For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
Inviting an author to review:
EPI64 protein functions as a physiological GTPase-activating protein for Rab27 protein and regulates amylase release in rat parotid acinar cells.
Find an author and click ‘Invite to review selected article’ near their name.
Search for authorsSearch for similar articles
19
views
56
references
 Top references
cited by
4
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
1 collections
    0
    shares
      4
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Identification of nuclear phosphoproteins as novel tobacco markers in mouse lung tissue following short-term exposure to tobacco smoke

      research-article
      Author(s): a , * , a , b , a , a , a , a , a , a ,   a , b , c , a , *
      Publication date (Electronic):
      Journal: FEBS Open Bio
      Publisher: Elsevier
      Keywords: COPD, chronic obstructive pulmonary disorder, FACTp140, FACT complex subunit SPT16, K18, keratin type 1 cytoskeletal 18, AFABP, adipocyte fatty acid-binding protein, OSF3, peroxiredoxin-1, SPTBN1, spectrin β chain brain 1, STAT, signal transducer and activator of transcription, IL, interleukin, K8, keratin type 2 cytoskeletal 8, PRP19, pre-mRNA-processing factor 19, CRP1, cysteine and glycine-rich protein 1, Jak2, tyrosine-protein kinase JAK2, pSTAT3-Tyr705, phosphorylated STAT3, TIM, mitochondrial import inner membrane translocase subunit Tim9, HIP1, Huntingtin-interacting protein 1, 60s-RP, 60s ribosomal protein L10E, TNF, tumor necrosis factor, ALDH2, aldehyde dehydrogenase, mitochondrial, PRP19, pre-mRNA-processing factor 19, ROS, reactive oxygen species, TNFR2, tumor necrosis factor receptor 2, JNK, c-Jun NH2-terminal kinase, ERK(1/2), extracellular signal regulated kinase 1/2, NF-κB, nuclear factor-kappa B, PKC-α, protein kinase C-α, p100, serine protease P100, MAPK3, mitogen-activated protein kinase 3, TGF-β, Transforming growth factor-β, TRAP1, heat shock protein 75 kDa, LIM, LIM/homeobox protein, Tobacco smoke exposure, Nuclear phosphoprotein, Phosphoproteomic analysis, Signaling pathways

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Graphical abstract

          Highlights

          • •

            We analyzed nuclear phosphoprotein expression activated by tobacco smoke exposure.

          • •

            253 phosphoproteins were identified in 1-day and 7-day exposure groups.

          • •

            Of these, 33 were significantly differentially expressed in control and exposed groups.

          • •

            Identified proteins were related to inflammation, response to stress and nicotine.

          • •

            OSF3 and spectrin β chain were identified as candidate tobacco smoke markers.

          Abstract

          Smoking is a risk factor for lung diseases, including chronic obstructive pulmonary disease and lung cancer. However, the molecular mechanisms mediating the progression of these diseases remain unclear. Therefore, we sought to identify signaling pathways activated by tobacco-smoke exposure, by analyzing nuclear phosphoprotein expression using phosphoproteomic analysis of lung tissue from mice exposed to tobacco smoke. Sixteen mice were exposed to tobacco smoke for 1 or 7 days, and the expression of phosphorylated peptides was analyzed by mass spectrometry. A total of 253 phosphoproteins were identified, including FACT complex subunit SPT16 in the 1-day exposure group, keratin type 1 cytoskeletal 18 (K18), and adipocyte fatty acid-binding protein, in the 7-day exposure group, and peroxiredoxin-1 (OSF3) and spectrin β chain brain 1 (SPTBN1), in both groups. Semi-quantitative analysis of the identified phosphoproteins revealed that 33 proteins were significantly differentially expressed between the control and exposed groups. The identified phosphoproteins were classified according to their biological functions. We found that the identified proteins were related to inflammation, regeneration, repair, proliferation, differentiation, morphogenesis, and response to stress and nicotine. In conclusion, we identified proteins, including OSF3 and SPTBN1, as candidate tobacco smoke-exposure markers; our results provide insights into the mechanisms of tobacco smoke-induced diseases.

