MAPK: Perbedaan antara revisi
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'''Kinase MAP''' ({{lang-en|mitogen-activated protein kinase; c-Jun N-terminal kinase; Dp38; ERK; ERK1; ERK2; extracellular signal-regulated kinase; JNK; JNK3α1; LeMPK3; MAP kinase; MAP-2 kinase; MAPK; MBP kinase I; MBP kinase II; microtubule-associated protein 2 kinase; microtubule-associated protein kinase; myelin basic protein kinase; p38δ; p38-2; p42 mitogen-activated protein kinase; p42<sup>mapk</sup>; PMK-1; PMK-2; PMK-3; pp42; pp44<sup>mapk</sup>; p44mpk; SAPK; STK26; stress-activated protein kinase; ATP:protein phosphotransferase (MAPKK-activated); Extracellular signal-regulated kinase, ERK,<ref>{{en}}{{cite web |
'''Kinase MAP''' ({{lang-en|mitogen-activated protein kinase; c-Jun N-terminal kinase; Dp38; ERK; ERK1; ERK2; extracellular signal-regulated kinase; JNK; JNK3α1; LeMPK3; MAP kinase; MAP-2 kinase; MAPK; MBP kinase I; MBP kinase II; microtubule-associated protein 2 kinase; microtubule-associated protein kinase; myelin basic protein kinase; p38δ; p38-2; p42 mitogen-activated protein kinase; p42<sup>mapk</sup>; PMK-1; PMK-2; PMK-3; pp42; pp44<sup>mapk</sup>; p44mpk; SAPK; STK26; stress-activated protein kinase; ATP:protein phosphotransferase (MAPKK-activated); Extracellular signal-regulated kinase, ERK,<ref>{{en}} {{cite web |
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| url = http://www.ncbi.nlm.nih.gov/pubmed/8261431 |
| url = http://www.ncbi.nlm.nih.gov/pubmed/8261431 |
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| title = X-irradiation, phorbol esters, and H2O2 stimulate mitogen-activated protein kinase activity in NIH-3T3 cells through the formation of reactive oxygen intermediates |
| title = X-irradiation, phorbol esters, and H2O2 stimulate mitogen-activated protein kinase activity in NIH-3T3 cells through the formation of reactive oxygen intermediates |
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| accessdate = 2011-07-10 |
| accessdate = 2011-07-10 |
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| work = Dana Farber Cancer Institute, Harvard Medical School; Stevenson MA, Pollock SS, Coleman CN, Calderwood SK. |
| work = Dana Farber Cancer Institute, Harvard Medical School; Stevenson MA, Pollock SS, Coleman CN, Calderwood SK. |
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}}</ref> MAPK; EC 2.7.11.24}}) adalah [[enzim]] [[protein|peptida]] dari jenis [[kinase protein]] yang teraktivasi sebagai respon |
}}</ref> MAPK; EC 2.7.11.24}}) adalah [[enzim]] [[protein|peptida]] dari jenis [[kinase protein]] yang teraktivasi sebagai respon seluler terhadap berbagai jenis [[hormon]] [[faktor pertumbuhan]],<ref>{{en}} {{cite book|title=Molecular Cell Biology|author=Harvey Lodish, Arnold Berk, S Lawrence Zipursky, Paul Matsudaira, David Baltimore, dan James Darnell|work=|isbn=0-7167-3136-3|edition=4|year=2000|page=MAP Kinase|publisher=W. H. Freeman and Company|url=http://www.ncbi.nlm.nih.gov/books/NBK21607/def-item/A7634|accessdate=2011-07-08}}</ref> dan mengkatalis reaksi [[fosforilasi]] terhadap jenis protein tertentu pada residu [[serina]]/[[treonina]],<ref name="PM2550926">{{en}} {{cite web |
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| url = http://www.ncbi.nlm.nih.gov/pubmed/2550926 |
| url = http://www.ncbi.nlm.nih.gov/pubmed/2550926 |
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| title = Evidence that pp42, a major tyrosine kinase target protein, is a mitogen-activated serine/threonine protein kinase |
| title = Evidence that pp42, a major tyrosine kinase target protein, is a mitogen-activated serine/threonine protein kinase |
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| accessdate = 2011-07-09 |
| accessdate = 2011-07-09 |
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| work = Department of Microbiology, University of Virginia School of Medicine; Rossomando AJ, Payne DM, Weber MJ, Sturgill TW. |
| work = Department of Microbiology, University of Virginia School of Medicine; Rossomando AJ, Payne DM, Weber MJ, Sturgill TW. |
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}}</ref> termasuk [[Kinase ribosomal s6|Rsk]]<ref>{{en}}{{cite web |
}}</ref> termasuk [[Kinase ribosomal s6|Rsk]]<ref>{{en}} {{cite web |
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| url = Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms |
| url = Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms |
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| title = Humoral Immunity |
| title = Humoral Immunity |
