75 research outputs found
GRP78 Mediates Cell Growth and Invasiveness in Endometrial Cancer.
- Author
- Publication venue
- 'Wiley'
- Publication date
- 01/01/2014
- Field of study
Abstract
Recent studies have indicated that endoplasmic reticulum stress, the unfolded protein response activation and altered GRP78 expression can play an important role in a variety of tumors development and progression. Very recently we reported for the first time that GRP78 is increased in endometrial tumors. However, whether GRP78 could play a role in the growth and/or invasiveness of endometrial cancer cells is still unknown. Here we report that the silencing of GRP78 expression affects both cell growth and invasiveness of Ishikawa and AN3CA cells, analyzed by the (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and transwell migration assay, respectively. At variance with Ishikawa cells, AN3CA cells showed, besides an endoplasmic reticulum, also a plasma membrane GRP78 localization, evidenced by both immunofluorescence and cell membrane biotinylation experiments. Intriguingly, flow cytometry experiments showed that the treatment with a specific antibody targeting GRP78 C-terminal domain caused apoptosis in AN3CA but not in Ishikawa cells. Induction of apoptosis in AN3CA cells was not mediated by the p53 pathway activation but was rather associated to reduced AKT phosphorylation. Interestingly, immunofluorescence analysis evidenced that endometrioid adenocarcinoma tissues displayed, similarly to AN3CA cells, also a GRP78 plasma membrane localization. These data suggest that GRP78 and its plasma membrane localization, might play a role in endometrial cancer development and progression and might constitute a novel target for the treatment of endometrial cancer
Adenoviral gene transfer of PLD1-D4 enhances insulin sensitivity in mice by disrupting phospholipase D1 interaction with PED/PEA-15.
- Author
- Publication venue
- 'Public Library of Science (PLoS)'
- Publication date
- 01/01/2013
- Field of study
Over-expression of phosphoprotein enriched in diabetes/phosphoprotein enriched in astrocytes (PED/PEA-15) causes insulin resistance by interacting with the D4 domain of phospholipase D1 (PLD1). Indeed, the disruption of this association restores insulin sensitivity in cultured cells over-expressing PED/PEA-15. Whether the displacement of PLD1 from PED/PEA-15 improves insulin sensitivity in vivo has not been explored yet. In this work we show that treatment with a recombinant adenoviral vector containing the human D4 cDNA (Ad-D4) restores normal glucose homeostasis in transgenic mice overexpressing PED/PEA-15 (Tg ped/pea-15) by improving both insulin sensitivity and secretion. In skeletal muscle of these mice, D4 over-expression inhibited PED/PEA-15-PLD1 interaction, decreased Protein Kinase C alpha activation and restored insulin induced Protein Kinase C zeta activation, leading to amelioration of insulin-dependent glucose uptake. Interestingly, Ad-D4 administration improved insulin sensitivity also in high-fat diet treated obese C57Bl/6 mice. We conclude that PED/PEA-15-PLD1 interaction may represent a novel target for interventions aiming at improving glucose tolerance
ANKRD26 and Its Interacting Partners TRIO, GPS2, HMMR and DIPA Regulate Adipogenesis in 3T3-L1 Cells
- Author
- A Debant
- BH Spain
- C Tolg
- C Tolg
- C Yu
- CA Maxwell
- CA Maxwell
- CA Maxwell
- Charissa Kahue
- CR Jefcoate
- DW Haslam
- DY Jin
- EA Turley
- GA Raciti
- Gregory A. Raciti
- I Prokopenko
- Ira Pastan
- J Li
- J Zhang
