrastructural, and molecular changes that occur at a pathological stage equivalent to the early stages of human AD. We studied the TgCRND8 mouse, a model of aggressive AD amyloidosis, at an early stage of plaque pathology (3 months of age) in comparison to their wildtype littermates and assessed changes in cognition, neuron and spine structure, and expression of synaptic glutamate receptor proteins. We found that, at this age, TgCRND8 mice display substantial plaque deposition in the neocortex and hippocampus and impairment on cued and contextual memory tasks. Of particular interest, we also observed a significant decrease in the number of neurons in the hippocampus. Furthermore, analysis of CA1 neurons revealed significant changes in apical and basal dendritic spine types, as well as altered expression of GluN1 and GluA2 receptors. This change in molecular architecture within the hippocampus may reflect a rising representation of inherently less stable thin spine populations, which can cause cognitive decline. These changes, taken together with toxic insults from amyloid- protein, may underlie the observed neuronal loss. J. Comp. Neurol. 522:2319-2335, 2014. (c) 2014 Wiley Periodicals, Inc.
Ponda MP, Mcgee D, Breslow JL
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Vitamin D-Binding Protein Levels Do Not Influence The Effect of Vitamin D Repletion on Serum PTH and Calcium: Data From a Randomized, Controlled Trial
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM 2014 JUL; 99(7):2494-2499
Context: Vitamin D deficiency, defined by the total serum 25-hydroxyvitamin D [25(OH)D] level, is common and more prevalent among Blacks than whites. Vitamin D-binding protein (DBP) levels vary with race and may modulate "bioavailable" levels of 25(OH)D. Objective: To determine the effect of DBP levels on the functional response to vitamin D. Setting and Design: A randomized, placebo-controlled trial of vitamin D repletion for 2 mo, which took place at an outpatient research unit. Participants included 150 vitamin D-deficient (25(OH)D <20 ng/mL) adults. Participants were randomly assigned to receive either 50,000 IU of vitamin D-3 or placebo weekly for 8 weeks. This is a post-hoc analysis using DBP, 25(OH)D, PTH, and calcium levels. Results: Blacks had lower total 25(OH)D (12 vs 15 ng/mL, P < .001) and DBP levels (119 vs 234 mu g/mL, < .001) than non-Blacks. DBP levels were similar before and after vitamin D-3 or placebo treatment (r = 0.98, P < .001). Baseline total 25(OH)D levels were a significant determinant of baseline PTH levels (P < .001). The change in total 25(OH)D was associated with the change in PTH (P < 0.001) and calcium levels (P = .05). In contrast, DBP levels were not a determinant of baseline PTH (P = .57) nor significantly related to changes in either PTH (P = .53) or calcium levels (P = .88). Conclusions: DBP levels are stable in Blacks and non-Blacks, and do not change with correction of vitamin D deficiency. Even for individuals with total 25(OH)D levels < 20 ng/mL, Blacks have significantly lower DBP levels than non-Blacks. However, within this range of total 25(OH)D, DBP levels do not influence the effect of vitamin D repletion on PTH or calcium levels.
