Mitogen-activated protein kinase kinase

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<StructureSection load='3os3' size='350' side='right' caption='Human MAP2K1 complex with an anticancer agent, ATP and Mg+2 ion (PDB entry [[3os3]])' scene='43/438474/Cv/4'>
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<StructureSection load='' size='350' side='right' caption='Human MAP2K1 complex with an anticancer agent, ATP and Mg+2 ion (PDB entry [[3os3]])' scene='43/438474/Cv/4'>
== Function ==
== Function ==
[[Mitogen-activated protein kinase kinase]] (MAP2K) are serine/threonine kinases which regulate various cellular activities in response to extracellular stimuli by mitogens, heat shock and more. MAP2K is part of the MAPK cascade which consists also of [[Mitogen-activated protein kinase|MAPK]] and [[Mitogen-activated protein kinase kinase kinase|MAP3K]] which are activated by phosphorylation. '''MAP2K''' activates [[Mitogen-activated protein kinase|MAPK]]<ref>PMID:9528964</ref>,<ref>PMID:8226933</ref>.
[[Mitogen-activated protein kinase kinase]] (MAP2K) are serine/threonine kinases which regulate various cellular activities in response to extracellular stimuli by mitogens, heat shock and more. MAP2K is part of the MAPK cascade which consists also of [[Mitogen-activated protein kinase|MAPK]] and [[Mitogen-activated protein kinase kinase kinase|MAP3K]] which are activated by phosphorylation. '''MAP2K''' activates [[Mitogen-activated protein kinase|MAPK]]<ref>PMID:9528964</ref>,<ref>PMID:8226933</ref>.
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**[[1wi0]] - mMAP2K5 PB1 domain – NMR<br />
**[[1wi0]] - mMAP2K5 PB1 domain – NMR<br />
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**[[1p38]] – hMAP2K5+hMAP2KK2<br />
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**[[5uoj]] – hMAP2K5+hMAP2KK2<br />
*MAP2K6
*MAP2K6

Revision as of 17:17, 28 December 2017

Human MAP2K1 complex with an anticancer agent, ATP and Mg+2 ion (PDB entry 3os3)

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3D Structures of Mitogen-activated protein kinase kinase

Updated on 28-December-2017

References

  1. ↑ Weyman CM, Wolfman A. Mitogen-activated protein kinase kinase (MEK) activity is required for inhibition of skeletal muscle differentiation by insulin-like growth factor 1 or fibroblast growth factor 2. Endocrinology. 1998 Apr;139(4):1794-800. PMID:9528964 doi:http://dx.doi.org/10.1210/endo.139.4.5950
  2. ↑ Zheng CF, Guan KL. Properties of MEKs, the kinases that phosphorylate and activate the extracellular signal-regulated kinases. J Biol Chem. 1993 Nov 15;268(32):23933-9. PMID:8226933
  3. ↑ Falchook GS, Lewis KD, Infante JR, Gordon MS, Vogelzang NJ, DeMarini DJ, Sun P, Moy C, Szabo SA, Roadcap LT, Peddareddigari VG, Lebowitz PF, Le NT, Burris HA 3rd, Messersmith WA, O'Dwyer PJ, Kim KB, Flaherty K, Bendell JC, Gonzalez R, Kurzrock R, Fecher LA. Activity of the oral MEK inhibitor trametinib in patients with advanced melanoma: a phase 1 dose-escalation trial. Lancet Oncol. 2012 Aug;13(8):782-9. doi: 10.1016/S1470-2045(12)70269-3. Epub 2012, Jul 16. PMID:22805292 doi:http://dx.doi.org/10.1016/S1470-2045(12)70269-3
  4. ↑ Su GH, Song JJ, Repasky EA, Schutte M, Kern SE. Mutation rate of MAP2K4/MKK4 in breast carcinoma. Hum Mutat. 2002 Jan;19(1):81. PMID:11754110 doi:http://dx.doi.org/10.1002/humu.9002
  5. ↑ Isshiki Y, Kohchi Y, Iikura H, Matsubara Y, Asoh K, Murata T, Kohchi M, Mizuguchi E, Tsujii S, Hattori K, Miura T, Yoshimura Y, Aida S, Miwa M, Saitoh R, Murao N, Okabe H, Belunis C, Janson C, Lukacs C, Schuck V, Shimma N. Design and synthesis of novel allosteric MEK inhibitor CH4987655 as an orally available anticancer agent. Bioorg Med Chem Lett. 2011 Jan 21. PMID:21316218 doi:10.1016/j.bmcl.2011.01.062

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