- K Djinovic-Carugo
- K Walder
- L Fajas
- LM Lanier
- O Bezy
- P Zimmet
- QG Medley
- R Brazas
- R Sordella
- Rebecca Berdeaux
- S Sanyal
- SR Hamilton
- Tapan K. Bera
- Thelma Escobar
- TK Bera
- TM Frayling
- WK Kim
- Xiu-Fen Liu
- Y Hahn
- Z Fei
- Zhaoliang Fei
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2012
- Field of study
Partial inactivation of the Ankyrin repeat domain 26 (Ankrd26) gene causes obesity and diabetes in mice and increases spontaneous and induced adipogenesis in mouse embryonic fibroblasts. However, it is not yet known how the Ankrd26 protein carries out its biological functions. We identified by yeast two-hybrid and immunoprecipitation assays the triple functional domain protein (TRIO), the G protein pathway suppressor 2 (GPS2), the delta-interacting protein A (DIPA) and the hyaluronan-mediated motility receptor (HMMR) as ANKRD26 interacting partners. Adipogenesis of 3T3-L1 cells was increased by selective down-regulation of Ankrd26, Trio, Gps2, Hmmr and Dipa. Furthermore, GPS2 and DIPA, which are normally located in the nucleus, were translocated to the cytoplasm, when the C-terminus of ANKRD26 was introduced into these cells. These findings provide biochemical evidence that ANKRD26, TRIO, GPS2 and HMMR are novel and important regulators of adipogenisis and identify new targets for the modulation of adipogenesis
ENPP1 Affects Insulin Action and Secretion: Evidences from In Vitro Studies
- Author
- A Belfiore
- A Marucci
- A Pizzuti
- A Virkamaki
- Antonella Marucci
- BA Maddux
- BA Maddux
- BA Maddux
- BF Voight
- BV Costanzo
- C Miele
- CA Aspinwall
- Claudia Dimatteo
- Claudia Iadicicco
- Claudia Miele
- CN Chin
- CR Kahn
- Cristina Parrino
- CW Liew
- Dora Sudano
- E Bernal-Mizrachi
- ES Stolerman
- F Andreozzi
- F Oriente
- FB Stentz
- Francesco Beguinot
- GA Raciti
- H Dong
- HH Zhou
- ID Goldfine
- J Liang
- JC Parker
- JH Warram
- JO Clausen
- K Almind
- K Maedler
- K Otani
- Kathrin Maedler
- L Clare
- L Frittitta
- L Frittitta
- Lucia Frittitta
- M Anello
- M Stumvoll
- ML Hribal
- N Abate
- N Grarup
- Nunzia Caporarello
- O Porzio
- P Marchetti
- P Marchetti
- Piero Marchetti
- R Baratta
- RA DeFronzo
- RN Kulkarni
- Rosa Di Paola
- S Bacci
- S Bacci
- S Del Guerra
- S Lillioja
- S Prudente
- S Prudente
- S Prudente
- S Prudente
- S Teno
- Sabrina Prudente
- Salvatore Piro
- Silvia Del Guerra
- T Okada
- Vincenzo Trischitta
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2011
- Field of study
The aim of this study was to deeper investigate the mechanisms through which
ENPP1, a negative modulator of insulin receptor (IR) activation, plays a role on
insulin signaling, insulin secretion and eventually glucose metabolism. ENPP1
cDNA (carrying either K121 or Q121 variant) was transfected in HepG2 liver-, L6
skeletal muscle- and INS1E beta-cells. Insulin-induced IR-autophosphorylation
(HepG2, L6, INS1E), Akt-Ser473,
ERK1/2-Thr202/Tyr204 and GSK3-beta Ser9
phosphorylation (HepG2, L6), PEPCK mRNA levels (HepG2) and
2-deoxy-D-glucose uptake (L6) was studied. GLUT 4 mRNA
(L6), insulin secretion and caspase-3 activation (INS1E) were also investigated.
Insulin-induced IR-autophosphorylation was decreased in HepG2-K, L6-K, INS1E-K
(20%, 52% and 11% reduction vs. untransfected cells) and
twice as much in HepG2-Q, L6-Q, INS1E-Q (44%, 92% and 30%).
Similar data were obtained with Akt-Ser473,
ERK1/2-Thr202/Tyr204 and GSK3-beta Ser9 in
HepG2 and L6. Insulin-induced reduction of PEPCK mRNA was progressively lower in
untransfected, HepG2-K and HepG2-Q cells (65%, 54%, 23%).