Reuman DC, Gislason H, Barnes C, Melin F, Jennings S
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The marine diversity spectrum
JOURNAL OF ANIMAL ECOLOGY 2014 JUL; 83(4):963-979
Distributions of species body sizes within a taxonomic group, for example, mammals, are widely studied and important because they help illuminate the evolutionary processes that produced these distributions. Distributions of the sizes of species within an assemblage delineated by geography instead of taxonomy (all the species in a region regardless of clade) are much less studied but are equally important and will illuminate a different set of ecological and evolutionary processes. We develop and test a mechanistic model of how diversity varies with body mass in marine ecosystems. The model predicts the form of the diversity spectrum', which quantifies the distribution of species' asymptotic body masses, is a species analogue of the classic size spectrum of individuals, and which we have found to be a new and widely applicable description of diversity patterns. The marine diversity spectrum is predicted to be approximately linear across an asymptotic mass range spanning seven orders of magnitude. Slope -0 center dot 5 is predicted for the global marine diversity spectrum for all combined pelagic zones of continental shelf seas, and slopes for large regions are predicted to lie between -0 center dot 5 and -0 center dot 1. Slopes of -0 center dot 5 and -0 center dot 1 represent markedly different communities: a slope of -0 center dot 5 depicts a 10-fold reduction in diversity for every 100-fold increase in asymptotic mass; a slope of -0 center dot 1 depicts a 1 center dot 6-fold reduction. Steeper slopes are predicted for larger or colder regions, meaning fewer large species per small species for such regions. Predictions were largely validated by a global empirical analysis. Results explain for the first time a new and widespread phenomenon of biodiversity. Results have implications for estimating numbers of species of small asymptotic mass, where taxonomic inventories are far from complete. Results show that the relationship between diversity and body mass can be explained from the dependence of predation behaviour, dispersal, and life history on body mass, and a neutral assumption about speciation and extinction.
Levran O, Peles E, Randesi M, Li Y, Rotrosen J, Ott J, Adelson M, Kreek MJ
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Stress-related genes and heroin addiction: A role for a functional FKBP5 haplotype
PSYCHONEUROENDOCRINOLOGY 2014 JUL; 45(?):67-76
Background: Stress is a critical risk factor affecting both the development of and the relapse to drug addictions. Drug addictions are caused by genetic, environmental and drug-induced factors. The objective of this hypothesis-driven association study was to determine if genetic variants in stress-related genes are associated with heroin addiction. Methods: 112 selected genetic variants in 26 stress-related genes were genotyped in 852 case subjects and 238 controls of predominantly European ancestry. The case subjects are former heroin addicts with a history of at least one year of daily multiple uses of heroin, treated at a methadone maintenance treatment program (MMTP). The two most promising SNPs were subsequently tested in an African-American sample comprising of 314 cases and 208 control individuals. Results: Nineteen single nucleotide polymorphisnris (SNPs) in 9 genes (AVP, AVPR1A, CRHR1, CRHR2, FKBP5, GAL, GLRA1, NPY1R and NR3C2) showed nominally significant association with heroin addiction. The associations of two FKBP5 SNPs that are part of one haplotype block, rs1360780 (intron 2) and rs3800373 (the 3' untranslated region), remained significant after correction for multiple testing (P corrected 0.03; OR = 2.35, P corrected = 0.0018; OR = 2.85, respectively). The two SNPs also showed nominally significant association (P < 0.05) with heroin addiction in an independent African-American cohort. FKBP5 is a co-chaperone that regulates glucocorticoid sensitivity. These FKBP5 SNPs were previously associated with diverse affective disorders and showed functional differences in gene expression and stress response. This study also supports our and others' previous reports of association of the GAL SNP rs694066 and the AVPR1A SNPs rs11174811, rs1587097 and rs10784339 with heroin and general drug addiction, respectively. Conclusions: This study suggests that variations in the FKBP5 gene contribute to the development of opiate addiction by modulating the stress response. These findings may enhance the understanding of the interaction between stress and heroin addiction. (C) 2014 Elsevier Ltd. All rights reserved.
