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- Publisher Website: 10.1016/j.jprot.2012.11.021
- Scopus: eid_2-s2.0-84871391215
- PMID: 23219901
- WOS: WOS:000316706800015
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Article: Proteomic profiling in Lipocalin 2 deficient mice under normal and inflammatory conditions
Title | Proteomic profiling in Lipocalin 2 deficient mice under normal and inflammatory conditions |
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Authors | |
Keywords | LCN2 Difference gel electrophoresis (DIGE) Lipocalin 2 NGAL Proteomics Liver injury |
Issue Date | 2013 |
Citation | Journal of Proteomics, 2013, v. 78, p. 188-196 How to Cite? |
Abstract | Lipocalin 2 (LCN2) belongs to the superfamily of lipocalins which represent a group of small secreted proteins classified as extracellular transport proteins expressed in many tissues. LCN2 is strongly increased in experimental models of acute and chronic liver injuries. To investigate the function of LCN2 in normal liver homeostasis and under conditions of inflammatory liver injury, we comparatively analyzed hepatic extracts taken from Lcn2-deficient and wild type mice under basal conditions and after stimulation with lipopolysaccharides. Liver was chemically and mechanically lysed and extracts were subjected to 2-D-DIGE after minimal labeling (G200 and G300 dyes) using an appropriate internal standard (G100). Afterwards MALDI TOF MS and MS/MS were used to identify differentially expressed proteins. Proteins that were identified to be differentially expressed include for example the chloride intracellular channel protein 4 (CLIC4), aminoacylase 1 and transketolase. The altered expression of respective genes was confirmed by Western blot analysis and further validated by quantitative real time PCR. Altogether, the complex expression alterations in mice lacking LCN2 under normal conditions and after exposure to inflammatory stimuli reveal that LCN2 has essential function in liver homeostasis and in the onset of inflammatory responses in which LCN2 expression dramatically increases. © 2012 Elsevier B.V. |
Persistent Identifier | http://hdl.handle.net/10722/292036 |
ISSN | 2021 Impact Factor: 3.855 2020 SCImago Journal Rankings: 1.067 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Labbus, Kirsten | - |
dc.contributor.author | Henning, Marc | - |
dc.contributor.author | Borkham-Kamphorst, Erawan | - |
dc.contributor.author | Geisler, Cordelia | - |
dc.contributor.author | Berger, Thorsten | - |
dc.contributor.author | Mak, Tak W. | - |
dc.contributor.author | Knüchel, Ruth | - |
dc.contributor.author | Meyer, Helmut E. | - |
dc.contributor.author | Weiskirchen, Ralf | - |
dc.contributor.author | Henkel, Corinna | - |
dc.date.accessioned | 2020-11-17T14:55:38Z | - |
dc.date.available | 2020-11-17T14:55:38Z | - |
dc.date.issued | 2013 | - |
dc.identifier.citation | Journal of Proteomics, 2013, v. 78, p. 188-196 | - |
dc.identifier.issn | 1874-3919 | - |
dc.identifier.uri | http://hdl.handle.net/10722/292036 | - |
dc.description.abstract | Lipocalin 2 (LCN2) belongs to the superfamily of lipocalins which represent a group of small secreted proteins classified as extracellular transport proteins expressed in many tissues. LCN2 is strongly increased in experimental models of acute and chronic liver injuries. To investigate the function of LCN2 in normal liver homeostasis and under conditions of inflammatory liver injury, we comparatively analyzed hepatic extracts taken from Lcn2-deficient and wild type mice under basal conditions and after stimulation with lipopolysaccharides. Liver was chemically and mechanically lysed and extracts were subjected to 2-D-DIGE after minimal labeling (G200 and G300 dyes) using an appropriate internal standard (G100). Afterwards MALDI TOF MS and MS/MS were used to identify differentially expressed proteins. Proteins that were identified to be differentially expressed include for example the chloride intracellular channel protein 4 (CLIC4), aminoacylase 1 and transketolase. The altered expression of respective genes was confirmed by Western blot analysis and further validated by quantitative real time PCR. Altogether, the complex expression alterations in mice lacking LCN2 under normal conditions and after exposure to inflammatory stimuli reveal that LCN2 has essential function in liver homeostasis and in the onset of inflammatory responses in which LCN2 expression dramatically increases. © 2012 Elsevier B.V. | - |
dc.language | eng | - |
dc.relation.ispartof | Journal of Proteomics | - |
dc.subject | LCN2 | - |
dc.subject | Difference gel electrophoresis (DIGE) | - |
dc.subject | Lipocalin 2 | - |
dc.subject | NGAL | - |
dc.subject | Proteomics | - |
dc.subject | Liver injury | - |
dc.title | Proteomic profiling in Lipocalin 2 deficient mice under normal and inflammatory conditions | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1016/j.jprot.2012.11.021 | - |
dc.identifier.pmid | 23219901 | - |
dc.identifier.scopus | eid_2-s2.0-84871391215 | - |
dc.identifier.volume | 78 | - |
dc.identifier.spage | 188 | - |
dc.identifier.epage | 196 | - |
dc.identifier.eissn | 1876-7737 | - |
dc.identifier.isi | WOS:000316706800015 | - |
dc.identifier.issnl | 1874-3919 | - |