Regulation of GLUT4 expression in denervated skeletal muscle
1 Department of Biology, Viterbo University, La Crosse, Wisconsin; 2 Departments of Exercise and Sport Science and 3 Physiology, Brody School of Medicine, East Carolina University, Greenville, North Carolina; 4 Deparment of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences C...
Saved in:
Published in | American journal of physiology. Regulatory, integrative and comparative physiology Vol. 296; no. 6; pp. R1820 - R1828 |
---|---|
Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
American Physiological Society
01.06.2009
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | 1 Department of Biology, Viterbo University, La Crosse, Wisconsin; 2 Departments of Exercise and Sport Science and 3 Physiology, Brody School of Medicine, East Carolina University, Greenville, North Carolina; 4 Deparment of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; and 5 Department of Molecular Biology, University of Texas Southwestern, Dallas, Texas; and 6 Duke University Medical School, Durham, North Carolina
Submitted 20 August 2008
; accepted in final form 23 March 2009
Denervation by sciatic nerve resection causes decreased muscle glucose transporter 4 (GLUT4) expression, but little is known about the signaling events that cause this decrease. Experiments were designed to test the hypothesis that decreased GLUT4 expression in denervated muscle occurs because of decreased calcium/CaMK activity, which would then lead to decreased activation of the transcription factors myocyte enhancer factor 2 (MEF2) and GLUT4 enhancer factor (GEF), which are required for normal GLUT4 expression. GLUT4 mRNA was elevated in mice expressing constitutively active CaMK isoform IV (CaMKIV) and decreased by denervation. Denervation decreased GEF binding to the promoter and the content of GEF in the nucleus, but there was no change in either MEF2 binding or MEF2 protein content. Expression of a MEF2-dependent reporter gene did not change in denervated skeletal muscle. To determine the domains of the GLUT4 promoter that respond to denervation, transgenic mice expressing the chloramphenicol acetyl transferase (CAT) reporter gene driven by different lengths of the human GLUT4 promoter were denervated. Using several different promoter/reporter gene constructs, we found that all areas of the GLUT4 promoter were truncated or missing, except for the MEF2 binding domain and the basal promoter. All of the GLUT4 promoter/CAT reporter constructs evaluated responded normally to denervation. Our data lead us to conclude that decreased CaMK activity is not the reason for decreased GLUT4 content in denervated muscle and that negative control of GLUT4 expression is not mediated through the MEF2 or GEF-binding domains. These findings indicate that withdrawal of a GEF- or MEF2-dependent signal is not likely a major determinant of the denervation effect on GLUT4 expression. Thus, the response to denervation may be mediated by other elements present in the basal promoter of the GLUT4 gene.
denervation; exercise; myocyte enhancer factor 2; GLUT4 enhancer factor; glucose
