| 词条 | Cytochalasin D |
| 释义 |
| Verifiedfields = changed | Watchedfields = changed | verifiedrevid = 399739879 | ImageFile=Cytochalasin D.png | ImageSize=200px | IUPACName= | OtherNames=Zygosporin A; Cytohalasin D; Lygosporin A |Section1={{Chembox Identifiers | ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}} | ChemSpiderID = 16736231 | ChEBI_Ref = {{ebicite|changed|EBI}} | ChEBI = 529996 | InChI = 1/C30H37NO6/c1-17-10-9-13-22-26(33)19(3)18(2)25-23(16-21-11-7-6-8-12-21)31-28(35)30(22,25)24(37-20(4)32)14-15-29(5,36)27(17)34/h6-9,11-15,17-18,22-26,33,36H,3,10,16H2,1-2,4-5H3,(H,31,35)/b13-9-,15-14+ | InChIKey = SDZRWUKZFQQKKV-JIIHXHDGBR | SMILES1 = CC(=O)OC4/C=C/C(C)(O)C(=O)C(C)C\\C=C/C2C(O)C(=C)C(C)C3C(Cc1ccccc1)NC(=O)C234 | StdInChI_Ref = {{stdinchicite|correct|chemspider}} | StdInChI = 1S/C30H37NO6/c1-17-10-9-13-22-26(33)19(3)18(2)25-23(16-21-11-7-6-8-12-21)31-28(35)30(22,25)24(37-20(4)32)14-15-29(5,36)27(17)34/h6-9,11-15,17-18,22-26,33,36H,3,10,16H2,1-2,4-5H3,(H,31,35)/b13-9-,15-14+ | StdInChIKey_Ref = {{stdinchicite|correct|chemspider}} | StdInChIKey = SDZRWUKZFQQKKV-JIIHXHDGSA-N | CASNo_Ref = {{cascite|correct|??}} | CASNo=22144-77-0 | PubChem=5458428 | SMILES=C[C@H]1C/C=C/[C@H]2[C@@H](C(=C)[C@H]([C@@H]3[C@@]2([C@@H](/C=C/[C@@](C1=O)(C)O)OC(=O)C)C(=O)N[C@H]3CC4=CC=CC=C4)C)O |Section2={{Chembox Properties | C=30 | H=37 | N=1 | O=6 | Appearance= | Density= | MeltingPt= | BoilingPt= | Solubility= |Section3={{Chembox Hazards | MainHazards= | FlashPt= | AutoignitionPt = }} Cytochalasin D is a member of the class of mycotoxins known as cytochalasins. Cytochalasin D is an alkaloid produced by Helminthosporium and other molds. Cytochalasin D is a cell-permeable and potent inhibitor of actin polymerization. It disrupts actin microfilaments and activates the p53-dependent pathways causing arrest of the cell cycle at the G1-S transition. It is believed to bind to F-actin polymer and prevent polymerization of actin monomers. [1] References1. ^{{cite journal | author = Heptinstall, J. A. May H. Ratan J. R. Glenn W. L| title = GPIIb-IIIa antagonists cause rapid disaggregation of platelets pre-treated with cytochalasin D. Evidence that the stability of platelet aggregates depends on normal cytoskeletal assembly. | journal = Platelets | volume = 9 | issue = 3 | pages = 227–32 | year = 1998 | pmid = 16793707| doi = 10.1080/09537109876744}} External links
3 : Mycotoxins|Actin inhibitors|Acetate esters |
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