Insulin-induced glucose uptake in untransfected L6 (60% increase over
basal), was totally abolished in L6-K and L6-Q cells. GLUT 4 mRNA was slightly
reduced in L6-K and twice as much in L6-Q (13% and 25% reduction
vs. untransfected cells). Glucose-induced insulin secretion was 60%
reduced in INS1E-K and almost abolished in INS1E-Q. Serum deficiency activated
caspase-3 by two, three and four folds in untransfected INS1E, INS1E-K and
INS1E-Q. Glyburide-induced insulin secretion was reduced by 50% in
isolated human islets from homozygous QQ donors as compared to those from KK and
KQ individuals. Our data clearly indicate that ENPP1, especially when the Q121
variant is operating, affects insulin signaling and glucose metabolism in
skeletal muscle- and liver-cells and both function and survival of insulin
secreting beta-cells, thus representing a strong pathogenic factor predisposing
to insulin resistance, defective insulin secretion and glucose metabolism
abnormalities
The importance of the cellular stress response in the pathogenesis and treatment of type 2 diabetes
- Author
- A Adami
- A Berdichevsky
- A Figueredo
- A Murshid
- A Nicolai
- A Panossian
- A Zisman
- AA Gupte
- AA Gupte
- AA Gupte
- AA Gupte
- AC Tsuei
- AH Lee
- AJ Bushell
- AK Sharma
- AL Hsu
- AL McMurtry
- AM Lehnen
- AM Petersen
- American Diabetes Association
- AV Nunn
- B Holmes
- BJ Gurd
- BW Tobin
- C Frosig
- CA Stuart
- CD Touchberry
- CJ Tanner
- CR Bruce
- D Ornish
- D Simar
- D Simar
- D Whitley
- DA Cunha
- DA Lepore
- DC Salo
- DH Lee
- DJ O’Gorman
- E Teixeira-Lemos
- E TeixeiradeLemos
- EA Richter
- EA Richter
- Eric Rivas
- G Balogh
- G Hu
- GA Dudley
- GA Raciti
- Gabor Balogh
- GM Strub
- GN Kraniou
- GP Holloway
- GS Hotamisligil
- HM Brown-Borg
- HR Seo
- HS Park
- I Horvath
- I Kurucz
- IP Tzanetakou
- J Campisi
- J Chung
- J Lee
- J Nishizawa
- J Rodrigues-Krause
- J Tang
- J Wang
- JA Hawley
- JC Longhurst
- JD Bartlett
- JF Tanti
- JF Wojtaszewski
- JG Eriksson
- JH Lee
- JI Joo
- JM Garcia-Lara
- JM Lash
- JO Holloszy
- JO Holloszy
- JO Holloszy
- JP McClung
- JP Yuan
- JR Daugaard
- JR Daugaard
- JR Pauli
- JR Zierath
- JS Marino
- JS Perona
- K Dokladny
- K Farmer
- K Kabayama
- K Kavanagh
- K Kavanagh
- K Kavanagh
- K Kavanagh
- K Sahin
- K Sakamoto
- K Yokoyama
- KC Silva
- KD Copps
- KD Salway
- KD Singleton
- KJ Milne
- Kylie Kavanagh
- L Brocca
- L Geurts
- L Vigh
- L Vigh
- L Wieten
- Laszlo Vigh
- M Atalay
- M Atalay
- M Balasubramanyam
- M Brameshuber
- M Furuhashi
- M Gaster
- M Kars
- M Khassaf
- M Li
- M Marini
- M Nakhjavani
- M Nakhjavani
- M Rincon
- M Ugurlucan
- MA Febbraio
- MA Kiraly
- MA Pahlavani
- MF Belotto
- MM Farnfield
- MP Harber
- MT Hamilton
- N Bobkova
- NF Wiernsperger
- NP Kadoglou
- P Garagnani
- P Wernstedt
- PC Lollo
- PD Gollnick
- PD Gollnick
- Philip L. Hooper
- PL Hooper
- PL Hooper
- PL Hooper
- PL Hooper
- PL Hooper
- R Beever
- R Mestril
- R Mestril
- RH Eckel
- RH Olsen
- RM Reznick
- RN Weijers
- RR Holman
- S Adak
- S Bhardwaj
- S Biro
- S Cho
- S Frame
- S Gielen
- S Gupta
- S Han
- S Kokura
- S Morino
- S Morino-Koga
- S Muller
- S Ringholm
- S Zanuso
- SA Leite
- SD Chou
- SE Hussey
- SH Schneider
- SZ Bathaie
- T Crul
- T Dai
- T Hara
- T Kondo
- T Mikami
- T Nomura
- T Ostergard
- T Shinohara
- TK Pandita
- U Ozcan
- V Volloch
- VL Gabai
- W Apro
- WC Knowler
- WH Dillmann
- X Xu
- XM Song
- Y Chen
- Y Liu
- Z Bromberg
- Z Luo
- Z Török
- Z Zhu
- ZP Chen
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2014
- Field of study