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| work = Division of Neuroscience, Children's Hospital, and Department of Neurobiology, Harvard Medical School; Bonni A, Brunet A, West AE, Datta SR, Takasu MA, Greenberg ME. |
| work = Division of Neuroscience, Children's Hospital, and Department of Neurobiology, Harvard Medical School; Bonni A, Brunet A, West AE, Datta SR, Takasu MA, Greenberg ME. |
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}}</ref> dan [[faktor transkripsi]] yang terdapat pada [[inti sel]],<ref>{{en}} {{cite book|title=Molecular Cell Biology|author=Harvey Lodish, Arnold Berk, S Lawrence Zipursky, Paul Matsudaira, David Baltimore, dan James Darnell|work=|isbn=0-7167-3136-3|edition=4|year=2000|page=Section 20.5 MAP Kinase Pathways|publisher=W. H. Freeman and Company|url=http://www.ncbi.nlm.nih.gov/books/NBK21529|accessdate=2011-07-08}}</ref> pada jenjang reaksi berikutnya:<ref>{{en}} {{cite web|url=http://www.chem.qmul.ac.uk/iubmb/enzyme/EC2/7/11/24.html|title=EC 2.7.11.24|accessdate=2011-07-08|work=Queen Mary University of London}}</ref> |
}}</ref> dan [[faktor transkripsi]] yang terdapat pada [[inti sel]],<ref>{{en}} {{cite book|title=Molecular Cell Biology|author=Harvey Lodish, Arnold Berk, S Lawrence Zipursky, Paul Matsudaira, David Baltimore, dan James Darnell|work=|isbn=0-7167-3136-3|edition=4|year=2000|page=Section 20.5 MAP Kinase Pathways|publisher=W. H. Freeman and Company|url=http://www.ncbi.nlm.nih.gov/books/NBK21529|accessdate=2011-07-08}}</ref> pada jenjang reaksi berikutnya:<ref>{{en}} {{cite web|url=http://www.chem.qmul.ac.uk/iubmb/enzyme/EC2/7/11/24.html|title=EC 2.7.11.24|accessdate=2011-07-08|work=Queen Mary University of London}}</ref> |
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:<math>\mbox{ATP} + \mbox{protein} \rightarrow \mbox{ADP} + \mbox{fosfoprotein} \, </math> |
:<math>\mbox{ATP} + \mbox{protein} \rightarrow \mbox{ADP} + \mbox{fosfoprotein} \, </math> |
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Pada [[fibroblas]], protein ini terlebih dahulu akan mengalami reaksi fosforilasi transien pada residu [[tirosina]] setelah adanya stimulasi [[fibroblas]] oleh berbagai [[mitogen]], seperti ''epidermal growth factor'', ''platelet-derived growth factor'', ''phorbol 12-myristate 13-acetate'', [[trombin]], dan ''insulin-like growth factor II''.<ref name="PM2550926" /> Induksi fosforilasi yang terjadi pada MAPK oleh begitu banyak jenis mitogen, membuat kita mengambil [[ |
Pada [[fibroblas]], protein ini terlebih dahulu akan mengalami reaksi fosforilasi transien pada residu [[tirosina]] setelah adanya stimulasi [[fibroblas]] oleh berbagai [[mitogen]], seperti ''epidermal growth factor'', ''platelet-derived growth factor'', ''phorbol 12-myristate 13-acetate'', [[trombin]], dan ''insulin-like growth factor II''.<ref name="PM2550926" /> Induksi fosforilasi yang terjadi pada MAPK oleh begitu banyak jenis mitogen, membuat kita mengambil [[hipotesis]] bahwa reaksi ini merupakan jenjang reaksi yang penting bagi transisi [[siklus sel|siklus]] [[sel (biologi)|sel]] dari [[fase]] G<sub>0</sub> menuju fase G<sub>1</sub>. |
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== Lintasan metabolisme == |
== Lintasan metabolisme == |
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Pada [[mamalia]], [[Lintasan metabolisme|lintasan]] MAPK mempengaruhi berbagai respon |
Pada [[mamalia]], [[Lintasan metabolisme|lintasan]] MAPK mempengaruhi berbagai respon seluler terhadap stimulus seperti [[mitogen]], [[stres]] dan perkembangan [[tubuh]], kopling terjadi pada jenjang [[enzim]] [[Kinase MAPKK|MAP3K]] → [[Kinase MAPK|MEK]] → MAPK.<ref>{{en}} {{cite web |
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| url = http://www.ncbi.nlm.nih.gov/pubmed/11784851 |
| url = http://www.ncbi.nlm.nih.gov/pubmed/11784851 |
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| title = Direct activation of mitogen-activated protein kinase kinase kinase MEKK1 by the Ste20p homologue GCK and the adapter protein TRAF2. |
| title = Direct activation of mitogen-activated protein kinase kinase kinase MEKK1 by the Ste20p homologue GCK and the adapter protein TRAF2. |
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| accessdate = 2011-07-10 |
| accessdate = 2011-07-10 |
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| work = Diabetes Research Laboratory, Medical Services, Massachusetts General Hospital, Harvard Medical School; Chadee DN, Yuasa T, Kyriakis JM. |
| work = Diabetes Research Laboratory, Medical Services, Massachusetts General Hospital, Harvard Medical School; Chadee DN, Yuasa T, Kyriakis JM. |
