Identification and molecular characterization of Mnk1b, a splice variant of human MAP kinase-interacting kinase Mnk1
In this paper, we report the identification and molecular characterization of a splice variant of human Mnk1 which has been named as Mnk1b. Human Mnk1b mRNA is homologous to human Mnk1 mRNA but lacking a region corresponding to exon 19, which causes a change in the reading frame generating a stop co...
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Veröffentlicht in: | Experimental cell research 2004-10, Vol.299 (2), p.343-355 |
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description | In this paper, we report the identification and molecular characterization of a splice variant of human Mnk1 which has been named as Mnk1b. Human Mnk1b mRNA is homologous to human Mnk1 mRNA but lacking a region corresponding to exon 19, which causes a change in the reading frame generating a stop codon. The resulting protein lacks the last 89 amino acids at the C-terminal region that are replaced by 12 amino acids with an entirely new sequence. The C-terminal end in Mnk1 corresponds to the extracellular signal-regulated kinase (ERK1/2) binding site. Although Mnk1b lacks this domain and, consequently, is not phosphorylated by ERK1/2, it is able, however, to phosphorylate eIF4E in vitro and in vivo in a mitogen-activated protein kinases-independent manner. This result suggests that Mnk1b may play a key role in regulating protein translation in the absence of stimuli. Interestingly, a significant population of cells shows Mnk1b within the nucleus whereas Mnk1 is always detected in the cytoplasm. This fact may be explained because Mnk1b maintains the nuclear localization signal (NLS) but lacks the nuclear export sequence (NES). |
doi_str_mv | 10.1016/j.yexcr.2004.06.006 |
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Human Mnk1b mRNA is homologous to human Mnk1 mRNA but lacking a region corresponding to exon 19, which causes a change in the reading frame generating a stop codon. The resulting protein lacks the last 89 amino acids at the C-terminal region that are replaced by 12 amino acids with an entirely new sequence. The C-terminal end in Mnk1 corresponds to the extracellular signal-regulated kinase (ERK1/2) binding site. Although Mnk1b lacks this domain and, consequently, is not phosphorylated by ERK1/2, it is able, however, to phosphorylate eIF4E in vitro and in vivo in a mitogen-activated protein kinases-independent manner. This result suggests that Mnk1b may play a key role in regulating protein translation in the absence of stimuli. Interestingly, a significant population of cells shows Mnk1b within the nucleus whereas Mnk1 is always detected in the cytoplasm. This fact may be explained because Mnk1b maintains the nuclear localization signal (NLS) but lacks the nuclear export sequence (NES).</description><identifier>ISSN: 0014-4827</identifier><identifier>EISSN: 1090-2422</identifier><identifier>DOI: 10.1016/j.yexcr.2004.06.006</identifier><identifier>PMID: 15350534</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Alternative Splicing ; Amino Acid Sequence ; Binding Sites ; Cell Nucleus ; eIF4E ; Eukaryotic Initiation Factor-4E - metabolism ; Genetic Variation - genetics ; Humans ; Intracellular Signaling Peptides and Proteins ; MAP kinases ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinases - metabolism ; Mnk1 ; Molecular Sequence Data ; Phosphorylation ; Protein Isoforms ; Protein translation ; Protein-Serine-Threonine Kinases - genetics ; Protein-Serine-Threonine Kinases - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Sequence Homology, Amino Acid</subject><ispartof>Experimental cell research, 2004-10, Vol.299 (2), p.343-355</ispartof><rights>2004 Elsevier Inc.