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PCTR3 Sale

(Synonyms: Protein Conjugates in Tissue Regeneration 3) 目录号 : GC44581

A specialized pro-resolving mediator

PCTR3 Chemical Structure

Cas No.:1810710-69-0

规格 价格 库存
10μg
¥2,141.00
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25μg
¥5,088.00
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50μg
¥9,645.00
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100μg
¥16,926.00
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Sample solution is provided at 25 µL, 10mM.

产品文档

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产品描述

Protein conjugates in tissue regeneration 3 (PCTR3) is a specialized pro-resolving mediator (SPM) synthesized from docosahexaenoic acid . DHA is oxidized to 16S,17S-epoxy-protectin, which is converted to PCTR1 by glutathione S-transferase and to PCTR2 and PCTR3 via peptidases. PCTR3 is found in infected mouse spleens and resolving exudate as well as isolated human spleen and septic plasma. It is also found in both M1 and M2 macrophages differentiated from isolated human monocytes.

Chemical Properties

Cas No. 1810710-69-0 SDF
别名 Protein Conjugates in Tissue Regeneration 3
Canonical SMILES CC/C=C\C[C@H](O)[C@H](SC[C@@H](C(O)=O)N)/C=C/C=C/C=C\C/C=C\C/C=C\CCC(O)=O
分子式 C25H37NO5S 分子量 463.6
溶解度 DMF: 50 mg/ml,DMSO: 50 mg/ml,Ethanol: 1 mg/ml,Ethanol:H20 (95:5): 2 mg/ml,PBS (pH 7.2): 0.1 mg/ml 储存条件 Store at -20°C
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.157 mL 10.7852 mL 21.5703 mL
5 mM 0.4314 mL 2.157 mL 4.3141 mL
10 mM 0.2157 mL 1.0785 mL 2.157 mL
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Research Update

Cysteinyl-specialized proresolving mediators link resolution of infectious inflammation and tissue regeneration via TRAF3 activation

Proc Natl Acad Sci U S A 2021 Mar 9;118(10):e2013374118.PMID:33649212DOI:PMC7958394

The recently elucidated proresolving conjugates in tissue regeneration (CTR) maresin-CTR (MCTR), protectin-CTR (PCTR), and resolvin-CTR (RCTR), termed cysteinyl-specialized proresolving mediators (cys-SPMs) each promotes regeneration, controls infection, and accelerates resolution of inflammation. Here, we sought evidence for cys-SPM activation of primordial pathways in planaria (Dugesia japonica) regeneration that might link resolution of inflammation and regeneration. On surgical resection, planaria regeneration was enhanced with MCTR3, PCTR3, or RCTR3 (10 nM), each used for RNA sequencing. The three cys-SPMs shared up-regulation of 175 known transcripts with fold-change > 1.25 and combined false discovery rate (FDR) < 0.002, and 199 canonical pathways (FDR < 0.25), including NF-κB pathways and an ortholog of human TRAF3 (TNFR-associated factor 3). Three separate pathway analyses converged on TRAF3 up-regulation by cys-SPMs. With human macrophages, three cys-SPMs each dose-dependently increased TRAF3 expression in a cAMP-PKA-dependent manner. TRAF3 overexpression in macrophages enhanced Interleukin-10 (IL-10) and phagocytosis of Escherichia coli IL-10 also increased phagocytosis in a dose-dependent manner. Silencing of mouse TRAF3 in vivo significantly reduced IL-10 and macrophage phagocytosis. TRAF3 silencing in vivo also relieved cys-SPMs' actions in limiting polymorphonuclear neutrophil in E. coli exudates. These results identify cys-SPM-regulated pathways in planaria regeneration, uncovering a role for TRAF3/IL-10 in regulating mammalian phagocyte functions in resolution. Cys-SPM activation of TRAF3 signaling is a molecular component of both regeneration and resolution of infectious inflammation.