Address for reprint requests and other correspondence: G. Lynis Dohm, Dept. of Physiology, Brody School of Medicine, East Carolina Univ., 6N98 600 Moye Blvd., Greenville, NC 27834 (e-mail: dohmg{at}ecu.edu ) |
---|---|
AbstractList | 1 Department of Biology, Viterbo University, La Crosse, Wisconsin; 2 Departments of Exercise and Sport Science and 3 Physiology, Brody School of Medicine, East Carolina University, Greenville, North Carolina; 4 Deparment of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; and 5 Department of Molecular Biology, University of Texas Southwestern, Dallas, Texas; and 6 Duke University Medical School, Durham, North Carolina
Submitted 20 August 2008
; accepted in final form 23 March 2009
Denervation by sciatic nerve resection causes decreased muscle glucose transporter 4 (GLUT4) expression, but little is known about the signaling events that cause this decrease. Experiments were designed to test the hypothesis that decreased GLUT4 expression in denervated muscle occurs because of decreased calcium/CaMK activity, which would then lead to decreased activation of the transcription factors myocyte enhancer factor 2 (MEF2) and GLUT4 enhancer factor (GEF), which are required for normal GLUT4 expression. GLUT4 mRNA was elevated in mice expressing constitutively active CaMK isoform IV (CaMKIV) and decreased by denervation. Denervation decreased GEF binding to the promoter and the content of GEF in the nucleus, but there was no change in either MEF2 binding or MEF2 protein content. Expression of a MEF2-dependent reporter gene did not change in denervated skeletal muscle. To determine the domains of the GLUT4 promoter that respond to denervation, transgenic mice expressing the chloramphenicol acetyl transferase (CAT) reporter gene driven by different lengths of the human GLUT4 promoter were denervated. Using several different promoter/reporter gene constructs, we found that all areas of the GLUT4 promoter were truncated or missing, except for the MEF2 binding domain and the basal promoter. All of the GLUT4 promoter/CAT reporter constructs evaluated responded normally to denervation. Our data lead us to conclude that decreased CaMK activity is not the reason for decreased GLUT4 content in denervated muscle and that negative control of GLUT4 expression is not mediated through the MEF2 or GEF-binding domains. These findings indicate that withdrawal of a GEF- or MEF2-dependent signal is not likely a major determinant of the denervation effect on GLUT4 expression. Thus, the response to denervation may be mediated by other elements present in the basal promoter of the GLUT4 gene.
denervation; exercise; myocyte enhancer factor 2; GLUT4 enhancer factor; glucose
Address for reprint requests and other correspondence: G. Lynis Dohm, Dept. of Physiology, Brody School of Medicine, East Carolina Univ., 6N98 600 Moye Blvd., Greenville, NC 27834 (e-mail: dohmg{at}ecu.edu ) Denervation by sciatic nerve resection causes decreased muscle glucose transporter 4 (GLUT4) expression, but little is known about the signaling events that cause this decrease. Experiments were designed to test the hypothesis that decreased GLUT4 expression in denervated muscle occurs because of decreased calcium/CaMK activity, which would then lead to