Organisms have evolved to survive rigorous environments and are not prepared to thrive in a world of caloric excess and sedentary behavior. A realization that physical exercise (or lack of it) plays a pivotal role in both the pathogenesis and therapy of type 2 diabetes mellitus (t2DM) has led to the provocative concept of therapeutic exercise mimetics. A decade ago, we attempted to simulate the beneficial effects of exercise by treating t2DM patients with 3 weeks of daily hyperthermia, induced by hot tub immersion. The short-term intervention had remarkable success, with a 1 % drop in HbA1, a trend toward weight loss, and improvement in diabetic neuropathic symptoms. An explanation for the beneficial effects of exercise and hyperthermia centers upon their ability to induce the cellular stress response (the heat shock response) and restore cellular homeostasis. Impaired stress response precedes major metabolic defects associated with t2DM and may be a near seminal event in the pathogenesis of the disease, tipping the balance from health into disease. Heat shock protein inducers share metabolic pathways associated with exercise with activation of AMPK, PGC1-a, and sirtuins. Diabetic therapies that induce the stress response, whether via heat, bioactive compounds, or genetic manipulation, improve or prevent all of the morbidities and comorbidities associated with the disease. The agents reduce insulin resistance, inflammatory cytokines, visceral adiposity, and body weight while increasing mitochondrial activity, normalizing membrane structure and lipid composition, and preserving organ function. Therapies restoring the stress response can re-tip the balance from disease into health and address the multifaceted defects associated with the disease
Tissue-specific methylation profile in obese patients with type 2 diabetes before and after Roux-en-Y gastric bypass
- Author
- A Bird
- A Festa
- AD Riggs
- AE Boström
- AJ Drake
- AP Feinberg
- AW Drong
- B Hidalgo
- B Lewin
- BE Bernstein
- BT Yang
- BT Yang
- C Ling
- CF Nicoletti
- CT Nguyen
- D Berglind
- Dan Linetzky Waitzberg
- Daniel Giannella-Neto
- Danielle Cristina Fonseca
- E Nilsson
- EK Nilsson
- FI Milagro
- G Toperoff
- GA Raciti
- GA Raciti
- Graziela Rosa Ravacci
- H Kirchner
- H Kirchner
- HH Hermsdorff
- I Dahlman
- J Li
- J Yan
- J Zhao
- JA Martínez
- JB Meigs
- JC Chambers
- JK Sethi
- K Hemminki
- L Shen
- LK Billings
- M Ahrens
- MC Benton
- MM Suzuki
- MS Almén
- N Ahuja
- P Kuehnen
- P Lofgren
- P Sala
- PC Sala
- PC Sala
- Priscila Sala
- R Barres
- R Barrès
- R Lister
- R Sladek
- Raquel Susana Matos de Miranda Torrinhas
- S Ito
- S Movérare-Skrtic
- S Stepanow
- SA Obermann-Borst
- SB Baylin
- SH Kao
- SH Kwak
- SJ Dijk van
- SJ Dijk van
- T Dayeh
- TA Dayeh
- VL Gloy
- WM Rideout III
- X Xu
- YF He
- ZH Liu
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Recommended from our members
Search for long-lived heavy neutral leptons with lepton flavour conserving or violating decays to a jet and a charged lepton
- Author
- Aarrestad TK
- Aarup Petersen H
- Abbaneo D
- Abbiendi G
- Abbott S
- Abbrescia M
- Abdalla H
- Abdullin S
- Abreu A
- Abu Zeid S
- Acharya H
- Acharya S
- Acosta D
- Adam W
- Adamidis K
- Adams MR
- Adams T
- Addesa FM
- Adloff C
- Adzic P
- Aebi D
- Afanasiev S
- Agapitos A
- Agarwal G
- Agram J-L
- Aguilar-Benitez M
- Agyel D
- Ahmad A
- Ahmad M
- Ahmed A
- Aimè C
- Ajmal S
- Akchurin N
- Akgun B
- Akpinar A
- Al Kadhim A
- Albrecht A
- Albrecht S
- Albrow M
- Alcaraz Maestre J
- Alcerro Alcerro LF
- Aldaya Martin M
- Aldá Júnior WL
- Aleksandrov A
- Alexander J
- Alhusseini M
- Alimena J