          Related collections

          Most cited references56

          • Record: found
          • Abstract: found
          • Article: not found

          Induction of apoptosis by ASK1, a mammalian MAPKKK that activates SAPK/JNK and p38 signaling pathways.

          H Ichijo, E Nishida, K Irie … (1997)
          Mitogen-activated protein (MAP) kinase cascades are activated in response to various extracellular stimuli, including growth factors and environmental stresses. A MAP kinase kinase kinase (MAPKKK), termed ASK1, was identified that activated two different subgroups of MAP kinase kinases (MAPKK), SEK1 (or MKK4) and MKK3/MAPKK6 (or MKK6), which in turn activated stress-activated protein kinase (SAPK, also known as JNK; c-Jun amino-terminal kinase) and p38 subgroups of MAP kinases, respectively. Overexpression of ASK1 induced apoptotic cell death, and ASK1 was activated in cells treated with tumor necrosis factor-alpha (TNF-alpha). Moreover, TNF-alpha-induced apoptosis was inhibited by a catalytically inactive form of ASK1. ASK1 may be a key element in the mechanism of stress- and cytokine-induced apoptosis.
          Article 0 comments Cited 392 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Structure, mechanism and regulation of peroxiredoxins.

            Zachary A Wood, Ewald Schroder, J Robin Harris … (2003)
            Peroxiredoxins (Prxs) are a ubiquitous family of antioxidant enzymes that also control cytokine-induced peroxide levels which mediate signal transduction in mammalian cells. Prxs can be regulated by changes to phosphorylation, redox and possibly oligomerization states. Prxs are divided into three classes: typical 2-Cys Prxs; atypical 2-Cys Prxs; and 1-Cys Prxs. All Prxs share the same basic catalytic mechanism, in which an active-site cysteine (the peroxidatic cysteine) is oxidized to a sulfenic acid by the peroxide substrate. The recycling of the sulfenic acid back to a thiol is what distinguishes the three enzyme classes. Using crystal structures, a detailed catalytic cycle has been derived for typical 2-Cys Prxs, including a model for the redox-regulated oligomeric state proposed to control enzyme activity.
            Article 0 comments Cited 208 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Multifaceted mechanisms in COPD: inflammation, immunity, and tissue repair and destruction.

              K F Chung, I M Adcock (2008)
              Chronic obstructive pulmonary disease is a leading global cause of morbidity and mortality that is characterised by inexorable deterioration of small airways obstruction with emphysema associated with cellular inflammation and structural remodelling. Other features include apoptosis as well as proliferation of cells, and both tissue repair and lack of tissue repair. Metalloprotease release, together with that of apoptotic factors, may underlie the emphysema, and, conversely, fibrosis of the small airways may be accounted for by the effects of growth factor activation. In advanced disease, influential factors include the development of autoimmunity, with activation of dendritic cells and T-helper cells of both type 1 and 2, and the senescence response. An inability of macrophages to ingest apoptosed cells and bacteria may exacerbate inflammatory responses. Systemic inflammation with concomitant cardiovascular disease and metabolic syndrome may reflect the effect of cigarette smoke on nonpulmonary cells. Corticosteroid resistance may be secondary to oxidative stress mechanisms, such as inactivation of histone deacetylases. The mechanisms of chronic obstructive pulmonary disease may be heterogeneous, according to severity, and clinical phenotypes need to be correlated with cellular and pathological processes. Treatments may be targeted to patients with specific mechanisms.
              Article 0 comments Cited 180 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Kanako Niimori-Kita
                Takaaki Ito
                Journal
                Journal ID (nlm-ta): FEBS Open Bio
                Journal ID (iso-abbrev): FEBS Open Bio
                Title: FEBS Open Bio
                Publisher: Elsevier
                ISSN (Electronic): 2211-5463
                Publication date PMC-release: 23 August 2014
                Publication date (Electronic): 23 August 2014
                Publication date Collection: 2014
                Volume: 4
                Pages: 746-754
                Affiliations
                [a ]Department of Pathology and Experimental Medicine, Kumamoto University, 1-1-1, Honjo, Kumamoto 860-8556, Japan
                [b ]AMR Incorporated, 2-13-18, Nakane, Meguro-ku, Tokyo 152-0031, Japan
                [c ]Isotope Research Center, Nippon Medical School, 1-1-5, Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan
                Author notes
                [* ]Corresponding authors. Tel.: +81 96 373 5086; fax: +81 96 373 5087. nimokana7@ 123456gmail.com takaito@ 123456kumamoto-u.ac.jp
                Article
                Publisher ID: S2211-5463(14)00076-X
                DOI: 10.1016/j.fob.2014.08.002
                PMC ID: 4208089
                PubMed ID: 25349779
                SO-VID: 652aca6c-1ebe-4da8-80a8-76b4800992fc
                Copyright © © 2014 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/).