decreased activation of the transcription factors myocyte enhancer factor 2 (MEF2) and GLUT4 enhancer factor (GEF), which are required for normal GLUT4 expression. GLUT4 mRNA was elevated in mice expressing constitutively active CaMK isoform IV (CaMKIV) and decreased by denervation. Denervation decreased GEF binding to the promoter and the content of GEF in the nucleus, but there was no change in either MEF2 binding or MEF2 protein content. Expression of a MEF2-dependent reporter gene did not change in denervated skeletal muscle. To determine the domains of the GLUT4 promoter that respond to denervation, transgenic mice expressing the chloramphenicol acetyl transferase (CAT) reporter gene driven by different lengths of the human GLUT4 promoter were denervated. Using several different promoter/reporter gene constructs, we found that all areas of the GLUT4 promoter were truncated or missing, except for the MEF2 binding domain and the basal promoter. All of the GLUT4 promoter/CAT reporter constructs evaluated responded normally to denervation. Our data lead us to conclude that decreased CaMK activity is not the reason for decreased GLUT4 content in denervated muscle and that negative control of GLUT4 expression is not mediated through the MEF2 or GEF-binding domains. These findings indicate that withdrawal of a GEF- or MEF2-dependent signal is not likely a major determinant of the denervation effect on GLUT4 expression. Thus, the response to denervation may be mediated by other elements present in the basal promoter of the GLUT4 gene. Denervation by sciatic nerve resection causes decreased muscle glucose transporter 4 (GLUT4) expression, but little is known about the signaling events that cause this decrease. Experiments were designed to test the hypothesis that decreased GLUT4 expression in denervated muscle occurs because of decreased calcium/CaMK activity, which would then lead to decreased activation of the transcription factors myocyte enhancer factor 2 (MEF2) and GLUT4 enhancer factor (GEF), which are required for normal GLUT4 expression. GLUT4 mRNA was elevated in mice expressing constitutively active CaMK isoform IV (CaMKIV) and decreased by denervation. Denervation decreased GEF binding to the promoter and the content of GEF in the nucleus, but there was no change in either MEF2 binding or MEF2 protein content. Expression of a MEF2-dependent reporter gene did not change in denervated skeletal muscle. To determine the domains of the GLUT4 promoter that respond to denervation, transgenic mice expressing the chloramphenicol acetyl transferase (CAT) reporter gene driven by different lengths of the human GLUT4 promoter were denervated. Using several different promoter/reporter gene constructs, we found that all areas of the GLUT4 promoter were truncated or missing, except for the MEF2 binding domain and the basal promoter. All of the GLUT4 promoter/CAT reporter constructs evaluated responded normally to denervation. Our data lead us to conclude that decreased CaMK activity is not the reason for decreased GLUT4 content in denervated muscle and that negative control of GLUT4 expression is not mediated through the MEF2 or GEF-binding domains. These findings indicate that withdrawal of a GEF- or MEF2-dependent signal is not likely a major determinant of the denervation effect on GLUT4 expression. Thus, the response to denervation may be mediated by other elements present in the basal promoter of the GLUT4 gene. [PUBLICATION ABSTRACT] |
