Differences in activity and phosphorylation of MAPK enzymes in esophageal squamous cells of GERD patients with and without Barrett's esophagus
We hypothesized that, in esophageal squamous epithelial cells, there are differences among individuals in the signal transduction pathways activated by acid reflux that might underlie the development of Barrett's esophagus. To explore that hypothesis, we immortalized nonneoplastic, esophageal s...
Gespeichert in:
Veröffentlicht in: | American journal of physiology: Gastrointestinal and liver physiology 2008-09, Vol.295 (3), p.G470-G478 |
---|---|
Hauptverfasser: | , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | G478 |
---|---|
container_issue | 3 |
container_start_page | G470 |
container_title | American journal of physiology: Gastrointestinal and liver physiology |
container_volume | 295 |
creator | Zhang, Hui Ying Zhang, Xi Chen, Xi Thomas, Deena Hormi-Carver, Kathy Elder, Frederick Spechler, Stuart J Souza, Rhonda F |
description | We hypothesized that, in esophageal squamous epithelial cells, there are differences among individuals in the signal transduction pathways activated by acid reflux that might underlie the development of Barrett's esophagus. To explore that hypothesis, we immortalized nonneoplastic, esophageal squamous cells from patients with gastroesophageal reflux disease (GERD) with (NES-B3T) and without (NES-G2T) Barrett's esophagus and used those cells to study acid effects on MAPK proteins. During endoscopy in patients with GERD with and without Barrett's esophagus, we took biopsy specimens from the distal squamous esophagus to study MAPK proteins before and after esophageal perfusion with 0.1 N HCl. We used immunoblotting and Western blotting to study MEK1/2 phosphorylation at two activating sites (serines 217/221), MEK1 phosphorylation at an inhibitory site (threonine 286), and MEK1/2 activity. After acid exposure, both cell lines exhibited increased MEK1/2 phosphorylation at the activating sites; the NES-B3T cells had higher levels of MEK1 phosphorylation at the inhibitory site, however, and only the NES-G2T cells showed an acid-induced increase in MEK1/2 activity. Similarly, in the squamous epithelium of patients with GERD with and without Barrett's esophagus, acid perfusion increased MEK1/2 phosphorylation at the activating sites in both patient groups; the Barrett's patients had higher levels of MEK1 phosphorylation at the inhibitory site, however, and only the patients without Barrett's demonstrated an acid-induced increase in ERK1/2 phosphorylation. In esophageal squamous cell lines and biopsies from patients with GERD with and without Barrett's esophagus, we have found differences in MAPK pathways activated by acid exposure. We speculate that these differences might underlie the development of Barrett's metaplasia. |
doi_str_mv | 10.1152/ajpgi.90262.2008 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2536777</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>69530581</sourcerecordid><originalsourceid>FETCH-LOGICAL-c421t-4baa8d358682889f89e48622ce6519486062b6089dc27ec55f7f4d1cef46f2dd3</originalsourceid><addsrcrecordid>eNpdkUuPFCEUhYnROO3o3pUhLnRVLVDFozYm83I0jtEYXROagm46VVAD1Jj2R_ibpbrb54Jwc_nOyb0cAJ5itMSYkldqO67dskWEkSVBSNwDi9ImFaYNvw8WCLd1hQXlJ-BRSluEECUYPwQnWDDMKWUL8OPSWWui8dok6DxUOrs7l3dQ-Q6Om5DKibteZRc8DBZ-OPv0Hhr_fTcceJPCuFFro3qYbic1hClBbfo-zfD11edLOBat8TnBby5v9rZzEaYMz1WMJueX6ZfLlB6DB1b1yTw53qfg65urLxdvq5uP1-8uzm4q3RCcq2allOhqKpggQrRWtKYRjBBtGMVtKREjK4ZE22nCjabUctt0WBvbMEu6rj4Frw--47QaTKfLgFH1coxuUHEng3Ly3xfvNnId7iShNeOcF4MXR4MYbieTshxcmhdX3pQ_kKylNaICF_D5f-A2TNGX5SSpCRVcMFYgdIB0DClFY39PgpGck5b7pOU-aTknXSTP_t7gj-AYbf0TJZSojA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>232587866</pqid></control><display><type>article</type><title>Differences in activity and phosphorylation of MAPK enzymes in esophageal squamous cells of GERD patients with and without Barrett's esophagus</title><source>MEDLINE</source><source>American Physiological Society</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Zhang, Hui Ying ; Zhang, Xi ; Chen, Xi ; Thomas, Deena ; Hormi-Carver, Kathy ; Elder, Frederick ; Spechler, Stuart J ; Souza, Rhonda