                History
                Date received : 4 April 2014
                Date revision received : 19 August 2014
                Date accepted : 19 August 2014
                Categories
                Subject: Article

                Keywords: copd, chronic obstructive pulmonary disorder,factp140, fact complex subunit spt16,k18, keratin type 1 cytoskeletal 18,afabp, adipocyte fatty acid-binding protein,osf3, peroxiredoxin-1,sptbn1, spectrin β chain brain 1,stat, signal transducer and activator of transcription,il, interleukin,k8, keratin type 2 cytoskeletal 8,prp19, pre-mrna-processing factor 19,crp1, cysteine and glycine-rich protein 1,jak2, tyrosine-protein kinase jak2,pstat3-tyr705, phosphorylated stat3,tim, mitochondrial import inner membrane translocase subunit tim9,hip1, huntingtin-interacting protein 1,60s-rp, 60s ribosomal protein l10e,tnf, tumor necrosis factor,aldh2, aldehyde dehydrogenase, mitochondrial,ros, reactive oxygen species,tnfr2, tumor necrosis factor receptor 2,jnk, c-jun nh2-terminal kinase,erk(1/2), extracellular signal regulated kinase 1/2,nf-κb, nuclear factor-kappa b,pkc-α, protein kinase c-α,p100, serine protease p100,mapk3, mitogen-activated protein kinase 3,tgf-β, transforming growth factor-β,trap1, heat shock protein 75 kda,lim, lim/homeobox protein,tobacco smoke exposure,nuclear phosphoprotein,phosphoproteomic analysis,signaling pathways
                Data availability:
                Keywords: copd, chronic obstructive pulmonary disorder, factp140, fact complex subunit spt16, k18, keratin type 1 cytoskeletal 18, afabp, adipocyte fatty acid-binding protein, osf3, peroxiredoxin-1, sptbn1, spectrin β chain brain 1, stat, signal transducer and activator of transcription, il, interleukin, k8, keratin type 2 cytoskeletal 8, prp19, pre-mrna-processing factor 19, crp1, cysteine and glycine-rich protein 1, jak2, tyrosine-protein kinase jak2, pstat3-tyr705, phosphorylated stat3, tim, mitochondrial import inner membrane translocase subunit tim9, hip1, huntingtin-interacting protein 1, 60s-rp, 60s ribosomal protein l10e, tnf, tumor necrosis factor, aldh2, aldehyde dehydrogenase, mitochondrial, ros, reactive oxygen species, tnfr2, tumor necrosis factor receptor 2, jnk, c-jun nh2-terminal kinase, erk(1/2), extracellular signal regulated kinase 1/2, nf-κb, nuclear factor-kappa b, pkc-α, protein kinase c-α, p100, serine protease p100, mapk3, mitogen-activated protein kinase 3, tgf-β, transforming growth factor-β, trap1, heat shock protein 75 kda, lim, lim/homeobox protein, tobacco smoke exposure, nuclear phosphoprotein, phosphoproteomic analysis, signaling pathways

                Comments

                Comment on this article

                scite_

                Similar content4

                See all similar

                Cited by4

                See all cited by