Author | Dohm, G. Lynis Jensen, Ellis B Bassel-Duby, Rhonda Olson, Ann Louise Williams, R. Sanders Zheng, Donghai Russell, Robert A |
AuthorAffiliation | 1 Department of Biology, Viterbo University, La Crosse, Wisconsin; 2 Departments of Exercise and Sport Science and 3 Physiology, Brody School of Medicine, East Carolina University, Greenville, North Carolina; 4 Deparment of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; and 5 Department of Molecular Biology, University of Texas Southwestern, Dallas, Texas; and 6 Duke University Medical School, Durham, North Carolina |
AuthorAffiliation_xml | – name: 1 Department of Biology, Viterbo University, La Crosse, Wisconsin; 2 Departments of Exercise and Sport Science and 3 Physiology, Brody School of Medicine, East Carolina University, Greenville, North Carolina; 4 Deparment of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; and 5 Department of Molecular Biology, University of Texas Southwestern, Dallas, Texas; and 6 Duke University Medical School, Durham, North Carolina |
Author_xml | – sequence: 1 fullname: Jensen, Ellis B – sequence: 2 fullname: Zheng, Donghai – sequence: 3 fullname: Russell, Robert A – sequence: 4 fullname: Bassel-Duby, Rhonda – sequence: 5 fullname: Williams, R. Sanders – sequence: 6 fullname: Olson, Ann Louise – sequence: 7 fullname: Dohm, G. Lynis |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19321702$$D View this record in MEDLINE/PubMed |
BookMark | eNpdkVFr2zAQx8XoWNNsX2APw_Shb86kky1bMAqlrN0gUAjts1Csc-JMkTLJbptvP6UJWdung7vf_bnjd0ZOnHdIyFdGJ4yV8F2vNgEXw0RSUbIJUFp_IKM0gJwVkp6QEeWC54IxeUrOYlxRSgte8E_klEkOrKIwIj9mKcHqvvMu8212O324LzJ8TsEx7nqdyww6DI-6R5PFP2ix1zZbD7Gx-Jl8bLWN-OVQx-Th5uf99a98enf7-_pqmjclhz4X85qx2nBjmkLqRla0NSXUVVu26c7WNBorLimwOZhaG8FTMaaiHI3hteR8TC73uZthvkbToOuDtmoTurUOW-V1p95OXLdUC_-oQEioUsKYXBwCgv87YOzVuosNWqsd-iEqUUENBd-B5-_AlR-CS88pAFlBCaVIEOyhJvgYA7bHSxhVOzPqYEa9mFE7M2np2-sf_q8cVCRgsgeW3WL51AVUm-U2ObB-sT0GghRKqBmrgfJ_9G6eUQ |
CODEN | AJPRDO |
CitedBy_id | crossref_primary_10_1530_JOE_18_0528 crossref_primary_10_1016_j_jmb_2011_11_011 crossref_primary_10_1080_13813455_2020_1861028 crossref_primary_10_14814_phy2_12359 crossref_primary_10_1016_j_biomaterials_2014_12_002 crossref_primary_10_7600_jpfsm_2_355 crossref_primary_10_1152_physrev_00038_2012 crossref_primary_10_1089_neu_2018_6144 crossref_primary_10_2337_db13_0229 crossref_primary_10_1007_s00441_013_1655_1 crossref_primary_10_1016_j_phymed_2022_154022 |