F</creator><creatorcontrib>Zhang, Hui Ying ; Zhang, Xi ; Chen, Xi ; Thomas, Deena ; Hormi-Carver, Kathy ; Elder, Frederick ; Spechler, Stuart J ; Souza, Rhonda F</creatorcontrib><description>We hypothesized that, in esophageal squamous epithelial cells, there are differences among individuals in the signal transduction pathways activated by acid reflux that might underlie the development of Barrett's esophagus. To explore that hypothesis, we immortalized nonneoplastic, esophageal squamous cells from patients with gastroesophageal reflux disease (GERD) with (NES-B3T) and without (NES-G2T) Barrett's esophagus and used those cells to study acid effects on MAPK proteins. During endoscopy in patients with GERD with and without Barrett's esophagus, we took biopsy specimens from the distal squamous esophagus to study MAPK proteins before and after esophageal perfusion with 0.1 N HCl. We used immunoblotting and Western blotting to study MEK1/2 phosphorylation at two activating sites (serines 217/221), MEK1 phosphorylation at an inhibitory site (threonine 286), and MEK1/2 activity. After acid exposure, both cell lines exhibited increased MEK1/2 phosphorylation at the activating sites; the NES-B3T cells had higher levels of MEK1 phosphorylation at the inhibitory site, however, and only the NES-G2T cells showed an acid-induced increase in MEK1/2 activity. Similarly, in the squamous epithelium of patients with GERD with and without Barrett's esophagus, acid perfusion increased MEK1/2 phosphorylation at the activating sites in both patient groups; the Barrett's patients had higher levels of MEK1 phosphorylation at the inhibitory site, however, and only the patients without Barrett's demonstrated an acid-induced increase in ERK1/2 phosphorylation. In esophageal squamous cell lines and biopsies from patients with GERD with and without Barrett's esophagus, we have found differences in MAPK pathways activated by acid exposure. We speculate that these differences might underlie the development of Barrett's metaplasia.</description><identifier>ISSN: 0193-1857</identifier><identifier>EISSN: 1522-1547</identifier><identifier>DOI: 10.1152/ajpgi.90262.2008</identifier><identifier>PMID: 18617556</identifier><identifier>CODEN: APGPDF</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Barrett Esophagus - enzymology ; Barrett Esophagus - etiology ; Barrett Esophagus - pathology ; Biochemistry ; Cell Line, Transformed ; Cell Proliferation ; Cells ; Cyclin-Dependent Kinase Inhibitor p21 - metabolism ; Disease Progression ; Dual Specificity Phosphatase 1 - metabolism ; Enzymes ; Epithelial Cells - drug effects ; Epithelial Cells - enzymology ; Epithelial Cells - pathology ; Epithelial Cells - radiation effects ; Esophagoscopy ; Esophagus ; Esophagus - drug effects ; Esophagus - enzymology ; Esophagus - pathology ; Esophagus - radiation effects ; Gastric Acid - metabolism ; Gastroesophageal reflux ; Gastroesophageal Reflux - complications ; Gastroesophageal Reflux - enzymology ; Gastroesophageal Reflux - pathology ; Humans ; Hydrochloric Acid - pharmacology ; MAP Kinase Kinase 1 - metabolism ; MAP Kinase Kinase 2 - metabolism ; MAP Kinase Signaling System - drug effects ; MAP Kinase Signaling System - radiation effects ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - metabolism ; Mitogen-Activated Protein Kinases - metabolism ; Mucosal Biology ; Phosphorylation ; Proteins ; Signal transduction ; Time Factors ; Tumor Suppressor Protein p53 - metabolism ; Ultraviolet Rays</subject><ispartof>American journal of physiology: Gastrointestinal and liver physiology, 2008-09, Vol.295 (3), p.G470-G478</ispartof><rights>Copyright American Physiological Society Sep 2008</rights><rights>Copyright © 2008, American Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-4baa8d358682889f89e48622ce6519486062b6089dc27ec55f7f4d1cef46f2dd3</citedby><cites>FETCH-LOGICAL-c421t-4baa8d358682889f89e48622ce6519486062b6089dc27ec55f7f4d1cef46f2dd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18617556$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Hui