- Alison J
- Allmond B
- Ally D
- Almond J
- Alpana A
- Alsufyani B
- Alvarez Gonzalez B
- Alverson G
- Alves Gallo Pereira M
- Alves GA
- Aly R
- Alyari M
- Amapane N
- Ambrozas M
- Ameen MM
- Amendola C
- Amoroso S
- Amram O
- Amsler C
- An S
- An Y
- Anagnostou G
- Andrea J
- Andreev V
- Andreev Y
- Andrejkovic JW
- Andrews MB
- Androsov K
- Anguiano J
- Antchev G
- Anthony D
- Antonello M
- Apollinari G
- Apparu D
- Appelt E
- Apresyan A
- Araujo M
- Aravind A
- Arcaro D
- Arcidiacono R
- Ardino R
- Argiro S
- Arneodo M
- Aruta C
- Asawatangtrakuldee C
- Asenov P
- Asghar MI
- Asilar E
- Askew A
- Assiouras P
- Assran Y
- Atakisi IO
- Attikis A
- Auffray E
- Aushev T
- Auzinger G
- Avati V
- Avery P
- Avila C
- Awais A
- Awan MIM
- Ayala E
- Ayala G
- Aydilek O
- Azarkin M
- Azzi P
- Azzurri P
- Baarmand MM
- Babaev A
- Babbar J
- Bacchetta N
- Bachtis M
- Backhaus M
- Baden A
- Baechler J
- Bagaturia I
- Bagliesi G
- Bahinipati S
- Bainbridge R
- Bak G
- Bakas G
- Bakhshiansohi H
- Bakshi AS
- Bala A
- Baldenegro Barrera C
- Ball AH
- Bam B
- Ban Y
- Band R
- Bandyopadhyay H
- Banerjee S
- Banerjee S
- Bansal S
- Baradia S
- Barbagli G
- Barberis E
- Barbosa Trujillo DA
- Bardelli G
- Bargassa P
- Baringer P
- Barman S
- Barnes VE
- Barney D
- Barria P
- Barroso Ferreira Filho M
- Bartek R
- Bartosik N
- Bartók M
- Barzdukas A
- Basnet A
- Bastos D
- Battilana C
- Baty A
- Bauer G
- Bauerdick LAT
- Bautista I
- Baxter S
- Bayatmakou M
- Bean A
- Beauceron S
- Beaudette F
- Becerril Gonzalez H
- Bedoya CF
- Behera PK
- Behera SC
- Behnke O
- Bein S
- Beirão Da Cruz E Silva C
- Belforte S
- Bell KW
- Bellan R
- Belloni A
- Bellora A
- Belvedere A
- Belyaev A
- Belyaev A
- Benaglia A
- Benato L
- Bencze G
- Bendavid J
- Benecke A
- Benelli G
- Benitez JF
- Bennett C
- Benussi L
- Bergauer T
- Beri SB
- Bermúdez Martínez A
- Bernardes CA
- Berry D
- Berryhill J
- Besancon M
- Bestintzanos I
- Bethani A
- Bevilacqua T
- Beyrouthy T
- Bhardwaj A
- Bharthuar S
- Bhat PC
- Bhatnagar V
- Bhattacharya R
- Bhattacharya S
- Bhattacharya S
- Bhattacharya S
- Bhowmik D
- Bhowmik S
- Bhyun JH
- Bialkowska H
- Bianchini L
- Bianco M
- Bianco S
- Biino C
- Bilei GM
- Bilin B
- Bin Anuar AA
- Bin Norjoharuddeen N
- Bisello D
- Black K
- Blanco Fernández S
- Blancon B
- Blekman F
- Blend D
- Blinov V
- Bloch D
- Bloch P
- Bloom K
- Bluj M
- Blumenfeld B
- Boccali T
- Bocci A
- Bodek A
- Boimska B
- Boldrini G
- Boletti A
- Bols ES
- Bonacorsi D
- Bonanomi M
- Bonilla J
- Boos E
- Boran F
- Borca C
- Borgonovi L
- Bornheim A
- Borras K
- Borshch V
- Bortignon P
- Bose T
- Bossini E
- Botta C
- Botta V
- Bouchamaoui H
- Boudoul G
- Bouhali O
- Bourilkov D
- Bower S
- Boyaryntsev A
- Bozzo M
- Bragagnolo A
- Braghieri A
- Brainerd C
- Brandao Malbouisson H
- Branson JG
- Breedon R
- Brennan L
- Brew C
- Bright-Thonney S
- Brigljevic V
- Brinkerhoff A
- Brivio F
- Brochero Cifuentes JA
- Brom J-M
- Brommer S
- Brondolin E
- Brooke JJ
- Brown CE
- Brown RM
- Bruno G
- Bruschini D
- Bryant P
- Brzhechko D
- Brücken E
- Bubanja I
- Bucci R
- Buchmuller O
- Buchot Perraguin A
- Budkouski D
- Bueghly J
- Bundock A
- Bunichev V
- Bunkowski K
- Buontempo S
- Burkart M
- Burkett K
- Bury F
- Busson P
- Busza W
- Butalla S
- Butler JN
- Butler PH
- Butz E
- Bylsma B
- Bärtschi P
- Cabrera A
- Cabrillo IJ
- Cacchio V
- Cadamuro L
- Cagnotta A
- Caillol C
- Cakir A
- Calandri A
- Calderon De La Barca Sanchez M
- Calderon A
- Cali IA
- Calligaris L
- Calzaferri S
- Camaiani B
- Caminada L
- Campagnari C
- Campana M
- Campanini R
- Campbell A
- Camporesi T