Cites_doi | 10.1172/JCI117823 10.1073/pnas.92.8.3096 10.1152/ajpendo.1993.264.4.E583 10.1016/S0021-9258(19)49746-9 10.1006/jmbi.2001.5091 10.1016/S0306-3623(98)00095-0 10.1073/pnas.140199597 10.2337/diab.44.5.555 10.1007/s001090050068 10.1074/jbc.M001452200 10.1038/35040593 10.1152/ajpendo.1997.273.4.E682 10.1152/ajpregu.1995.269.5.R1148 10.1152/jappl.1995.79.6.1936 10.2337/diab.45.1.23 10.1113/jphysiol.2006.111757 10.1093/emboj/19.9.1963 10.1093/emboj/20.22.6414 10.1074/jbc.270.40.23491 10.1152/ajpendo.00080.2004 10.1083/jcb.200408128 10.1006/bbrc.1997.7587 10.1172/JCI8551 10.1007/BF00402546 10.1126/science.1071163 10.2337/diabetes.50.3.593 10.1016/S0021-9258(18)46957-8 10.1113/jphysiol.2003.054171 10.1152/ajpcell.00248.2004 10.2337/diab.45.1.28 10.2337/diabetes.48.5.1061 10.1128/MCB.20.18.6904-6912.2000 10.1146/annurev.biochem.71.110601.135410 10.1074/jbc.273.23.14285 10.1152/ajpendo.1991.261.4.E437 10.1007/BF00401526 10.1016/S0021-9258(18)43974-9 10.2337/diabetes.51.4.901 10.1172/JCI115465 10.2337/db07-0843 10.1172/JCI117673 10.1096/fj.05-4671fje 10.1210/endo.131.4.1396328 10.1152/jappl.1998.84.5.1661 10.1152/ajpcell.00188.2006 10.1152/jappl.1993.74.2.776 10.1242/dev.126.10.2045 10.1249/01.mss.0000233798.62153.50 |
ContentType | Journal Article |
Copyright | Copyright American Physiological Society Jun 2009 Copyright © 2009, American Physiological Society |
Copyright_xml | – notice: Copyright American Physiological Society Jun 2009 – notice: Copyright © 2009, American Physiological Society |
DBID | CGR CUY CVF ECM EIF NPM AAYXX CITATION 7QP 7QR 7TS 7U7 8FD C1K FR3 P64 7X8 5PM |
DOI | 10.1152/ajpregu.90651.2008 |
DatabaseName | Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed CrossRef Calcium & Calcified Tissue Abstracts Chemoreception Abstracts Physical Education Index Toxicology Abstracts Technology Research Database Environmental Sciences and Pollution Management Engineering Research Database Biotechnology and BioEngineering Abstracts MEDLINE - Academic PubMed Central (Full Participant titles) |
DatabaseTitle | MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) CrossRef Technology Research Database Toxicology Abstracts Chemoreception Abstracts Engineering Research Database Calcium & Calcified Tissue Abstracts Physical Education Index Biotechnology and BioEngineering Abstracts Environmental Sciences and Pollution Management MEDLINE - Academic |
DatabaseTitleList | CrossRef MEDLINE Technology Research Database |
Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Anatomy & Physiology |
EISSN | 1522-1490 |
EndPage | R1828 |
ExternalDocumentID | 1726796071 10_1152_ajpregu_90651_2008 19321702 ajpregu_296_6_R1820 |
Genre | Research Support, Non-U.S. Gov't Journal Article Research Support, N.I.H., Extramural |
GrantInformation_xml | – fundername: NIDDK NIH HHS grantid: R01 DK046121 – fundername: NIDDK NIH HHS grantid: R01 DK062341 |
GroupedDBID | 02 23M 2WC 39C 4.4 5GY 5VS ACIWK ACPRK ADBBV AFFNX AFRAH ALMA_UNASSIGNED_HOLDINGS BAWUL BKOMP C1A DIK DL EBS EJD F5P KQ8 O0- OK1 P2P PQEST PQQKQ RAP RHF RHI RPL UKR WH7 WOQ 53G 6J9 8M5 AAFWJ BKKCC BTFSW CGR CUY CVF ECM EIF EMOBN H13 ITBOX NPM RPRKH TAE TR2 W8F XSW YSK YYP ~02 AAYXX CITATION 7QP 7QR 7TS 7U7 8FD C1K FR3 P64 7X8 5PM |
ID | FETCH-LOGICAL-c532t-6b8118d3ddc49ac970fd5287f5f490fdcae739021b2d8ad632d8dd703edd38933 |
ISSN | 0363-6119 |
IngestDate | Tue Sep 17 20:42:42 EDT 2024 Fri Oct 25 08:25:24 EDT 2024 Thu Oct 10 22:05:56 EDT 2024 Fri Nov 22 01:04:38 EST 2024 Sat Sep 28 07:44:50 EDT 2024 Tue Jan 05 17:52:14 EST 2021 |
IsDoiOpenAccess | false |
IsOpenAccess | true |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 6 |
Language | English |
LinkModel | OpenURL |