Ying</creatorcontrib><creatorcontrib>Zhang, Xi</creatorcontrib><creatorcontrib>Chen, Xi</creatorcontrib><creatorcontrib>Thomas, Deena</creatorcontrib><creatorcontrib>Hormi-Carver, Kathy</creatorcontrib><creatorcontrib>Elder, Frederick</creatorcontrib><creatorcontrib>Spechler, Stuart J</creatorcontrib><creatorcontrib>Souza, Rhonda F</creatorcontrib><title>Differences in activity and phosphorylation of MAPK enzymes in esophageal squamous cells of GERD patients with and without Barrett's esophagus</title><title>American journal of physiology: Gastrointestinal and liver physiology</title><addtitle>Am J Physiol Gastrointest Liver Physiol</addtitle><description>We hypothesized that, in esophageal squamous epithelial cells, there are differences among individuals in the signal transduction pathways activated by acid reflux that might underlie the development of Barrett's esophagus. To explore that hypothesis, we immortalized nonneoplastic, esophageal squamous cells from patients with gastroesophageal reflux disease (GERD) with (NES-B3T) and without (NES-G2T) Barrett's esophagus and used those cells to study acid effects on MAPK proteins. During endoscopy in patients with GERD with and without Barrett's esophagus, we took biopsy specimens from the distal squamous esophagus to study MAPK proteins before and after esophageal perfusion with 0.1 N HCl. We used immunoblotting and Western blotting to study MEK1/2 phosphorylation at two activating sites (serines 217/221), MEK1 phosphorylation at an inhibitory site (threonine 286), and MEK1/2 activity. After acid exposure, both cell lines exhibited increased MEK1/2 phosphorylation at the activating sites; the NES-B3T cells had higher levels of MEK1 phosphorylation at the inhibitory site, however, and only the NES-G2T cells showed an acid-induced increase in MEK1/2 activity. Similarly, in the squamous epithelium of patients with GERD with and without Barrett's esophagus, acid perfusion increased MEK1/2 phosphorylation at the activating sites in both patient groups; the Barrett's patients had higher levels of MEK1 phosphorylation at the inhibitory site, however, and only the patients without Barrett's demonstrated an acid-induced increase in ERK1/2 phosphorylation. In esophageal squamous cell lines and biopsies from patients with GERD with and without Barrett's esophagus, we have found differences in MAPK pathways activated by acid exposure. We speculate that these differences might underlie the development of Barrett's metaplasia.</description><subject>Barrett Esophagus - enzymology</subject><subject>Barrett Esophagus - etiology</subject><subject>Barrett Esophagus - pathology</subject><subject>Biochemistry</subject><subject>Cell Line, Transformed</subject><subject>Cell Proliferation</subject><subject>Cells</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</subject><subject>Disease Progression</subject><subject>Dual Specificity Phosphatase 1 - metabolism</subject><subject>Enzymes</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - enzymology</subject><subject>Epithelial Cells - pathology</subject><subject>Epithelial Cells - radiation effects</subject><subject>Esophagoscopy</subject><subject>Esophagus</subject><subject>Esophagus - drug effects</subject><subject>Esophagus - enzymology</subject><subject>Esophagus - pathology</subject><subject>Esophagus - radiation effects</subject><subject>Gastric Acid - metabolism</subject><subject>Gastroesophageal reflux</subject><subject>Gastroesophageal Reflux - complications</subject><subject>Gastroesophageal Reflux - enzymology</subject><subject>Gastroesophageal Reflux - pathology</subject><subject>Humans</subject><subject>Hydrochloric Acid - pharmacology</subject><subject>MAP Kinase Kinase 1 - metabolism</subject><subject>MAP Kinase Kinase 2 - metabolism</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>MAP Kinase Signaling System - radiation effects</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Mucosal Biology</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>Time Factors</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Ultraviolet