- Candelise V
- Canelli MF
- Canepa A
- Cankocak K
- Capiluppi P
- Cappati A
- Caputo C
- Caraway B
- Cardini A
- Cardwell B
- Carlin R
- Carnahan T
- Carnevali F
- Carrera Jarrin E
- Carrigan M
- Carrillo Montoya CA
- Cartiglia N
- Carvalho W
- Casarsa M
- Cassese A
- Castaldi R
- Castaneda Hernandez A
- Castells S
- Castilla-Valdez H
- Cavallari F
- Cavallo FR
- Cavallo N
- Cavanaugh R
- Cazzaniga C
- Ceard L
- Ceccarelli R
- Cepaitis V
- Cepeda M
- Cerati GB
- Cerci S
- Cerminara G
- Cerrada M
- Cerri O
- Cetorelli F
- Chabert EC
- Chadeeva M
- Chahal GS
- Chandra S
- Chang P
- Chanon N
- Chao Y
- Charlot C
- Chatagnon P
- Chatterjee RM
- Chatterjee S
- Chatterjee S
- Chatzistavrou T
- Chaudhary G
- Chauhan S
- Chawla R
- Checchia P
- Chekhovsky V
- Chen GM
- Chen HS
- Chen KF
- Chen M
- Chen PS
- Chen X
- Chen Y
- Chen YM
- Chen Z
- Chen ZG
- Chenarani S
- Cheng C
- Cheng T
- Cherepanov V
- Chernyavskaya N
- Chertok M
- Cheung HWK
- Chhetri A
- Chiarito B
- Chinellato J
- Chistov R
- Chitroda BK
- Chiusi M
- Chlebana F
- Choi J
- Choi J
- Choi M
- Choi S
- Chou JP
- Choudhary BC
- Christoforou K
- Chudasama R
- Chwalek T
- Ciangottini D
- Ciocci MA
- Cipriani M
- Citron M
- Cittolin S
- Ciulli V
- Civinini C
- Claes DR
- Clare R
- Clement E
- Clerbaux B
- Cockerill DJA
- Coelho E
- Colaleo A
- Coldham K
- Cole JE
- Colino N
- Collard C
- Colling D
- Colombina F
- Connor P
- Consuegra Rodríguez S
- Contardo D
- Conway J
- Cooke C
- Cooper SI
- Cooperstein S
- Corcodilos L
- Cormier K
- Correia Silva G
- Cosby C
- Cossutti F
- Costa M
- Costa S
- Coubez X
- Couderc F
- Cousins R
- Covarelli R
- Cox B
- Cox PT
- Cranshaw DJ
- Creanza D
- Cremaldi LM
- Cremonesi M
- Crossman B
- Crotte Ledesma H
- Csanád M
- Csorgo T
- Cuevas J
- Cuffiani M
- Cumalat JP
- Cummings G
- Cunqueiro Mendez L
- Cussans D
- Cutts D
- Czellar S
- Da Costa EM
- Da Molin G
- Da Silveira GG
- Dabrowski A
- Dallavalle GM
- Damanakis K
- Damas F
- Damgov J
- Dancu JS
- Dansana S
- Darwish MR
- Das A
- Das AK
- Das I
- Das P
- Das S
- Daskalakis G
- Dasu S
- Datta A
- Datta K
- Dauncey P
- David A
- Davies G
- Davies J
- Davignon O
- Davis J
- de Barbaro P
- De Bruyn I
- De Coen M
- De Cosa A
- De Filippis N
- De Guio F
- De Iorio A
- De Jesus Damiao D
- De La Cruz B
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- Publication venue
- Springer Nature on behalf of SISSA
- Publication date
- 19/03/2024
- Field of study
A preprint version of the article is available at arXiv:2312.07484v3 [hep-ex], https://arxiv.org/abs/2312.07484 . Comments: Replaced with the published version. Added the journal reference and the DOI. All the figures and tables can be found at https://cms-results.web.cern.ch/cms-results/public-results/publications/EXO-21-013 (CMS Public Pages)A search for long-lived heavy neutral leptons (HNLs) is presented, which considers the hadronic final state and coupling scenarios involving all three lepton generations in the 2-20 GeV HNL mass range for the first time. Events comprising two leptons (electrons or muons) and jets are analyzed in a data sample of proton-proton collisions, recorded with the CMS experiment at the CERN LHC at a centre-of-mass energy of 13 TeV, corresponding to an integrated luminosity of 138 fb−1. A novel jet tagger, based on a deep neural network, has been developed to identify jets from an HNL decay using various features of the jet and its constituent particles. The network output can be used as a powerful discriminating tool to probe a broad range of HNL lifetimes and masses. Contributions from background