CAS: 145-13-1; Pregnenolone

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豆甾醇置于cytochrome P450Scc,还原型辅酶ii(Nadph)四钠盐体系中,用 Aq. Phosphate Buffer 用作溶剂,化学反应 0.5H,反应生成孕烯醇酮
参考文献:Ile351,Leu355 And Ile461 Residues Are Essential For Catalytic Activity Of Bovine Cytochrome P450Scc (Cyp11A1)
标题:Ile351,Leu355 And Ile461 Residues Are Essential For Catalytic Activity Of Bovine Cytochrome P450Scc (Cyp11A1)
摘要:Cytochrome P450Scc (Cyp11A1) Is A Mammalian Mitochondrial Enzyme Which Catalyzes Cholesterol Side Chain Cleavage To Form Pregnenolone. Along With Cholesterol,Some Other Steroids Including Sterols With A Branched Side Chain Like Beta-Sitosterol Are The Substrates For The Enzyme,But The Activity Towards Beta-Sitosterol Is Rather Low. Modification Of The Catalytic Site Conformation Could Provide More Effective Beta-Sitosterol Bioconversion By The Enzyme. This Study Was Aimed To Find Out The Amino Acid Residues Substitution Of Which Could Modify The Conformation Of The Active Site Providing Possible Higher Enzyme Activity Towards .Beta-Sitosterol. After Structural And Bioinformatics Analysis Three Amino Acid Residues I351,L355,I461 Were Chosen. Molecular Dynamics Simulations Of P450Scc Evidenced The Stability Of The Wild Type,Double (I351A/l355A) And Triple (I351A/l355A/i461A) Mutants. Mutant Variants Of Cdna Encoding P450Scc With The Single,Double And Triple Mutations Were Obtained By Site-Directed Mutagenesis. However,The Experimental Data Indicate That The Introduced Single Mutations Ile351A,Leu355A And Ile461A Dramatically Decrease The Target Catalytic Activity Of Cyp11A1,And No Activity Was Observed For Double And Triple Mutants Obtained. Therefore,Isoleucine Residues 351 And 461,And Leucine Residue 355 Are Important For The Cytochrome P450Scc Functioning Towards Sterols Both With Unbranched (Cholesterol) And Branched (Sitosterol) Side Chains.
Doi:10.1016/j.Steroids.2019.01.002

专利信息

专利号:US-8889840-B2
优先权日:2009-10-29
标题 :Vascular leakage inhibitor
发明人：KWON YOUNG-GUEN; SUH YOUNG-GER
权利人:KWON YOUNG-GUEN; SUH YOUNG-GER; UNIV YONSEI IACF
摘要:The present disclosure relates to a novel vascular leakage inhibitor. The novel vascular leakage inhibitor of the present disclosure inhibits the apoptosis of vascular endothelial cells, inhibits the formation of actin stress fibers induced by VEGF, enhances the cortical actin ring structure, and improves the stability of the tight junctions (TJs) between vascular cells, thereby inhibiting vascular leakage. The vascular leakage inhibitor of the present disclosure has the activity of not only reducing vascular permeability but also recovering the integrity of damaged blood vessels. Accordingly, the vascular leakage inhibitor of the present disclosure can prevent or treat various diseases caused by vascular leakage. Since the vascular leakage inhibitor of the present disclosure is synthesized from commercially available or easily synthesizable cholesterols, it has remarkably superior feasibility of commercial synthesis.