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}}</ref> Awalnya, [[Ras]], sejenis [[protein]] yang membentuk [[ikatan kovalen]] dengan [[gugus fungsional|gugus]] [[farnesil]] [[molekul]] [[asam lemak]] pada sisi dalam [[membran plasma]] sel, setelah teraktivasi oleh [[RTK]] akan mengikat pada domain terminal-N dari [[Raf]].<ref>{{en}}{{cite book |
}}</ref> Awalnya, [[Ras]], sejenis [[protein]] yang membentuk [[ikatan kovalen]] dengan [[gugus fungsional|gugus]] [[farnesil]] [[molekul]] [[asam lemak]] pada sisi dalam [[membran plasma]] sel, setelah teraktivasi oleh [[RTK]] akan mengikat pada domain terminal-N dari [[Raf]].<ref>{{en}} {{cite book |
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|title = Molecular Cell Biology |
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|author = Harvey Lodish, Arnold Berk, S Lawrence Zipursky, Paul Matsudaira, David Baltimore, and James Darnell. |
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|work = |
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|isbn = 0--7167-3136-3 |
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|edition = 4 |
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|year = 2000 |
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|page = Section 20.5MAP Kinase Pathways |
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|publisher = W. H. Freeman and Company. |
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|url = http://www.ncbi.nlm.nih.gov/books/NBK21529/#A5846 |
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|accessdate = 2011-07-09 |
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}}</ref> Kemudian, Raf akan mengikat dan menginduksi fosforilasi pada MEK, setelah itu MEK akan menginduksi fosforilasi MAPK pada residu [[tirosina]] pY185 dan [[treonina]] pT183 dan membuat MAPK teraktivasi. Setelah itu MAPK akan mengaktivasi [[ETS]].<ref>{{en}}{{cite web |
}}</ref> Kemudian, Raf akan mengikat dan menginduksi fosforilasi pada MEK, setelah itu MEK akan menginduksi fosforilasi MAPK pada residu [[tirosina]] pY185 dan [[treonina]] pT183 dan membuat MAPK teraktivasi. Setelah itu MAPK akan mengaktivasi [[ETS]].<ref>{{en}} {{cite web |
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| url = http://www.ncbi.nlm.nih.gov/pubmed/15572696 |
| url = http://www.ncbi.nlm.nih.gov/pubmed/15572696 |
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| title = Ras/mitogen-activated protein kinase signaling activates Ets-1 and Ets-2 by CBP/p300 recruitment. |
| title = Ras/mitogen-activated protein kinase signaling activates Ets-1 and Ets-2 by CBP/p300 recruitment. |
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[[Kategori:Enzim]] |
[[Kategori:Enzim]] |
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[[cs:MAP kináza]] |
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[[en:Mitogen-activated protein kinase]] |
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[[ja:分裂促進因子活性化タンパク質キナーゼ]] |
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[[pl:Kinazy aktywowane mitogenami]] |
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[[sr:Mitogenom-aktivirane proteinske kinaze]] |
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[[ur:انقسامیہ مفاعل لحمیاتی حرمرہ]] |
Revisi terkini sejak 29 November 2019 12.32
Kinase MAP (bahasa Inggris: mitogen-activated protein kinase; c-Jun N-terminal kinase; Dp38; ERK; ERK1; ERK2; extracellular signal-regulated kinase; JNK; JNK3α1; LeMPK3; MAP kinase; MAP-2 kinase; MAPK; MBP kinase I; MBP kinase II; microtubule-associated protein 2 kinase; microtubule-associated protein kinase; myelin basic protein kinase; p38δ; p38-2; p42 mitogen-activated protein kinase; p42mapk; PMK-1; PMK-2; PMK-3; pp42; pp44mapk; p44mpk; SAPK; STK26; stress-activated protein kinase; ATP:protein phosphotransferase (MAPKK-activated); Extracellular signal-regulated kinase, ERK,[1] MAPK; EC 2.7.11.24) adalah enzim peptida dari jenis kinase protein yang teraktivasi sebagai respon seluler terhadap berbagai jenis hormon faktor pertumbuhan,[2] dan mengkatalis reaksi fosforilasi terhadap jenis protein tertentu pada residu serina/treonina,[3] termasuk Rsk[4] dan faktor transkripsi yang terdapat pada inti sel,[5] pada jenjang reaksi berikutnya:[6]
Pada fibroblas, protein ini terlebih dahulu akan mengalami reaksi fosforilasi transien pada residu tirosina setelah adanya stimulasi fibroblas oleh berbagai mitogen, seperti epidermal growth factor, platelet-derived growth factor, phorbol 12-myristate 13-acetate, trombin, dan insulin-like growth factor II.[3] Induksi fosforilasi yang terjadi pada MAPK oleh begitu banyak jenis mitogen, membuat kita mengambil hipotesis bahwa reaksi ini merupakan jenjang reaksi yang penting bagi transisi siklus sel dari fase G0 menuju fase G1.