processes are determined from data. No excess of events in data over the expected background is observed. Upper limits on the HNL production cross section are derived as functions of the HNL mass and the three coupling strengths VℓN to each lepton generation ℓ and presented as exclusion limits in the coupling-mass plane, as lower limits on the HNL lifetime, and on the HNL mass. In this search, the most stringent limit on the coupling strength is obtained for pure muon coupling scenarios; values of |VμN|2 > 5 (4) × 10−7 are excluded for Dirac (Majorana) HNLs with a mass of 10 GeV at a confidence level of 95% that correspond to proper decay lengths of 17 (10) mm.SCOAP3
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Measurement of the Higgs boson production via vector boson fusion and its decay into bottom quarks in proton-proton collisions at s = 13 TeV
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- Publication venue
- Springer Nature on behalf of SISSA
- Publication date
- 30/01/2024
- Field of study
A preprint version of the article is available at arXiv:2308.01253v2 [hep-ex], https://arxiv.org/abs/2308.01253v2 . Comments: Replaced with the published version. Added the journal reference and the DOI. All the figures and tables can be found at https://cms-results.web.cern.ch/cms-results/public-results/publications/HIG-22-009 (CMS Public Pages). Report number: CMS-HIG-22-009, CERN-EP-2023-110.A measurement of the Higgs boson (H) production via vector boson fusion (VBF) and its decay into a bottom quark-antiquark pair (bb¯) is presented using proton-proton collision data recorded by the CMS experiment at s√ = 13 TeV and corresponding to an integrated luminosity of 90.8 fb−1. Treating the gluon-gluon fusion process as a background and constraining its rate to the value expected in the standard model (SM) within uncertainties, the signal strength of the VBF process, defined as the ratio of the observed signal rate to that predicted by the SM, is measured to be μqqHHbb¯ = 1.01 +0.55−0.46. The VBF signal is observed with a significance of 2.4 standard deviations relative to the background prediction, while the expected significance is 2.7 standard deviations. Considering inclusive Higgs boson production and decay into bottom quarks, the signal strength is measured to be μincl.Hbb¯ = 0.99 +0.48−0.41, corresponding to an observed (expected) significance of 2.6 (2.9) standard deviations.SCOAP3, STFC; Marie-Curie program and the European Research Council and Horizon 2020 Gran
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Evidence for tWZ production in proton-proton collisions at √s=13 TeV in multilepton final states
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- Yohay R
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- Yoo J
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- Yuldashev BS
- Yusuff I
- Zabi A
- Zabolotny W
- Zacharopoulou A
- Zaleski S
- Zalewski P
- Zanetti M
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- Zehetner P
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- Zghiche A
- Zhang F
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- Ziemons T
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- Zisopoulos I
- Zoi I
- Zolkapli Z
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- Zorbilmez C
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- Zou R
- Zucchetta A
- Zuo X
- Zuolo D
- Zygala L
- Publication venue
- Elsevier BV
- Publication date
- 21/06/2024
- Field of study