</rights><rights>Copyright 2004 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c386t-cb7150e9c37e0a6a8d8f598bdee54146acab52b747e71f563ba343f38544b0693</citedby><cites>FETCH-LOGICAL-c386t-cb7150e9c37e0a6a8d8f598bdee54146acab52b747e71f563ba343f38544b0693</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.yexcr.2004.06.006$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,782,786,3554,27933,27934,46004</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15350534$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>O'Loghlen, Ana</creatorcontrib><creatorcontrib>González, Vı́ctor M.</creatorcontrib><creatorcontrib>Piñeiro, David</creatorcontrib><creatorcontrib>Pérez-Morgado, M.Isabel</creatorcontrib><creatorcontrib>Salinas, Matilde</creatorcontrib><creatorcontrib>Martı́n, M.Elena</creatorcontrib><title>Identification and molecular characterization of Mnk1b, a splice variant of human MAP kinase-interacting kinase Mnk1</title><title>Experimental cell research</title><addtitle>Exp Cell Res</addtitle><description>In this paper, we report the identification and molecular characterization of a splice variant of human Mnk1 which has been named as Mnk1b. Human Mnk1b mRNA is homologous to human Mnk1 mRNA but lacking a region corresponding to exon 19, which causes a change in the reading frame generating a stop codon. The resulting protein lacks the last 89 amino acids at the C-terminal region that are replaced by 12 amino acids with an entirely new sequence. The C-terminal end in Mnk1 corresponds to the extracellular signal-regulated kinase (ERK1/2) binding site. Although Mnk1b lacks this domain and, consequently, is not phosphorylated by ERK1/2, it is able, however, to phosphorylate eIF4E in vitro and in vivo in a mitogen-activated protein kinases-independent manner. This result suggests that Mnk1b may play a key role in regulating protein translation in the absence of stimuli. Interestingly, a significant population of cells shows Mnk1b within the nucleus whereas Mnk1 is always detected in the cytoplasm. This fact may be explained because Mnk1b maintains the nuclear localization signal (NLS) but lacks the nuclear export sequence (NES).</description><subject>Alternative Splicing</subject><subject>Amino Acid Sequence</subject><subject>Binding Sites</subject><subject>Cell Nucleus</subject><subject>eIF4E</subject><subject>Eukaryotic Initiation Factor-4E - metabolism</subject><subject>Genetic Variation - genetics</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins</subject><subject>MAP kinases</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Mnk1</subject><subject>Molecular Sequence Data</subject><subject>Phosphorylation</subject><subject>Protein Isoforms</subject><subject>Protein translation</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Sequence Homology, Amino Acid</subject><issn>0014-4827</issn><issn>1090-2422</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhi0EotvCL0BCPnEiYRx_xDlwqKoClVrBAc7WxJlQbxNnsZOq5deT7a7EDU4jeZ73HckPY28ElAKE-bAtH-nBp7ICUCWYEsA8YxsBDRSVqqrnbAMgVKFsVZ-w05y3AGCtMC_ZidBSg5Zqw-arjuIc-uBxDlPkGDs-TgP5ZcDE_S0m9DOl8Puwnnp-E-9E-54jz7sheOL3mALGeb-6XUaM_Ob8G78LETMVIa7ZtSDEn8enp_gr9qLHIdPr4zxjPz5dfr_4Ulx__Xx1cX5deGnNXPi2Fhqo8bImQIO2s71ubNsRaSWUQY-trtpa1VSLXhvZolSyl1Yr1YJp5Bl7d-jdpenXQnl2Y8iehgEjTUt2xlgNqqn_C4ra6loDrKA8gD5NOSfq3S6FEdOjE-D2VtzWPVlxeysOjFutrKm3x_qlHan7mzlqWIGPB4DW37gPlFz2gaKnLiTys-um8M8DfwBWX5-1</recordid><startdate>20041001</startdate><enddate>20041001</enddate><creator>O'Loghlen, Ana</creator><creator>González, Vı́ctor M.