3tti: Difference between revisions

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'''Unreleased structure'''


The entry 3tti is ON HOLD
==Crystal Structure of JNK3 complexed with CC-930, an orally active anti-fibrotic JNK inhibitor==
<StructureSection load='3tti' size='340' side='right'caption='[[3tti]], [[Resolution|resolution]] 2.20&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[3tti]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3TTI OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3TTI FirstGlance]. <br>
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.2&#8491;</td></tr>
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=KBI:TRANS-4-({9-[(3S)-TETRAHYDROFURAN-3-YL]-8-[(2,4,6-TRIFLUOROPHENYL)AMINO]-9H-PURIN-2-YL}AMINO)CYCLOHEXANOL'>KBI</scene></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=3tti FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3tti OCA], [https://pdbe.org/3tti PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3tti RCSB], [https://www.ebi.ac.uk/pdbsum/3tti PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3tti ProSAT]</span></td></tr>
</table>
== Disease ==
[https://www.uniprot.org/uniprot/MK10_HUMAN MK10_HUMAN] Defects in MAPK10 are a cause of epileptic encephalopathy Lennox-Gastaut type (EELG) [MIM:[https://omim.org/entry/606369 606369]. Epileptic encephalopathies of the Lennox-Gastaut group are childhood epileptic disorders characterized by severe psychomotor delay and seizures. Note=A chromosomal aberration involving MAPK10 has been found in a single patient. Translocation t(Y;4)(q11.2;q21) which causes MAPK10 truncation.
== Function ==
[https://www.uniprot.org/uniprot/MK10_HUMAN MK10_HUMAN] Serine/threonine-protein kinase involved in various processes such as neuronal proliferation, differentiation, migration and programmed cell death. Extracellular stimuli such as proinflammatory cytokines or physical stress stimulate the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK10/JNK3. In turn, MAPK10/JNK3 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN and ATF2 and thus regulates AP-1 transcriptional activity. Plays regulatory roles in the signaling pathways during neuronal apoptosis. Phosphorylates the neuronal microtubule regulator STMN2. Acts in the regulation of the beta-amyloid precursor protein/APP signaling during neuronal differentiation by phosphorylating APP. Participates also in neurite growth in spiral ganglion neurons.<ref>PMID:11718727</ref>


Authors: Plantevin Krenitsky, V, Nadolny, L, Delgado, M, Ayala, L, Clareen, S, Hilgraf, R, Albers, R, Hegde, S, D'Sidocky, N, Sapienza, J, Wright, J, McCarrick, M, Bahmanyar, S, Chamberlain, P, Delker, SL, Muir, J, Giegel, D, Xu, L, Celeridad, M, Lachowitzer, J, Bennett, B, Moghaddam, M, Khatsenko, O, Katz, J, Fan, R, Bai, A, Tang, Y, Shirley, MA, Benish, B, Bodine, T, Blease, K, Raymon, H, Cathers, BE, Satoh,Y
==See Also==
 
*[[Mitogen-activated protein kinase 3D structures|Mitogen-activated protein kinase 3D structures]]
Description: Crystal Structure of JNK3 complexed with CC-930, an orally active anti-fibrotic JNK inhibitor
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Albers R]]
[[Category: Ayala L]]
[[Category: Bahmanyar S]]
[[Category: Bai A]]
[[Category: Benish B]]
[[Category: Bennett B]]
[[Category: Blease K]]
[[Category: Bodine T]]
[[Category: Cathers BE]]
[[Category: Celeridad M]]
[[Category: Chamberlain P]]
[[Category: Clareen S]]
[[Category: D'Sidocky N]]
[[Category: Delgado M]]
[[Category: Delker SL]]
[[Category: Fan R]]
[[Category: Giegel D]]
[[Category: Hegde S]]
[[Category: Hilgraf R]]
[[Category: Katz J]]
[[Category: Khatsenko O]]
[[Category: Lachowitzer J]]
[[Category: McCarrick M]]
[[Category: Moghaddam M]]
[[Category: Muir J]]
[[Category: Nadolny L]]
[[Category: Plantevin-Krenitsky V]]
[[Category: Raymon H]]
[[Category: Sapienza J]]
[[Category: Satoh Y]]
[[Category: Shirley MA]]
[[Category: Tang Y]]
[[Category: Wright J]]
[[Category: Xu L]]

Latest revision as of 13:11, 1 March 2024

Crystal Structure of JNK3 complexed with CC-930, an orally active anti-fibrotic JNK inhibitorCrystal Structure of JNK3 complexed with CC-930, an orally active anti-fibrotic JNK inhibitor

Structural highlights

3tti is a 1 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA. For a guided tour on the structure components use FirstGlance.
Method:X-ray diffraction, Resolution 2.2Å
Ligands:,
Resources:FirstGlance, OCA, PDBe, RCSB, PDBsum, ProSAT

Disease

MK10_HUMAN Defects in MAPK10 are a cause of epileptic encephalopathy Lennox-Gastaut type (EELG) [MIM:606369. Epileptic encephalopathies of the Lennox-Gastaut group are childhood epileptic disorders characterized by severe psychomotor delay and seizures. Note=A chromosomal aberration involving MAPK10 has been found in a single patient. Translocation t(Y;4)(q11.2;q21) which causes MAPK10 truncation.

Function

MK10_HUMAN Serine/threonine-protein kinase involved in various processes such as neuronal proliferation, differentiation, migration and programmed cell death. Extracellular stimuli such as proinflammatory cytokines or physical stress stimulate the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK10/JNK3. In turn, MAPK10/JNK3 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN and ATF2 and thus regulates AP-1 transcriptional activity. Plays regulatory roles in the signaling pathways during neuronal apoptosis. Phosphorylates the neuronal microtubule regulator STMN2. Acts in the regulation of the beta-amyloid precursor protein/APP signaling during neuronal differentiation by phosphorylating APP. Participates also in neurite growth in spiral ganglion neurons.[1]

See Also

References

  1. ↑ Neidhart S, Antonsson B, Gillieron C, Vilbois F, Grenningloh G, Arkinstall S. c-Jun N-terminal kinase-3 (JNK3)/stress-activated protein kinase-beta (SAPKbeta) binds and phosphorylates the neuronal microtubule regulator SCG10. FEBS Lett. 2001 Nov 16;508(2):259-64. PMID:11718727

3tti, resolution 2.20Å

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