Jehi SE, Wu F, Li BB
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Trypanosoma brucei TIF2 suppresses VSG switching by maintaining subtelomere integrity
CELL RESEARCH 2014 JUL; 24(7):870-885
Subtelomeres consist of sequences adjacent to telomeres and contain genes involved in important cellular functions, as subtelomere instability is associated with several human diseases. Balancing between subtelomere stability and plasticity is particularly important for Trypanosoma brucei, a protozoan parasite that causes human African trypanosomiasis. T. brucei regularly switches its major variant surface antigen, variant surface glycoprotein (VSG), to evade the host immune response, and VSGs are expressed exclusively from subtelomeres in a strictly monoallelic fashion. Telomere proteins are important for protecting chromosome ends from illegitimate DNA processes. However, whether they contribute to subtelomere integrity and stability has not been well studied. We have identified a novel T. brucei telomere protein, T. brucei TRF-Interacting Factor 2 (TbTIF2), as a functional homolog of mammalian TIN2. A transient depletion of TbTIF2 led to an elevated VSG switching frequency and an increased amount of DNA double-strand breaks (DSBs) in both active and silent subtelomeric bloodstream form expression sites (BESs). Therefore, TbTIF2 plays an important role in VSG switching regulation and is important for subtelomere integrity and stability. TbTIF2 depletion increased the association of TbRAD51 with the telomeric and subtelomeric chromatin, and TbRAD51 deletion further increased subtelomeric DSBs in TbTIF2-depleted cells, suggesting that TbRAD51-mediated DSB repair is the underlying mechanism of subsequent VSG switching. Surprisingly, significantly more TbRAD51 associated with the active BES than with the silent BESs upon TbTIF2 depletion, and TbRAD51 deletion induced much more DSBs in the active BES than in the silent BESs in TbTIF2-depleted cells, suggesting that TbRAD51 preferentially repairs DSBs in the active BES.
Aaltonen T, Amerio S, Amidei D, Anastassov A, Annovi A, Antos J, Apollinari G, Appel JA, Arisawa T, Artikov A, Asaadi J, Ashmanskas W, Auerbach B, Aurisano A, Azfar F, Badgett W, Bae T, Barbaro-Galtieri A, Barnes VE, Barnett BA, Barria P, Bartos P, Bauce M, Bedeschi F, Behari S, Bellettini G, Bellinger J, Benjamin D, Beretvas A, Bhatti A, Bland KR, Blumenfeld B, Bocci A, Bodek A, Bortoletto D, Boudreau J, Boveia A, Brigliadori L, Bromberg C, Brucken E, Budagov J, Budd HS, Burkett K, Busetto G, Bussey P, Butti P, Buzatu A, Calamba A, Camarda S, Campanelli M, Canelli F, Carls B, Carlsmith D, Carosi R, Carrillo S, Casal B, Casarsa M, Castro A, Catastini P, Cauz D, Cavaliere V, Cavalli-Sforza M, Cerri A, Cerrito L, Chen YC, Chertok M, Chiarelli G, Chlachidze G, Cho K, Chokheli D, Clark A, Clarke C, Convery ME, Conway J, Corbo M, Cordelli M, Cox CA, Cox DJ, Cremonesi M, Cruz D, Cuevas J, Culbertson R, d'Ascenzo N, Datta M, de Barbaro P, Demortier L, Deninno M, Devoto F, D'Errico M, Di Canto A, Di Ruzza B, Dittmann JR, D'Onofrio M, Donati S, Dorigo M, Driutti A, Ebina K, Edgar R, Elagin A, Erbacher R, Errede S, Esham B, Farrington S, Feindt M, Ramos JPF, Field R, Flanagan G, Forrest R, Franklin M, Freeman JC, Frisch H, Funakoshi Y, Galloni C, Garfinkel AF, Garosi P, Gerberich H, Gerchtein E, Giagu S, Giakoumopoulou V, Gibson K, Ginsburg CM, Giokaris N, Giromini P, Giurgiu G, Glagolev