MergedId | FETCHMERGED-LOGICAL-c532t-6b8118d3ddc49ac970fd5287f5f490fdcae739021b2d8ad632d8dd703edd38933 |
Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Address for reprint requests and other correspondence: G. Lynis Dohm, Dept. of Physiology, Brody School of Medicine, East Carolina Univ., 6N98 600 Moye Blvd., Greenville, NC 27834 (e-mail: dohmg@ecu.edu) |
OpenAccessLink | https://thescholarship.ecu.edu/bitstream/10342/3022/1/RegGLUT4ExSkelMuscleJensenetal.pdf |
PMID | 19321702 |
PQID | 229725256 |
PQPubID | 48263 |
ParticipantIDs | pubmed_primary_19321702 proquest_miscellaneous_67282439 pubmedcentral_primary_oai_pubmedcentral_nih_gov_2692789 crossref_primary_10_1152_ajpregu_90651_2008 proquest_journals_229725256 highwire_physiology_ajpregu_296_6_R1820 |
PublicationCentury | 2000 |
PublicationDate | 2009-06-01 |
PublicationDateYYYYMMDD | 2009-06-01 |
PublicationDate_xml | – month: 06 year: 2009 text: 2009-06-01 day: 01 |
PublicationDecade | 2000 |
PublicationPlace | United States |
PublicationPlace_xml | – name: United States – name: Bethesda |
PublicationTitle | American journal of physiology. Regulatory, integrative and comparative physiology |
PublicationTitleAlternate | Am J Physiol Regul Integr Comp Physiol |
PublicationYear | 2009 |
Publisher | American Physiological Society |
Publisher_xml | – name: American Physiological Society |
References | 18184930 - Diabetes. 2008 Apr;57(4):860-7 11246879 - Diabetes. 2001 Mar;50(3):593-600 1601840 - J Biol Chem. 1992 Jun 15;267(17):11673-6 10825161 - J Biol Chem. 2000 Aug 4;275(31):23666-73 14565989 - J Physiol. 2003 Nov 15;553(Pt 1):303-9 1939643 - J Clin Invest. 1991 Nov;88(5):1546-52 16368714 - FASEB J. 2006 Feb;20(2):348-9 11916905 - Diabetes. 2002 Apr;51(4):901-9 9603935 - J Biol Chem. 1998 Jun 5;273(23):14285-92 7814644 - J Clin Invest. 1995 Jan;95(1):429-32 7961994 - J Biol Chem. 1994 Nov 25;269(47):29956-61 9405224 - Biochem Biophys Res Commun. 1997 Dec 8;241(1):1-6 11707412 - EMBO J. 2001 Nov 15;20(22):6414-23 7545962 - J Biol Chem. 1994 Nov 11;269(45):28514-21 9357795 - Am J Physiol. 1997 Oct;273(4 Pt 1):E682-7 9809466 - Gen Pharmacol. 1998 Nov;31(5):705-13 7503304 - Am J Physiol. 1995 Nov;269(5 Pt 2):R1148-53 10869435 - Proc Natl Acad Sci U S A. 2000 Jul 5;97(14):7835-40 15165992 - Am J Physiol Endocrinol Metab. 2004 Oct;287(4):E739-43 1396328 - Endocrinology. 1992 Oct;131(4):1821-5 8956150 - J Mol Med (Berl). 1996 Nov;74(11):639-52 8476037 - Am J Physiol. 1993 Apr;264(4 Pt 1):E583-93 16690701 - J Physiol. 2006 Aug 1;574(Pt 3):889-903 8522055 - Diabetes. 1996 Jan;45(1):23-7 8458795 - J Appl Physiol (1985). 1993 Feb;74(2):776-81 1547918 - Diabetologia. 1992 Feb;35(2):143-7 16985263 - Am J Physiol Endocrinol Metab. 2007 Feb;292(2):E413-20 10331411 - Diabetes. 1999 May;48(5):1061-9 17095928 - Med Sci Sports Exerc. 2006 Nov;38(11):1945-9 9572814 - J Appl Physiol (1985). 1998 May;84(5):1661-6 11081517 - Nature. 2000 Nov 2;408(6808):106-11 11718554 - J Mol Biol. 2001 Nov 23;314(2):195-204 1959709 - Diabetologia. 1991 Oct;34(10):763-5 10958686 - Mol Cell Biol. 2000 Sep;20(18):6904-12 10790363 - EMBO J. 2000 May 2;19(9):1963-73 8847256 - J Appl Physiol (1985). 