関: BFA

WordNet

the 1st letter of the Roman alphabet (同)a
the blood group whose red cells carry the A antigen (同)type_A, group A

PrepTutorEJDIC

answer / ampere
arsenicの化学記号

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/10/09 15:20:35」(JST)

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Brefeldin A is a lactone antibiotic produced by fungal organisms such as Eupenicillium brefeldianum.^[1] Brefeldin A inhibits protein transport from the endoplasmic reticulum to the Golgi apparatus indirectly by preventing formation of COPI-mediated^[2] transport vesicles. Brefeldin A was initially isolated as an anti-viral antibiotic^[3] but is now primarily used in biological research to study protein transport.

Physical data

Brefeldin A forms a clear colorless solution at 10 mg/ml in both dichloromethane and methanol.^[4]

Biological effects

In mammalian and yeast cells, the main target of brefeldin A appears to be a Guanine nucleotide exchange factor called GBF1.^[5] GBF1 mediates formation of transport vesicles by recruiting COPI coat proteins to cargo-bound receptor proteins found in the membrane of the Golgi. Inhibition of GBF1 activity induced the retrograde movement of secretory proteins from the golgi to the ER. The collapse of the Golgi into the ER triggers activation of unfolded protein response (UPR) (or ER stress)^[6]^[7] which can result in apoptosis.

References

^ Hutchinson, C. R.; Shu-Wen, L.; McInnes, A. G.; Walter, J. A. (1983). "Comparative biochemistry of fatty acid and macrolide antibiotic (brefeldin a). Formation in penicillium brefeldianum". Tetrahedron 39 (21): 3507. doi:10.1016/S0040-4020(01)88660-9.
^ http://www.cellsignal.com/pdf/9972.pdf
^ Tamura G, Ando K, Suzuki S, Takatsuki A, Arima K (February 1968). "Antiviral activity of brefeldin A and verrucarin A". J. Antibiot. 21 (2): 160–1. doi:10.7164/antibiotics.21.160. PMID 4299889.
^ Brefeldin A product page from Fermentek
^ http://www.genecards.org/cgi-bin/carddisp.pl?gene=GBF1
^ Pahl HL, Baeuerle (Jun 1995). "A novel signal transduction pathway from the endoplasmic reticulum to the nucleus is mediated by transcription factor NF-kappa B". EMBO J. 14 (11): 2580–8. PMID 7781611.
^ Kober L, Zehe C, Bode J (October 2012). "Development of a novel ER stress based selection system for the isolation of highly productive clones". Biotechnol. Bioeng. 109 (10): 2599–611. doi:10.1002/bit.24527. PMID 22510960.

External links

Klausner RD, Donaldson JG, Lippincott-Schwartz J (March 1992). "Brefeldin A: insights into the control of membrane traffic and organelle structure". J. Cell Biol. 116 (5): 1071–80. doi:10.1083/jcb.116.5.1071. PMC 2289364. PMID 1740466.
Nebenführ A, Ritzenthaler C, Robinson DG (November 2002). "Brefeldin A: deciphering an enigmatic inhibitor of secretion". Plant Physiol. 130 (3): 1102–8. doi:10.1104/pp.011569. PMC 1540261. PMID 12427977.
NCI Frederick, Structure and Data for Brefeldin A. (Image)

English Journal

A8.9 Rheumatoid arthritis synovial IL-21 + CD4+ t cells specifically induce matrix metalloproteinase production by fibroblast-like synoviocytes.

Cristina Lebre M, Vieira PL, Aarrass S, Newsom-Davis T, Tak PP, Screaton GR.Author information Amsterdam Rheumatology & Immunology Center.AbstractBACKGROUND/PURPOSE: IL-21 is a cytokine produced by activated CD4+ T cells and T follicular helper cells (TFh) that has been implicated in several autoimmune diseases including rheumatoid arthritis (RA). IL-21 regulates antibody production by B cells and induces osteoclastogenesis, mechanisms that contribute to rheumatoid arthritis (RA) pathology. Importantly, IL-21R blockade ameliorates arthritis in mice. Here we investigated the functional characteristics of synovial CD4+ IL-21 + T cells in RA.
Annals of the rheumatic diseases.Ann Rheum Dis.2014 Mar 1;73 Suppl 1:A79. doi: 10.1136/annrheumdis-2013-205124.183.
BACKGROUND/PURPOSE: IL-21 is a cytokine produced by activated CD4+ T cells and T follicular helper cells (TFh) that has been implicated in several autoimmune diseases including rheumatoid arthritis (RA). IL-21 regulates antibody production by B cells and induces osteoclastogenesis, mechanisms that c
PMID 24489312

Biogenesis of the demarcation membrane system (DMS) in megakaryocytes.