</creator><creator>Piñeiro, David</creator><creator>Pérez-Morgado, M.Isabel</creator><creator>Salinas, Matilde</creator><creator>Martı́n, M.Elena</creator><general>Elsevier Inc</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>7TM</scope><scope>7X8</scope></search><sort><creationdate>20041001</creationdate><title>Identification and molecular characterization of Mnk1b, a splice variant of human MAP kinase-interacting kinase Mnk1</title><author>O'Loghlen, Ana ; González, Vı́ctor M. ; Piñeiro, David ; Pérez-Morgado, M.Isabel ; Salinas, Matilde ; Martı́n, M.Elena</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c386t-cb7150e9c37e0a6a8d8f598bdee54146acab52b747e71f563ba343f38544b0693</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Alternative Splicing</topic><topic>Amino Acid Sequence</topic><topic>Binding Sites</topic><topic>Cell Nucleus</topic><topic>eIF4E</topic><topic>Eukaryotic Initiation Factor-4E - metabolism</topic><topic>Genetic Variation - genetics</topic><topic>Humans</topic><topic>Intracellular Signaling Peptides and Proteins</topic><topic>MAP kinases</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Mnk1</topic><topic>Molecular Sequence Data</topic><topic>Phosphorylation</topic><topic>Protein Isoforms</topic><topic>Protein translation</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Sequence Homology, Amino Acid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>O'Loghlen, Ana</creatorcontrib><creatorcontrib>González, Vı́ctor M.</creatorcontrib><creatorcontrib>Piñeiro, David</creatorcontrib><creatorcontrib>Pérez-Morgado, M.Isabel</creatorcontrib><creatorcontrib>Salinas, Matilde</creatorcontrib><creatorcontrib>Martı́n, M.Elena</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental cell research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>O'Loghlen, Ana</au><au>González, Vı́ctor M.</au><au>Piñeiro, David</au><au>Pérez-Morgado, M.Isabel</au><au>Salinas, Matilde</au><au>Martı́n, M.Elena</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identification and molecular characterization of Mnk1b, a splice variant of human MAP kinase-interacting kinase Mnk1</atitle><jtitle>Experimental cell research</jtitle><addtitle>Exp Cell Res</addtitle><date>2004-10-01</date><risdate>2004</risdate><volume>299</volume><issue>2</issue><spage>343</spage><epage>355</epage><pages>343-355</pages><issn>0014-4827</issn><eissn>1090-2422</eissn><abstract>In this paper, we report the identification and molecular characterization of a splice variant of human Mnk1 which has been named as Mnk1b. Human Mnk1b mRNA is homologous to human Mnk1 mRNA but lacking a region corresponding to exon 19, which causes a change in the reading frame generating a stop codon. The resulting protein lacks the last 89 amino acids at the C-terminal region that are replaced by 12 amino acids with an entirely new sequence. The C-terminal end in Mnk1 corresponds to the extracellular signal-regulated kinase (ERK1/2) binding site. Although Mnk1b lacks this domain and, consequently, is not phosphorylated by ERK1/2, it is able, however, to phosphorylate eIF4E in vitro and in vivo in a mitogen-activated protein kinases-independent manner. This result suggests that Mnk1b may play a key role in regulating protein translation in the absence of stimuli. Interestingly, a significant population of cells shows Mnk1b within the nucleus whereas Mnk1 is always detected in the cytoplasm. This fact may be explained because Mnk1b maintains the nuclear localization signal (NLS) but lacks the nuclear export sequence (NES).</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15350534</pmid><doi>10.1016/j.yexcr.2004.06.006</doi><tpages>13</tpages></addata></record> |
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subjects | Alternative Splicing Amino Acid Sequence Binding Sites Cell Nucleus eIF4E Eukaryotic Initiation Factor-4E - metabolism Genetic Variation - genetics Humans Intracellular Signaling Peptides and Proteins MAP kinases Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases - metabolism Mnk1 Molecular Sequence Data Phosphorylation Protein Isoforms Protein translation Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Reverse Transcriptase Polymerase Chain Reaction Sequence Homology, Amino Acid |
title | Identification and molecular characterization of Mnk1b, a splice variant of human MAP kinase-interacting kinase Mnk1 |
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