This old version of Proteopedia is provided for student assignments while the new version is undergoing repairs. Content and edits done in this old version of Proteopedia after March 1, 2026 will eventually be lost when it is retired in about June of 2026.


Apply for new accounts at the new Proteopedia. Your logins will work in both the old and new versions.


1jnk

From Proteopedia

(Difference between revisions)
Jump to: navigation, search
m (Protected "1jnk" [edit=sysop:move=sysop])
Line 1: Line 1:
-
[[Image:1jnk.png|left|200px]]
 
- 
{{STRUCTURE_1jnk| PDB=1jnk | SCENE= }}
{{STRUCTURE_1jnk| PDB=1jnk | SCENE= }}
- 
===THE C-JUN N-TERMINAL KINASE (JNK3S) COMPLEXED WITH MGAMP-PNP===
===THE C-JUN N-TERMINAL KINASE (JNK3S) COMPLEXED WITH MGAMP-PNP===
 +
{{ABSTRACT_PUBMED_9739089}}
-
{{ABSTRACT_PUBMED_9739089}}
+
==Disease==
 +
[[http://www.uniprot.org/uniprot/MK10_HUMAN MK10_HUMAN]] Defects in MAPK10 are a cause of epileptic encephalopathy Lennox-Gastaut type (EELG) [MIM:[http://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==
 +
[[http://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>
==About this Structure==
==About this Structure==
Line 11: Line 13:
==Reference==
==Reference==
-
<ref group="xtra">PMID:009739089</ref><ref group="xtra">PMID:010794408</ref><ref group="xtra">PMID:015048824</ref><references group="xtra"/>
+
<ref group="xtra">PMID:009739089</ref><ref group="xtra">PMID:010794408</ref><ref group="xtra">PMID:015048824</ref><references group="xtra"/><references/>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Su, M S.S.]]
[[Category: Su, M S.S.]]

Revision as of 04:46, 25 March 2013

Template:STRUCTURE 1jnk

Contents

THE C-JUN N-TERMINAL KINASE (JNK3S) COMPLEXED WITH MGAMP-PNP

Template:ABSTRACT PUBMED 9739089

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]

About this Structure

1jnk is a 1 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA.

Reference

  • Xie X, Gu Y, Fox T, Coll JT, Fleming MA, Markland W, Caron PR, Wilson KP, Su MS. Crystal structure of JNK3: a kinase implicated in neuronal apoptosis. Structure. 1998 Aug 15;6(8):983-91. PMID:9739089
  • Caffrey DR, O'Neill LA, Shields DC. A method to predict residues conferring functional differences between related proteins: application to MAP kinase pathways. Protein Sci. 2000 Apr;9(4):655-70. PMID:10794408 doi:10.1110/ps.9.4.655
  • Hicks JM, Hsu VL. The extended left-handed helix: a simple nucleic acid-binding motif. Proteins. 2004 May 1;55(2):330-8. PMID:15048824 doi:10.1002/prot.10630
  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

Proteopedia Page Contributors and Editors (what is this?)

OCA

Personal tools