Lintasan metabolisme
[sunting | sunting sumber]Pada mamalia, lintasan MAPK mempengaruhi berbagai respon seluler terhadap stimulus seperti mitogen, stres dan perkembangan tubuh, kopling terjadi pada jenjang enzim MAP3K → MEK → MAPK.[7] Awalnya, Ras, sejenis protein yang membentuk ikatan kovalen dengan gugus farnesil molekul asam lemak pada sisi dalam membran plasma sel, setelah teraktivasi oleh RTK akan mengikat pada domain terminal-N dari Raf.[8] Kemudian, Raf akan mengikat dan menginduksi fosforilasi pada MEK, setelah itu MEK akan menginduksi fosforilasi MAPK pada residu tirosina pY185 dan treonina pT183 dan membuat MAPK teraktivasi. Setelah itu MAPK akan mengaktivasi ETS.[9]
Rujukan
[sunting | sunting sumber]- ^ (Inggris) "X-irradiation, phorbol esters, and H2O2 stimulate mitogen-activated protein kinase activity in NIH-3T3 cells through the formation of reactive oxygen intermediates". Dana Farber Cancer Institute, Harvard Medical School; Stevenson MA, Pollock SS, Coleman CN, Calderwood SK. Diakses tanggal 2011-07-10.
- ^ (Inggris) Harvey Lodish, Arnold Berk, S Lawrence Zipursky, Paul Matsudaira, David Baltimore, dan James Darnell (2000). Molecular Cell Biology (edisi ke-4). W. H. Freeman and Company. hlm. MAP Kinase. ISBN 0-7167-3136-3. Diakses tanggal 2011-07-08.
- ^ a b (Inggris) "Evidence that pp42, a major tyrosine kinase target protein, is a mitogen-activated serine/threonine protein kinase". Department of Microbiology, University of Virginia School of Medicine; Rossomando AJ, Payne DM, Weber MJ, Sturgill TW. Diakses tanggal 2011-07-09.
- ^ (Inggris) [Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms "Humoral Immunity"] Periksa nilai
|url=
(bantuan). Division of Neuroscience, Children's Hospital, and Department of Neurobiology, Harvard Medical School; Bonni A, Brunet A, West AE, Datta SR, Takasu MA, Greenberg ME. Diakses tanggal 2011-07-09. - ^ (Inggris) Harvey Lodish, Arnold Berk, S Lawrence Zipursky, Paul Matsudaira, David Baltimore, dan James Darnell (2000). Molecular Cell Biology (edisi ke-4). W. H. Freeman and Company. hlm. Section 20.5 MAP Kinase Pathways. ISBN 0-7167-3136-3. Diakses tanggal 2011-07-08.
- ^ (Inggris) "EC 2.7.11.24". Queen Mary University of London. Diakses tanggal 2011-07-08.
- ^ (Inggris) "Direct activation of mitogen-activated protein kinase kinase kinase MEKK1 by the Ste20p homologue GCK and the adapter protein TRAF2". Diabetes Research Laboratory, Medical Services, Massachusetts General Hospital, Harvard Medical School; Chadee DN, Yuasa T, Kyriakis JM. Diakses tanggal 2011-07-10.
- ^ (Inggris) Harvey Lodish, Arnold Berk, S Lawrence Zipursky, Paul Matsudaira, David Baltimore, and James Darnell. (2000). Molecular Cell Biology (edisi ke-4). W. H. Freeman and Company. hlm. Section 20.5MAP Kinase Pathways. ISBN 0--7167-3136-3. Diakses tanggal 2011-07-09.
- ^ (Inggris) "Ras/mitogen-activated protein kinase signaling activates Ets-1 and Ets-2 by CBP/p300 recruitment". Huntsman Cancer Institute, 2000 Circle of Hope, University of Utah; Foulds CE, Nelson ML, Blaszczak AG, Graves BJ. Diakses tanggal 2011-07-23.