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O-GlcNAc protein modification in cancer cells increases in response to glucose deprivation through glycogen degradation
DC Field | Value | Language |
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dc.contributor.author | 김현실 | - |
dc.contributor.author | 육종인 | - |
dc.date.accessioned | 2015-04-24T17:34:40Z | - |
dc.date.available | 2015-04-24T17:34:40Z | - |
dc.date.issued | 2009 | - |
dc.identifier.issn | 0021-9258 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/105665 | - |
dc.description.abstract | When cellular glucose concentrations fall below normal levels, in general the extent of protein O-GlcNAc modification (O-GlcNAcylation) decreases. However, recent reports demonstrated increased O-GlcNAcylation by glucose deprivation in HepG2 and Neuro-2a cells. Here, we report increased O-GlcNAcylation in non-small cell lung carcinoma A549 cells and various other cells in response to glucose deprivation. Although the level of O-GlcNAc transferase was unchanged, the enzyme contained less O-GlcNAc, and its activity was increased. Moreover, O-GlcNAcase activity was reduced. The studied cells contain glycogen, and we show that its degradation in response to glucose deprivation provides a source for UDP-GlcNAc required for increased O-GlcNAcylation under this condition. This required active glycogen phosphorylase and resulted in increased glutamine:fructose-6-phosphate amidotransferase, the first and rate-limiting enzyme in the hexosamine biosynthetic pathway. Interestingly, glucose deprivation reduced the amount of phosphofructokinase 1, a regulatory glycolytic enzyme, and blocked ATP synthesis. These findings suggest that glycogen is the source for increased O-GlcNAcylation but not for generating ATP in response to glucose deprivation and that this may be useful for cancer cells to survive. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 34777~34784 | - |
dc.relation.isPartOf | JOURNAL OF BIOLOGICAL CHEMISTRY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | AMP-Activated Protein Kinases/metabolism | - |
dc.subject.MESH | Acetylglucosamine/metabolism* | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Cell Line | - |
dc.subject.MESH | Glucose/metabolism* | - |
dc.subject.MESH | Glycogen/metabolism* | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | N-Acetylglucosaminyltransferases/metabolism | - |
dc.subject.MESH | Neoplasms/metabolism* | - |
dc.subject.MESH | Protein Processing, Post-Translational* | - |
dc.title | O-GlcNAc protein modification in cancer cells increases in response to glucose deprivation through glycogen degradation | - |
dc.type | Article | - |
dc.contributor.college | College of Dentistry (치과대학) | - |
dc.contributor.department | Dept. of Oral Pathology (구강병리학) | - |
dc.contributor.googleauthor | Jeong Gu Kang | - |
dc.contributor.googleauthor | Sang Yoon Park | - |
dc.contributor.googleauthor | Suena Ji | - |
dc.contributor.googleauthor | Insook Jang | - |
dc.contributor.googleauthor | Sujin Park | - |
dc.contributor.googleauthor | Hyun Sil Kim | - |
dc.contributor.googleauthor | Sung-Min Kim | - |
dc.contributor.googleauthor | Jong In Yook | - |
dc.contributor.googleauthor | Yong-Il Park | - |
dc.contributor.googleauthor | Ju¨rgen Roth | - |
dc.contributor.googleauthor | Jin Won Cho | - |
dc.identifier.doi | 10.1074/jbc.M109.026351 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A01121 | - |
dc.contributor.localId | A02536 | - |
dc.relation.journalcode | J01258 | - |
dc.identifier.eissn | 1083-351X | - |
dc.identifier.pmid | 19833729 | - |
dc.contributor.alternativeName | Kim, Hyun Sil | - |
dc.contributor.alternativeName | Yook, Jong In | - |
dc.contributor.affiliatedAuthor | Kim, Hyun Sil | - |
dc.contributor.affiliatedAuthor | Yook, Jong In | - |
dc.citation.volume | 284 | - |
dc.citation.number | 50 | - |
dc.citation.startPage | 34777 | - |
dc.citation.endPage | 34784 | - |
dc.identifier.bibliographicCitation | JOURNAL OF BIOLOGICAL CHEMISTRY, Vol.284(50) : 34777-34784, 2009 | - |
dc.identifier.rimsid | 42649 | - |
dc.type.rims | ART | - |
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