Rays</subject><issn>0193-1857</issn><issn>1522-1547</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUuPFCEUhYnROO3o3pUhLnRVLVDFozYm83I0jtEYXROagm46VVAD1Jj2R_ibpbrb54Jwc_nOyb0cAJ5itMSYkldqO67dskWEkSVBSNwDi9ImFaYNvw8WCLd1hQXlJ-BRSluEECUYPwQnWDDMKWUL8OPSWWui8dok6DxUOrs7l3dQ-Q6Om5DKibteZRc8DBZ-OPv0Hhr_fTcceJPCuFFro3qYbic1hClBbfo-zfD11edLOBat8TnBby5v9rZzEaYMz1WMJueX6ZfLlB6DB1b1yTw53qfg65urLxdvq5uP1-8uzm4q3RCcq2allOhqKpggQrRWtKYRjBBtGMVtKREjK4ZE22nCjabUctt0WBvbMEu6rj4Frw--47QaTKfLgFH1coxuUHEng3Ly3xfvNnId7iShNeOcF4MXR4MYbieTshxcmhdX3pQ_kKylNaICF_D5f-A2TNGX5SSpCRVcMFYgdIB0DClFY39PgpGck5b7pOU-aTknXSTP_t7gj-AYbf0TJZSojA</recordid><startdate>20080901</startdate><enddate>20080901</enddate><creator>Zhang, Hui Ying</creator><creator>Zhang, Xi</creator><creator>Chen, Xi</creator><creator>Thomas, Deena</creator><creator>Hormi-Carver, Kathy</creator><creator>Elder, Frederick</creator><creator>Spechler, Stuart J</creator><creator>Souza, Rhonda F</creator><general>American Physiological Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20080901</creationdate><title>Differences in activity and phosphorylation of MAPK enzymes in esophageal squamous cells of GERD patients with and without Barrett's esophagus</title><author>Zhang, Hui Ying ; Zhang, Xi ; Chen, Xi ; Thomas, Deena ; Hormi-Carver, Kathy ; Elder, Frederick ; Spechler, Stuart J ; Souza, Rhonda F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-4baa8d358682889f89e48622ce6519486062b6089dc27ec55f7f4d1cef46f2dd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Barrett Esophagus - enzymology</topic><topic>Barrett Esophagus - etiology</topic><topic>Barrett Esophagus - pathology</topic><topic>Biochemistry</topic><topic>Cell Line, Transformed</topic><topic>Cell Proliferation</topic><topic>Cells</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</topic><topic>Disease Progression</topic><topic>Dual Specificity Phosphatase 1 - metabolism</topic><topic>Enzymes</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - enzymology</topic><topic>Epithelial Cells - pathology</topic><topic>Epithelial Cells - radiation effects</topic><topic>Esophagoscopy</topic><topic>Esophagus</topic><topic>Esophagus - drug effects</topic><topic>Esophagus - enzymology</topic><topic>Esophagus - pathology</topic><topic>Esophagus - radiation effects</topic><topic>Gastric Acid - metabolism</topic><topic>Gastroesophageal reflux</topic><topic>Gastroesophageal Reflux - complications</topic><topic>Gastroesophageal Reflux - enzymology</topic><topic>Gastroesophageal Reflux - pathology</topic><topic>Humans</topic><topic>Hydrochloric Acid - pharmacology</topic><topic>MAP Kinase Kinase 1 - metabolism</topic><topic>MAP Kinase Kinase 2 - metabolism</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>MAP Kinase Signaling System - radiation effects</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Mucosal Biology</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Signal transduction</topic><topic>Time Factors</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Ultraviolet Rays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Hui Ying</creatorcontrib><creatorcontrib>Zhang, Xi</creatorcontrib><creatorcontrib>Chen, Xi</creatorcontrib><creatorcontrib>Thomas, Deena</creatorcontrib><creatorcontrib>Hormi-Carver, Kathy</creatorcontrib><creatorcontrib>Elder, Frederick</creatorcontrib><creatorcontrib>Spechler, Stuart J</creatorcontrib><creatorcontrib>Souza, Rhonda F</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of physiology: Gastrointestinal and liver physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Hui Ying</au><au>Zhang, Xi</au><au>Chen, Xi</au><au>Thomas, Deena</au><au>Hormi-Carver, Kathy</au><au>Elder, Frederick</au><au>Spechler, Stuart J</au><au>Souza, Rhonda F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differences in activity and phosphorylation of MAPK enzymes in esophageal squamous cells of GERD patients with and without Barrett's esophagus</atitle><jtitle>American journal of physiology: Gastrointestinal and liver physiology</jtitle><addtitle>Am J Physiol Gastrointest Liver Physiol</addtitle><date>2008-09-01</date><risdate>2008</risdate><volume>295</volume><issue>3</issue><spage>G470</spage><epage>G478</epage><pages>G470-G478</pages><issn>0193-1857</issn><eissn>1522-1547</eissn><coden>APGPDF</coden><abstract>We hypothesized that, in esophageal squamous epithelial cells, there are differences among individuals in the signal transduction