Eckly A, Heijnen H, Pertuy F, Geerts W, Proamer F, Rinckel JY, Léon C, Lanza F, Gachet C.Author information Unité mixte de recherche S949 Institut National de la Santé et de la Recherche Médicale, Université de Strasbourg, Etablissement Français du Sang-Alsace, Strasbourg, France;AbstractThe demarcation membrane system (DMS) in megakaryocytes forms the plasma membrane (PM) of future platelets. Using confocal microscopy, electron tomography, and large volume focused ion beam/scanning electron microscopy (FIB/SEM), we determined the sequential steps of DMS formation. We identified a pre-DMS that initiated at the cell periphery and was precisely located between the nuclear lobes. At all developmental stages, the DMS remained continuous with the cell surface. The number of these connections correlated well with the nuclear lobulation, suggesting a relationship with cleavage furrow formation and abortive cytokinesis. On DMS expansion, Golgi complexes assembled around the pre-DMS, and fusion profiles between trans-golgi network-derived vesicles and the DMS were observed. Brefeldin-A reduced DMS expansion, indicating that the exocytic pathway is essential for DMS biogenesis. Close contacts between the endoplasmic reticulum (ER) and the DMS were detected, suggesting physical interaction between the 2 membrane systems. FIB/SEM revealed that the DMS forms an intertwined tubular membrane network resembling the platelet open canalicular system. We thus propose the following steps in DMS biogenesis: (1) focal membrane assembly at the cell periphery; (2) PM invagination and formation of a perinuclear pre-DMS; (3) expansion through membrane delivery from Golgi complexes; and (4) ER-mediated lipid transfer.
Blood.Blood.2014 Feb 6;123(6):921-30. doi: 10.1182/blood-2013-03-492330. Epub 2013 Oct 23.
The demarcation membrane system (DMS) in megakaryocytes forms the plasma membrane (PM) of future platelets. Using confocal microscopy, electron tomography, and large volume focused ion beam/scanning electron microscopy (FIB/SEM), we determined the sequential steps of DMS formation. We identified a p
PMID 24152908

Brefeldin A Limits N-Hexanoylsphingosine-Induced Accumulation of Natural Ceramide via the Salvage Pathway by Enhancing Glucosylation.

Spinedi A.Author information Dipartimento di Biologia, Università di Roma 'Tor Vergata', Via della Ricerca Scientifica 1, 00133, Rome, Italy, spinedi@uniroma2.it.AbstractCells actively metabolize exogenously administered N-hexanoylsphingosine (C6-Cer) to natural (i.e. long-chain) ceramide (LC-Cer) via the sphingosine (Sph) salvage pathway, namely via C6-Cer deacylation and Sph reacylation with a long-chain fatty acid. Based on the observation that the mycotoxin brefeldin A (BFA), a Golgi complex disassembler, impairs C6-Cer-evoked LC-Cer accumulation, it has been hypothesized that the integrity of the above-mentioned organelle might be necessary for C6-Cer processing via the salvage pathway and that BFA might block the phenomenon at the step short-chain ceramide deacylation. The present study shows that BFA indeed attenuates C6-Cer-evoked LC-Cer accumulation in human neurotumor CHP-100 cells: evidence is however provided that the phenomenon is not due to impaired synthesis of LC-Cer, but to its enhanced conversion to glucosylceramide. The possibility is discussed that this outcome might be a consequence of the BFA well-established property to induce the merging of the cis-Golgi region with endoplasmic reticulum, namely the compartments in which glucosylceramide synthase and ceramide synthases have been reported to reside.
Lipids.Lipids.2014 Feb;49(2):207-10. doi: 10.1007/s11745-013-3858-3. Epub 2013 Nov 6.
Cells actively metabolize exogenously administered N-hexanoylsphingosine (C6-Cer) to natural (i.e. long-chain) ceramide (LC-Cer) via the sphingosine (Sph) salvage pathway, namely via C6-Cer deacylation and Sph reacylation with a long-chain fatty acid. Based on the observation that the mycotoxin bref
PMID 24194457

Japanese Journal

Dynamic Regulation of Endocytic Vesicle Recycling and PIN2 Localization in <i>Arabidopsis</i> Roots under Varying Light Qualities

Environmental Control in Biology 54(1), 51-55, 2016
NAID 130005122798

Involvement of an intracellular vesicular transport process in naked-sgRNA-mediated TRUE gene silencing.

Molecular medicine reports 12(4), 6365-6369, 2015-10
NAID 120005740329

Phosphatidylinositol 4-kinase Ⅲ beta is the target of oxoglaucine and pachypodol (Ro 09-0179) for their anti-poliovirus activities, and is located at upstream of the target step of brefeldin A

Microbiology and immunology 59(6), 338-347, 2015-06
NAID 40020510073

「BFA」

Brefeldin A
Names
	IUPAC name (1R,2E,6S,10E,11aS,13S,14aR)-1,13-Dihydroxy-6-methyl-1,6,7,8,9,11a,12,13,14,14a-decahydro-4H-cyclopenta[f]oxacyclotridecin-4-one
	Other names γ,4-Dihydroxy-2-(6-hydroxy-1-heptenyl)-4-cyclopentanecrotonic acid λ-lactone
Identifiers
CAS Registry Number	20350-15-6
ChEBI	CHEBI:48080
ChEMBL	ChEMBL19980
ChemSpider	4449949
DrugBank	DB07348
	InChI InChI=1S/C16H24O4/c1-11-5-3-2-4-6-12-9-13(17)10-14(12)15(18)7-8-16(19)20-11/h4,6-8,11-15,17-18H,2-3,5,9-10H2,1H3/b6-4+,8-7+/t11-,12+,13-,14+,15+/m0/s1 ; Key: KQNZDYYTLMIZCT-KQPMLPITSA-N ; InChI=1/C16H24O4/c1-11-5-3-2-4-6-12-9-13(17)10-14(12)15(18)7-8-16(19)20-11/h4,6-8,11-15,17-18H,2-3,5,9-10H2,1H3/b6-4+,8-7+/t11-,12+,13-,14+,15+/m0/s1; Key: KQNZDYYTLMIZCT-KQPMLPITBH ;
Jmol-3D images	Image
PubChem	5287620
	SMILES O=C/1O[C@H](CCC/C=C/[C@H]2[C@H]([C@H](O)/C=C\1)C[C@@H](O)C2)C ;
Properties
Chemical formula	C16H24O4
Molar mass	280.36 g/mol
Appearance	White to off-white crystalline powder
Melting point	204 to 205 °C (399 to 401 °F; 477 to 478 K)
	Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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	Infobox references