V, Glenzinski D, Gold M, Goldin D, Golossanov A, Gomez G, Gomez-Ceballos G, Goncharov M, Lopez OG, Gorelov I, Goshaw AT, Goulianos K, Gramellini E, Grinstein S, Grosso-Pilcher C, Group RC, da Costa JG, Hahn SR, Han JY, Happacher F, Hara K, Hare M, Harr RF, Harrington-Taber T, Hatakeyama K, Hays C, Heck M, Heinrich J, Herndon M, Hocker A, Hong Z, Hopkins W, Hou S, Hughes RE, Husemann U, Hussein M, Huston J, Introzzi G, Iori M, Ivanov A, James E, Jang D, Jayatilaka B, Jeon EJ, Jindariani S, Jones M, Joo KK, Jun SY, Junk TR, Kambeitz M, Kamon T, Karchin PE, Kasmi A, Kato Y, Ketchum W, Keung J, Kilminster B, Kim DH, Kim HS, Kim JE, Kim MJ, Kim SB, Kim SH, Kim YK, Kim YJ, Kimura N, Kirby M, Knoepfel K, Kondo K, Kong DJ, Konigsberg J, Kotwal AV, Kreps M, Kroll J, Kruse M, Kuhr T, Kurata M, Laasanen AT, Lammel S, Lancaster M, Lannon K, Latino G, Lee HS, Lee JS, Leo S, Leone S, Lewis JD, Limosani A, Lipeles E, Lister A, Liu H, Liu Q, Liu T, Lockwitz S, Loginov A, Luca A, Lucchesi D, Lueck J, Lujan P, Lukens P, Lungu G, Lys J, Lysak R, Madrak R, Maestro P, Malik S, Manca G, Manousakis-Katsikakis A, Marchese L, Margaroli F, Marino P, Martinez M, Matera K, Mattson ME, Mazzacane A, Mazzanti P, McNulty R, Mehta A, Mehtala P, Mesropian C, Miao T, Mietlicki D, Mitra A, Miyake H, Moed S, Moggi N, Moon CS, Moore R, Morello MJ, Mukherjee A, Muller T, Murat P, Mussini M, Nachtman J, Nagai Y, Naganoma J, Nakano I, Napier A, Nett J, Neu C, Nigmanov T, Nodulman L, Noh SY, Norniella O, Oakes L, Oh SH, Oh YD, Oksuzian I, Okusawa T, Orava R, Ortolan L, Pagliarone C, Palencia E, Palni P, Papadimitriou V, Parker W, Pauletta G, Paulini M, Paus C, Phillips TJ, Piacentino G, Pianori E, Pilot J, Pitts K, Plager C, Pondrom L, Poprocki S, Potamianos K, Prokoshin F, Pranko A, Ptohos F, Punzi G, Ranjan N, Fernandez I, Renton P, Rescigno M, Rimondi F, Ristori L, Robson A, Rodriguez T, Rolli S, Ronzani M, Roser R, Rosner JL, Ruffini F, Ruiz A, Russ J, Rusu V, Sakumoto WK, Sakurai Y, Santi L, Sato K, Saveliev V, Savoy-Navarro A, Schlabach P, Schmidt EE, Schwarz T, Scodellaro L, Scuri F, Seidel S, Seiya Y, Semenov A, Sforza F, Shalhout SZ, Shears T, Shepard PF, Shimojima M, Shochet M, Shreyber-Tecker I, Simonenko A, Sliwa K, Smith JR, Snider FD, Sorin V, Song H, Stancari M, St Denis R, Stentz D, Strologas J, Sudo Y, Sukhanov A, Suslov I, Takemasa K, Takeuchi Y, Tang J, Tecchio M, Teng PK, Thom J, Thomson E, Thukral V, Toback D, Tokar S, Tollefson K, Tomura T, Tonelli D, Torre S, Torretta D, Totaro P, Trovato M, Ukegawa F, Uozumi S, Vazquez F, Velev G, Vellidis C, Vernieri C, Vidal M, Vilar R, Vizan J, Vogel M, Volpi G, Wagner P, Wallny R, Wang SM, Waters D, Wester WC, Whiteson D, Wicklund AB, Wilbur S, Williams HH, Wilson JS, Wilson P, Winer BL, Wittich P, Wolbers S, Wolfe H, Wright T, Wu X, Wu Z, Yamamoto K, Yamato D, Yang T, Yang UK, Yang YC, Yao WM, Yeh GP, Yi K, Yoh J, Yorita K, Yoshida T, Yu GB, Yu I, Zanetti AM, Zeng Y, Zhou C, Zucchelli S
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Study of orbitally excited B mesons and evidence for a new B pi resonance
PHYSICAL REVIEW D 2014 JUL 28; 90(1):? Article 012013