pathways activated by acid reflux that might underlie the development of Barrett's esophagus. To explore that hypothesis, we immortalized nonneoplastic, esophageal squamous cells from patients with gastroesophageal reflux disease (GERD) with (NES-B3T) and without (NES-G2T) Barrett's esophagus and used those cells to study acid effects on MAPK proteins. During endoscopy in patients with GERD with and without Barrett's esophagus, we took biopsy specimens from the distal squamous esophagus to study MAPK proteins before and after esophageal perfusion with 0.1 N HCl. We used immunoblotting and Western blotting to study MEK1/2 phosphorylation at two activating sites (serines 217/221), MEK1 phosphorylation at an inhibitory site (threonine 286), and MEK1/2 activity. After acid exposure, both cell lines exhibited increased MEK1/2 phosphorylation at the activating sites; the NES-B3T cells had higher levels of MEK1 phosphorylation at the inhibitory site, however, and only the NES-G2T cells showed an acid-induced increase in MEK1/2 activity. Similarly, in the squamous epithelium of patients with GERD with and without Barrett's esophagus, acid perfusion increased MEK1/2 phosphorylation at the activating sites in both patient groups; the Barrett's patients had higher levels of MEK1 phosphorylation at the inhibitory site, however, and only the patients without Barrett's demonstrated an acid-induced increase in ERK1/2 phosphorylation. In esophageal squamous cell lines and biopsies from patients with GERD with and without Barrett's esophagus, we have found differences in MAPK pathways activated by acid exposure. We speculate that these differences might underlie the development of Barrett's metaplasia.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>18617556</pmid><doi>10.1152/ajpgi.90262.2008</doi><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0193-1857 |
ispartof | American journal of physiology: Gastrointestinal and liver physiology, 2008-09, Vol.295 (3), p.G470-G478 |
issn | 0193-1857 1522-1547 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2536777 |
source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
subjects | Barrett Esophagus - enzymology Barrett Esophagus - etiology Barrett Esophagus - pathology Biochemistry Cell Line, Transformed Cell Proliferation Cells Cyclin-Dependent Kinase Inhibitor p21 - metabolism Disease Progression Dual Specificity Phosphatase 1 - metabolism Enzymes Epithelial Cells - drug effects Epithelial Cells - enzymology Epithelial Cells - pathology Epithelial Cells - radiation effects Esophagoscopy Esophagus Esophagus - drug effects Esophagus - enzymology Esophagus - pathology Esophagus - radiation effects Gastric Acid - metabolism Gastroesophageal reflux Gastroesophageal Reflux - complications Gastroesophageal Reflux - enzymology Gastroesophageal Reflux - pathology Humans Hydrochloric Acid - pharmacology MAP Kinase Kinase 1 - metabolism MAP Kinase Kinase 2 - metabolism MAP Kinase Signaling System - drug effects MAP Kinase Signaling System - radiation effects Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - metabolism Mitogen-Activated Protein Kinases - metabolism Mucosal Biology Phosphorylation Proteins Signal transduction Time Factors Tumor Suppressor Protein p53 - metabolism Ultraviolet Rays |
title | Differences in activity and phosphorylation of MAPK enzymes in esophageal squamous cells of GERD patients with and without Barrett's esophagus |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-23T10%3A48%3A37IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Differences%20in%20activity%20and%20phosphorylation%20of%20MAPK%20enzymes%20in%20esophageal%20squamous%20cells%20of%20GERD%20patients%20with%20and%20without%20Barrett's%20esophagus&rft.jtitle=American%20journal%20of%20physiology:%20Gastrointestinal%20and%20liver%20physiology&rft.au=Zhang,%20Hui%20Ying&rft.date=2008-09-01&rft.volume=295&rft.issue=3&rft.spage=G470&rft.epage=G478&rft.pages=G470-G478&rft.issn=0193-1857&rft.eissn=1522-1547&rft.coden=APGPDF&rft_id=info:doi/10.1152/ajpgi.90262.2008&rft_dat=%3Cproquest_pubme%3E69530581%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=232587866&rft_id=info:pmid/18617556&rfr_iscdi=true |