4jgm: Difference between revisions
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{{STRUCTURE_4jgm| PDB=4jgm | SCENE= }} | |||
===Crystal structure of RelB double mutants: Y300F/I335V=== | |||
{{ABSTRACT_PUBMED_23485337}} | |||
The | ==Function== | ||
[[http://www.uniprot.org/uniprot/RELB_MOUSE RELB_MOUSE]] NF-kappa-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. NF-kappa-B heterodimeric RelB-p50 and RelB-p52 complexes are transcriptional activators. RELB neither associates with DNA nor with RELA/p65 or REL. Stimulates promoter activity in the presence of NFKB2/p49 (By similarity). As a member of the NUPR1/RELB/IER3 survival pathway, may allow the development of pancreatic intraepithelial neoplasias.<ref>PMID:22565310</ref> | |||
==About this Structure== | |||
[[4jgm]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4JGM OCA]. | |||
==Reference== | |||
<ref group="xtra">PMID:023485337</ref><references group="xtra"/><references/> | |||
[[Category: Ghosh, G.]] | |||
[[Category: Huang, D B.]] | |||
[[Category: Vu, D.]] | |||
[[Category: Intertwined dimer]] | |||
[[Category: Side-by side dimer]] | |||
[[Category: Transcription]] | |||
[[Category: Transcription factor]] | |||
Revision as of 11:08, 15 January 2014
Crystal structure of RelB double mutants: Y300F/I335VCrystal structure of RelB double mutants: Y300F/I335V
Template:ABSTRACT PUBMED 23485337
FunctionFunction
[RELB_MOUSE] NF-kappa-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. NF-kappa-B heterodimeric RelB-p50 and RelB-p52 complexes are transcriptional activators. RELB neither associates with DNA nor with RELA/p65 or REL. Stimulates promoter activity in the presence of NFKB2/p49 (By similarity). As a member of the NUPR1/RELB/IER3 survival pathway, may allow the development of pancreatic intraepithelial neoplasias.[1]
About this StructureAbout this Structure
4jgm is a 1 chain structure. Full crystallographic information is available from OCA.
ReferenceReference
- ↑ Vu D, Huang DB, Vemu A, Ghosh G. A Structural Basis for Selective Dimerization by NF-kappaB RelB. J Mol Biol. 2013 Feb 26. pii: S0022-2836(13)00122-8. doi:, 10.1016/j.jmb.2013.02.020. PMID:23485337 doi:10.1016/j.jmb.2013.02.020
- ↑ Hamidi T, Algul H, Cano CE, Sandi MJ, Molejon MI, Riemann M, Calvo EL, Lomberk G, Dagorn JC, Weih F, Urrutia R, Schmid RM, Iovanna JL. Nuclear protein 1 promotes pancreatic cancer development and protects cells from stress by inhibiting apoptosis. J Clin Invest. 2012 Jun 1;122(6):2092-103. doi: 10.1172/JCI60144. Epub 2012 May, 8. PMID:22565310 doi:10.1172/JCI60144