Using the full CDF Run II data sample, we report evidence for a new resonance, which we refer to as B(5970), found simultaneously in the B-0 pi(+) and B+pi(-) mass distributions with a significance of 4.4 standard deviations. We further report the first study of resonances consistent with orbitally excited B+ mesons and an updated measurement of the properties of orbitally excited B-0 and B-s(0) mesons. We measure the masses and widths of all states, as well as the relative production rates of the B-1, B-2*, and B(5970) states and the branching fraction of the B-s2*(0) B-s2*(0) state to either B*K-+(-) and B+K-. Furthermore, we measure the production rates of the orbitally excited B-0,B-+ states relative to the B-0,B-+ ground state. The masses of the new B(5970) resonances are 5978 +/- 5(stat) +/- 12(syst)MeV/c(2) for the neutral state and 5961 +/- 5(stat) +/- 12(syst) MeV/c(2) for the charged state, assuming that the resonance decays into B pi final states. The properties of the orbitally excited and the new B(5970)(0,+) states are compatible with isospin symmetry.
Wang WW, Whorton MR, MacKinnon R
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Quantitative analysis of mammalian GIRK2 channel regulation by G proteins, the signaling lipid PIP2 and Na+ in a reconstituted system
ELIFE 2014 JUL 20; 3(?):?
GIRK channels control spike frequency in atrial pacemaker cells and inhibitory potentials in neurons. By directly responding to G proteins, PIP2 and Na+, GIRK is under the control of multiple signaling pathways. In this study, the mammalian GIRK2 channel has been purified and reconstituted in planar lipid membranes and effects of G alpha, G beta gamma, PIP2 and Na+ analyzed. G beta gamma and PIP2 must be present simultaneously to activate GIRK2. Na+ is not essential but modulates the effect of G beta gamma and PIP2 over physiological concentrations. G alpha(i1)(GTP gamma S) has no effect, whereas G alpha(i1)(GDP) closes the channel through removal of G beta gamma. In the presence of G beta gamma, GIRK2 opens as a function of PIP2 mole fraction with Hill coefficient 2.5 and an affinity that poises GIRK2 to respond to natural variations of PIP2 concentration. The dual requirement for G beta gamma and PIP2 can help to explain why GIRK2 is activated by G(i/o), but not G(q) coupled GPCRs.
Heler R, Marraffini LA, Bikard D
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Adapting to new threats: the generation of memory by CRISPR-Cas immune systems
MOLECULAR MICROBIOLOGY 2014 JUL; 93(1):1-9
Clustered, regularly interspaced, short palindromic repeats (CRISPR) loci and their associated genes (cas) confer bacteria and archaea with adaptive immunity against phages and other invading genetic elements. A fundamental requirement of any immune system is the ability to build a memory of past infections in order to deal more efficiently with recurrent infections. The adaptive feature of CRISPR-Cas immune systems relies on their ability to memorize DNA sequences of invading molecules and integrate them in between the repetitive sequences of the CRISPR array in the form of 'spacers'. The transcription of a spacer generates a small antisense RNA that is used by RNA-guided Cas nucleases to cleave the invading nucleic acid in order to protect the cell from infection. The acquisition of new spacers allows the CRISPR-Cas immune system to rapidly adapt against new threats and is therefore termed 'adaptation'. Recent studies have begun to elucidate the genetic requirements for adaptation and have demonstrated that rather than being a stochastic process, the selection of new spacers is influenced by several factors. We review here our current knowledge of the CRISPR adaptation mechanism.