1995 Dec;79(6):1936-8 7724522 - Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3096-9 7729615 - Diabetes. 1995 May;44(5):555-60 1928336 - Am J Physiol. 1991 Oct;261(4 Pt 1):E437-43 10207130 - Development. 1999 May;126(10):2045-52 8522056 - Diabetes. 1996 Jan;45(1):28-36 11951046 - Science. 2002 Apr 12;296(5566):349-52 7706456 - J Clin Invest. 1995 Apr;95(4):1512-8 15229108 - Am J Physiol Cell Physiol. 2004 Nov;287(5):C1311-9 7559512 - J Biol Chem. 1995 Oct 6;270(40):23491-5 12045104 - Annu Rev Biochem. 2002;71:473-510 10811847 - J Clin Invest. 2000 May;105(10):1395-406 15767461 - J Cell Biol. 2005 Mar 14;168(6):887-97 R21 R20 R23 R22 R25 R24 R27 R26 R29 R28 R1 R2 R3 R4 R5 R6 R7 R8 R9 R30 R32 R31 R34 R33 R36 R35 R38 R37 R39 R41 R40 R43 R42 R45 R44 R47 R46 R49 R48 R10 R12 R11 R14 R13 R16 R15 R18 R17 R19 |
References_xml | – ident: R7 doi: 10.1172/JCI117823 – ident: R15 doi: 10.1073/pnas.92.8.3096 – ident: R29 doi: 10.1152/ajpendo.1993.264.4.E583 – ident: R23 doi: 10.1016/S0021-9258(19)49746-9 – ident: R38 doi: 10.1006/jmbi.2001.5091 – ident: R49 doi: 10.1016/S0306-3623(98)00095-0 – ident: R8 doi: 10.1073/pnas.140199597 – ident: R13 doi: 10.2337/diab.44.5.555 – ident: R19 doi: 10.1007/s001090050068 – ident: R33 doi: 10.1074/jbc.M001452200 – ident: R27 doi: 10.1038/35040593 – ident: R17 doi: 10.1152/ajpendo.1997.273.4.E682 – ident: R28 doi: 10.1152/ajpregu.1995.269.5.R1148 – ident: R39 – ident: R11 doi: 10.1152/jappl.1995.79.6.1936 – ident: R21 doi: 10.2337/diab.45.1.23 – ident: R37 doi: 10.1113/jphysiol.2006.111757 – ident: R47 doi: 10.1093/emboj/19.9.1963 – ident: R48 doi: 10.1093/emboj/20.22.6414 – ident: R32 doi: 10.1074/jbc.270.40.23491 – ident: R9 doi: 10.1152/ajpendo.00080.2004 – ident: R24 doi: 10.1083/jcb.200408128 – ident: R6 doi: 10.1006/bbrc.1997.7587 – ident: R34 doi: 10.1172/JCI8551 – ident: R5 doi: 10.1007/BF00402546 – ident: R46 doi: 10.1126/science.1071163 – ident: R3 doi: 10.2337/diabetes.50.3.593 – ident: R22 doi: 10.1016/S0021-9258(18)46957-8 – ident: R36 doi: 10.1113/jphysiol.2003.054171 – ident: R1 doi: 10.1152/ajpcell.00248.2004 – ident: R43 doi: 10.2337/diab.45.1.28 – ident: R16 doi: 10.2337/diabetes.48.5.1061 – ident: R44 doi: 10.1128/MCB.20.18.6904-6912.2000 – ident: R14 doi: 10.1146/annurev.biochem.71.110601.135410 – ident: R41 doi: 10.1074/jbc.273.23.14285 – ident: R10 doi: 10.1152/ajpendo.1991.261.4.E437 – ident: R20 doi: 10.1007/BF00401526 – ident: R42 doi: 10.1016/S0021-9258(18)43974-9 – ident: R30 doi: 10.2337/diabetes.51.4.901 – ident: R2 doi: 10.1172/JCI115465 – ident: R26 doi: 10.2337/db07-0843 – ident: R35 doi: 10.1172/JCI117673 – ident: R25 doi: 10.1096/fj.05-4671fje – ident: R4 doi: 10.1210/endo.131.4.1396328 – ident: R18 doi: 10.1152/jappl.1998.84.5.1661 – ident: R40 doi: 10.1152/ajpcell.00188.2006 – ident: R12 doi: 10.1152/jappl.1993.74.2.776 – ident: R31 doi: 10.1242/dev.126.10.2045 – ident: R45 doi: 10.1249/01.mss.0000233798.62153.50 |
SSID | ssj0004343 |
Score | 2.0421958 |
Snippet | 1 Department of Biology, Viterbo University, La Crosse, Wisconsin; 2 Departments of Exercise and Sport Science and 3 Physiology, Brody School of Medicine, East... Denervation by sciatic nerve resection causes decreased muscle glucose transporter 4 (GLUT4) expression, but little is known about the signaling events that... |
