Catalogue Number
BN-O1109
Analysis Method
Specification
98%(HPLC)
Storage
2-8°C
Molecular Weight
266.29
Appearance
Botanical Source
Structure Type
Category
SMILES
C1C2(COC(O1)CCC#N)COC(OC2)CCC#N
Synonyms
3,9-bis-(2-cyan-ethyl)-2,4,8,10-tetraoxa-spiro<5,5>undecan/3,9-Bis-(2-cyan-aethyl)-2,4,8,10-tetraoxa-spiro[5.5]undecan/CTU/Biscyanoethyltetraoxaspiro/2,4,8,10-Tetraoxaspiro[5.5]undecane-3,9-bis(propiononitrile)/3-[9-(2-cyanoethyl)-2,4,8,10-tetraoxaspiro[5.5]undecan-3-yl]propionitrile/3-[9-(2-cyanoethyl)-2,4,8,10-tetraoxaspiro[5.5]undecan-3-yl]propanenitrile/2,4,8,10-Tetraoxaspiro[5.5]undecane-3,9-dipropanenitrile/3,9-bis-(2-cyano-ethyl)-2,4,8,10-tetraoxa-spiro[5.5]undecane/2,4,8,10-Tetraoxaspiro[5.5]undecane-3,9-dipropionitrile/3,8-Bis-<2-cyanaethyl>-2,4,7,9-tetraoxospiro<5,5>undecan/Biscyanoethylteraoxaspiro/2,4,8,10-tetraoxaspiro[5.5]undecane-3,9-dipropiononitrile
IUPAC Name
Density
1.21g/cm3
Solubility
Flash Point
201.5ºC
Boiling Point
492.3ºC at 760mmHg
Melting Point
InChl
InChl Key
WGK Germany
RID/ADR
HS Code Reference
Personal Projective Equipment
Correct Usage
For Reference Standard and R&D, Not for Human Use Directly.
Meta Tag
provides coniferyl ferulate(CAS#:3058-04-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
No Technical Documents Available For This Product.
27348585
The nonsense-mediated RNA decay pathway is disrupted in inflammatory myofibroblastic tumors
The nonsense-mediated RNA decay pathway is disrupted in inflammatory myofibroblastic tumors
JingWei Lu,1,2 Terra-Dawn Plank,3 Fang Su,4 XiuJuan Shi,1 Chen Liu,5 Yuan Ji,6 ShuaiJun Li,1 Andrew Huynh,3 Chao Shi,4 Bo Zhu,4 Guang Yang,1 YanMing Wu,1 Miles F. Wilkinson,3,7 and YanJun Lu1
2016 Aug 1;
4562752
Methanol stimulates the hydrolysis of GTP catalyzed by bacterial ribosomes in the presence of the chain elongation factor T (EF-T). The methanol-stimulated activity is uncoupled from aminoacyl-tRNA binding to the ribosomes and does not require the presence of either synthetic polynucleotide messenger or aminoacyl-tRNA. When these reactants are present, along with EF-T, GTP, and methanol, the ribosomal binding of aminoacyl-tRNA is inhibited by thiostrepton but the uncoupled, EF-T-dependent hydrolysis of GTP is resistant to the antibiotic.
Elongation Factor T-Dependent Hydrolysis of Guanosine Triphosphate Resistant to Thiostrepton
Juan P. G. Ballesta and David Vazquez
1972 Oct;
7760802
The beta receptor for platelet-derived growth factor (beta PDGFR) is activated by binding of PDGF and undergoes phosphorylation at multiple tyrosine residues. The tyrosine-phosphorylated receptor associates with numerous SH2-domain-containing proteins which include phospholipase C-gamma 1 (PLC gamma), the GTPase-activating protein of Ras (GAP), the p85 subunit of phosphatidylinositol 3 kinase (PI3K), the phosphotyrosine phosphatase Syp, and several other proteins. Our previous studies indicated that PI3K and PLC gamma were required for relay of the mitogenic signal of beta PDGFR, whereas GAP and Syp did not appear to be required for this response. In this study, we further investigated the role of GAP and Syp in mitogenic signaling by beta PDGFR. Focusing on the PLC gamma-dependent branch of beta PDGFR signaling, we constructed a series of mutant beta PDGFRs that contained the binding sites for pairs of the receptor-associated proteins: PLC gamma and PI3K, PLC gamma and GAP, or PLC gamma and Syp. Characterization of these mutants showed that while all receptors were catalytically active and bound similar amounts of PLC gamma, they differed dramatically in their ability to initiate DNA synthesis. This signaling deficiency related to an inability to efficiently tyrosine phosphorylate and activate PLC gamma. Surprisingly, the crippled receptor was the one that recruited PLC gamma and GAP. Thus, GAP functions to suppress signal relay by the beta PDGFR, and it does so by silencing PLC gamma. These findings demonstrate that the biological response to PDGF depends not only on the ability of the beta PDGFR to recruit signal relay enzymes but also on the blend of these receptor-associated proteins.
The GTPase-activating protein of Ras suppresses platelet-derived growth factor beta receptor signaling by silencing phospholipase C-gamma 1.
M Valius, J P Secrist, and A Kazlauskas
1995 Jun;
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