Data availability - https://www.sciencedirect.com/science/article/pii/S0370269324003733?via%3Dihub#dav0001 [Release and preservation of data used by the CMS Collaboration as the basis for publications is guided by the CMS data preservation, re-use and open access policy (https://cms-docdb.cern.ch/cgi-bin/PublicDocDB/RetrieveFile?docid=6032&filename=CMSDataPolicyV1.2.pdf&version=2)]The first evidence for the standard model production of a top quark in association with a W boson and a Z boson is reported. The measurement is performed in multilepton final states, where the Z boson is reconstructed via its decays to electron or muon pairs. At least one W boson, associated or from top quark decay, decays leptonically, too. The analysed data were recorded by the CMS experiment at the CERN LHC in 2016–2018 in proton-proton collisions at √s=13 TeV, and correspond to an integrated luminosity of 138 fb−1. The measured cross section is 354±54(stat)±95(syst) fb, and corresponds to a statistical significance of 3.4 standard deviations.SCOAP
Recommended from our members
Search for new Higgs bosons via same-sign top quark pair production in association with a jet in proton-proton collisions at √s = 13 TeV
- Author
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- Aarup Petersen H
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- Yoo J
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- Yuldashev BS
- Yusuff I
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- Zehetner P
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- Zejdl P
- Zeuner WD
- Zghiche A
- Zhang F
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- Zhizhin I
- Zhokin A
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- Zorbakir IS
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- Zucchetta A
- Zumerle G
- Zuo X
- Zuolo D
- Zygala L
- Publication venue
- Elsevier
- Publication date
- 02/02/2024
- Field of study
Data availability:
Release and preservation of data used by the CMS Collaboration as the basis for publications is guided by the CMS policy as stated in “CMS data preservation, re-use and open access policy” available online at: https://cms-docdb.cern.ch/cgi-bin/PublicDocDB/RetrieveFile?docid=6032&filename=CMSDataPolicyV1.2.pdf&version=2 .A preprint of this article is available online at arXiv:2311.03261v2 [hep-ex] https://arxiv.org/abs/2311.03261v2 . Comments: Replaced with the published version. Added the journal reference and the DOI. All the figures and tables can be found at https://cms-results.web.cern.ch/cms-results/public-results/publications/TOP-22-010 (CMS Public Pages)A search is presented for new Higgs bosons in proton-proton (pp) collision events in which a same-sign top quark pair is produced in association with a jet, via the pp → tH/A → tt¯c and pp → tH/A → tt¯u processes. Here, H and A represent the extra scalar and pseudoscalar boson, respectively, of the second Higgs doublet in the generalized two-Higgs-doublet model (g2HDM). The search is based on pp collision data collected at a center-of-mass energy of 13 TeV with the CMS detector at the LHC, corresponding to an integrated luminosity of 138 fb−1. Final states with a same-sign lepton pair in association with jets and missing transverse momentum are considered. New Higgs bosons in the 200-1000 GeV mass range and new Yukawa couplings between 0.1 and 1.0 are targeted in the search, for scenarios in which either H or A appear alone, or in which they coexist and interfere. No significant excess above the standard model prediction is observed. Exclusion limits are derived in the context of the g2HDM.SCOAP3
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