SourceID | pubmedcentral proquest crossref pubmed highwire |
SourceType | Open Access Repository Aggregation Database Index Database Publisher |
StartPage | R1820 |
SubjectTerms | Animals Binding Sites Calcium-Calmodulin-Dependent Protein Kinase Type 4 - genetics Calcium-Calmodulin-Dependent Protein Kinase Type 4 - metabolism Chloramphenicol O-Acetyltransferase - genetics DNA-Binding Proteins - metabolism Down-Regulation Exercise and Respiratory Physiology Experiments Genes, Reporter Glucose Glucose Transporter Type 4 - genetics Glucose Transporter Type 4 - metabolism Humans Mice Mice, Inbred C57BL Mice, Transgenic Muscle Denervation Muscle, Skeletal - innervation Muscle, Skeletal - metabolism Musculoskeletal system Myogenic Regulatory Factors - genetics Myogenic Regulatory Factors - metabolism Neurons Promoter Regions, Genetic Ribonucleic acid RNA RNA, Messenger - metabolism Rodents Sciatic Nerve - surgery Signal Transduction Transcription Factors - metabolism |
Title | Regulation of GLUT4 expression in denervated skeletal muscle |
URI | http://ajpregu.physiology.org/cgi/content/abstract/296/6/R1820 https://www.ncbi.nlm.nih.gov/pubmed/19321702 https://www.proquest.com/docview/229725256 https://search.proquest.com/docview/67282439 https://pubmed.ncbi.nlm.nih.gov/PMC2692789 |
Volume | 296 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lc9MwENaEcuHCAOVhysMHBg4ZB1u2LHuGS9oCHV4DmWSmN49tyU1KI3dwfCg_lV_D6mU7kAP04iS2_Ij282p3tfsJoRcwCBckqKhX-BXxoiLEHljVpVeE4Mb5QcJCrrJ8v8Qni-jDKTkdjX4NspbaTTEpf-6sK7mOVGEfyFVWyf6HZLuLwg74DvKFLUgYtv8k45leSN7YfO8_LeaRpOzXqa1CJ7oKFXUFs7L5DiOMLH1ct429jqWftdM2Ax4JFfJQMffJ2Nyn1lPulmFC5hyZqriOQLw_q0vN4cIGeS4uVs34cNLHqrlWNMe1OFvmq27up20aMxui877H0-6cw1we845bTQg6W9Y2pGAjF2mfYTUoFpCq3j6agqXJVh3oQTnVHAdGs3Kjp8GHBufOHypyrNfGNYgdquWZpKkfjPHyd7J7ACGSkDY_B1GdtZMUDDQVRNhqDCC4XCtISes3oD7uB1ObQPD18xGOU1lmfAPdlCSNcl2Hj98GTPahzui0f84WdBH8-u-7K2pbfatt-8lyWu_yj_5M8x3YTfM76LZxeNypRu9dNOLiHtqfCoDT-sp96XZiudpHb3pAu3XlKkC7PaDdlXB7QLsW0K4G9H20ePd2fnTimeU9vJKEeOPFRRJIZcBYGaV5mVK_YgQc-IpUINiKlTmnYQo2aIFZkrM4hA_GYITijEkzO3yA9kQt-CPkBkXh84SyKoyTCNrlNKVVwAjFZS4pKh00tp2WXWoWl0x5vwRnprcz1dtqVVYHvbL9mvWvTdcQYJbFmYKUgw5st2fmDW0yjFOKCbgSDnreHQWlLWficsHrtsliihMMroCDHmoR9U9lxOwguiW8roGkg98-IlZLRQtv8Pb42mceoFv9a_oE7W1-tPwpmNyb4pnC7m-0Yt0a |
link.rule.ids | 230,314,780,784,885,27924,27925 |
linkProvider | Colorado Alliance of Research Libraries |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Regulation+of+GLUT4+expression+in+denervated+skeletal+muscle&rft.jtitle=American+journal+of+physiology.+Regulatory%2C+integrative+and+comparative+physiology&rft.au=Jensen%2C+Ellis+B.&rft.au=Zheng%2C+Donghai&rft.au=Russell%2C+Robert+A.&rft.au=Bassel-Duby%2C+Rhonda&rft.date=2009-06-01&rft.pub=American+Physiological+Society&rft.issn=0363-6119&rft.eissn=1522-1490&rft.volume=296&rft.issue=6&rft.spage=R1820&rft.epage=R1828&rft_id=info:doi/10.1152%2Fajpregu.90651.2008&rft_id=info%3Apmid%2F19321702&rft.externalDBID=PMC2692789 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0363-6119&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0363-6119&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0363-6119&client=summon |