1mpv: Difference between revisions
No edit summary |
No edit summary |
||
Line 1: | Line 1: | ||
==Structure of bhpBR3, the BAFF-binding loop of BR3 embedded in a beta-hairpin peptide== | ==Structure of bhpBR3, the BAFF-binding loop of BR3 embedded in a beta-hairpin peptide== | ||
<StructureSection load='1mpv' size='340' side='right' caption='[[1mpv]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''> | <StructureSection load='1mpv' size='340' side='right'caption='[[1mpv]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[1mpv]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1MPV OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1MPV FirstGlance]. <br> | <table><tr><td colspan='2'>[[1mpv]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1MPV OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1MPV FirstGlance]. <br> | ||
Line 24: | Line 24: | ||
__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
[[Category: Large Structures]] | |||
[[Category: Cochran, A G]] | [[Category: Cochran, A G]] | ||
[[Category: Dixit, V M]] | [[Category: Dixit, V M]] |
Revision as of 10:56, 31 July 2019
Structure of bhpBR3, the BAFF-binding loop of BR3 embedded in a beta-hairpin peptideStructure of bhpBR3, the BAFF-binding loop of BR3 embedded in a beta-hairpin peptide
Structural highlights
Disease[TR13C_HUMAN] Defects in TNFRSF13C are the cause of immunodeficiency common variable type 4 (CVID4) [MIM:613494]; also called antibody deficiency due to BAFFR defect. CVID4 is a primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. The defect results from a failure of B-cell differentiation and impaired secretion of immunoglobulins; the numbers of circulating B-cells is usually in the normal range, but can be low.[1] Function[TR13C_HUMAN] B-cell receptor specific for TNFSF13B/TALL1/BAFF/BLyS. Promotes the survival of mature B-cells and the B-cell response.[2] [3] Publication Abstract from PubMedThe TNF-like ligand BAFF/BLyS is a potent survival factor for B cells. It binds three receptors: TACI, BCMA, and BR3. We show that BR3 signaling promotes processing of the transcription factor NF-kappaB2/p100 to p52. NF-kappaB2/p100 cleavage was abrogated in B cells from A/WySnJ mice possessing a mutant BR3 gene, but not in TACI or BCMA null B cells. Furthermore, wild-type mice injected with BAFF-neutralizing BR3-Fc protein showed reduced basal NF-kappaB2 activation. BR3-Fc treatment of NZB/WF1 mice, which develop a fatal lupus-like syndrome, inhibited NF-kappaB2 processing and attenuated the disease process. Since inhibiting the BR3-BAFF interaction has therapeutic ramifications, the ligand binding interface of BR3 was investigated and found to reside within a 26 residue core domain. When stabilized within a structured beta-hairpin peptide, six of these residues were sufficient to confer binding to BAFF. BAFF/BLyS receptor 3 binds the B cell survival factor BAFF ligand through a discrete surface loop and promotes processing of NF-kappaB2.,Kayagaki N, Yan M, Seshasayee D, Wang H, Lee W, French DM, Grewal IS, Cochran AG, Gordon NC, Yin J, Starovasnik MA, Dixit VM Immunity. 2002 Oct;17(4):515-24. PMID:12387744[4] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. References
|
|