A Daidzein Metabolite, 6,7,4 '-Trihydroxyisoflavone Inhibits Cellular Proliferation through Cell Cycle Arrest and Apoptosis Induction in MCF10CA1a Human Breast Cancer Cells PUMID/DOI：DOI:10.1007/s13765-013-3164-z Lee J H, Hong J L. A daidzein metabolite, 6,7,4′-trihydroxyisoflavone inhibits cellular proliferation through cell cycle arrest and apoptosis induction in MCF10CA1a human breast cancer cells[J]. Journal of the Korean Society for Applied Biological Chemistry, 2013, 56(6):695-700. Despite recent findings of hepatic daidzein metabolites on prevention of skin and colon cancers, little study has been performed on breast cancer. In this study, we found that 6,7,4'-trihydroxyisoflavone, one of the major hepatic metabolite of the daidzein more significantly inhibited proliferation of MCF10CA1a human estrogen receptor (ER)-negative breast cancer cells, which was derived from arresting cell cycle at S- and G2/M phase. Cyclins and cyclin-dependent kinases (CDKs) involved in S- and G2/M phases, including cyclins A, B, E, CDK1 and CDK2 were regulated by 6,7,4'-trihydroxyisoflavone as well as CDK inhibitor, p21 and p27, in a dose-dependent manner. In addition, 6,7,4'-trihydroxyisoflavone induced apoptosis by enhancing death receptor4 (DR4) expression and suppressing the X-linked inhibitor of apoptosis protein, leading to poly ADP-ribose polymerase cleavage. Taken together, 6,7,4'-trihydroxyisoflavone inhibits cell proliferation via arresting cell cycle at S- and G2/M phases and inducing apoptosis in MCF10CA1a human breast cancer cells. These results suggest that the hepatic metabolite of daidzein, 6,7,4'-trihydroxyisoflavone, may be considered as a more potent agent in inhibiting ER-negative breast carcinogenesis. 6,7,4 '-Trihydroxyisoflavone from Doenjang inhibits lipid accumulation PUMID/DOI：DOI:10.1016/j.foodchem.2011.04.082 Roh C, Jung U, Jo S K. 6,7,4′-Trihydroxyisoflavone from Doenjang inhibits lipid accumulation[J]. Food Chemistry, 2011, 129(1):183-187. Doenjang is a unique traditional Korean fermented soybean paste. 6,7,4'-Trihydroxyisoflavone was identified from traditional Korean fermented Doenjang. The four products isolated from 100 g Korean Doenjang using acetonitrile and methanol (70/30, v/v) was identified as daidzein, genistein, glycitein and 6,7,4'-trihydroxyisoflavone. The products were structurally elucidated by GC-MS and (1)H NMR analysis. 6,7,4'-Trihydroxyisoflavone was evaluated for antioxidant activity against the free radical 1,1-diphenyl-2-picrylhydrazyl (DPPH) scavenging and superoxide radical scavenging activity. Among four products isolated, 6,7,4'-trihydroxyisoflavone had remarkable antioxidant activity with IC(50) values of 31.5 mu M, 50.0 mu M, respectively. Furthermore, 6,7,4'-trihydroxyisoflavone was found to inhibit fat droplet formation triglyceride accumulation in 3T3-L1 adipocytes. Accordingly, 6,7,4'-trihydroxyisoflavone compound is of growing scientific interest due to its attractive biological properties. Identifying 6,7,4 '-trihydroxyisoflavone as a potent tyrosinase inhibitor PUMID/DOI：DOI:10.1271/bbb.69.1999 Biosci Biotechnol Biochem. 2005 Oct;69(10):1999-2001. A known biotransformed compound, 6,7,4'-trihydroxyisoflavone, was identified as a potent tyrosinase inhibitor. It inhibited mushroom tyrosinase with an IC50 value of 9.2 Km, which is six times the anti-tyrosinase activity of kojic acid (IC50 = 54.4 mu m). The inhibition kinetics, analyzed by Lineweaver-Burk plots, indicated 6,7,4'-trihydroxyisoflavone to be a competitive inhibitor of tyrosinase when L-tyrosine was used as a substrate. Its biosynthesis precursors and analogs, including glycitein, daidzein, and genistein, showed little anti-tyrosinase activity. The results suggest that hydroxyl groups at the C-6 and C-7 positions of the isoflavone skeleton might play an important role in the expression of tyrosinase inhibitory activity. 6,7,4-Trihydroxyisoflavone, a daidzein metabolites, regulated glycogen synthase kinase 3 beta/beta-catenin signaling and inhibited cell proliferation in MCF10DCIS.com human breast cancer cells PUMID/DOI：DOI:10.1158/1538-7445.AM2014-4228 Park H C, Cheng B, Ko J, et al. Abstract 4228: 6,7,4-Trihydroxyisoflavone, a daidzein metabolites, regulated glycogen synthase kinase 3β/β-catenin signaling and inhibited cell proliferation in MCF10DCIS.com human breast cancer cells[J]. Cancer Research, 2014, 74(19 Supplement):4228-4228. Recent studies have demonstrated that hepatic daidzein metabolites exerted significant activities in regulating different types of cancer including skin and colon. However, the role of daidzein metabolites on breast cancer has not been extensively studied. In this study, we found that 6,7,4′-trihydroxyisoflavone exerted the strongest inhibitory effect on the proliferation of MCF10DCIS.com human breast cancer cells among the daidzein metabolites we tested. Cell cycle at S and G2/M phase were arrested by 6,7,4-trihydroxyisoflavone, which were derived from regulating cyclins and cyclin dependent kinases (CDKs) including cyclin B, CDK1 and CDK2, as well as CDK inhibitor, p27 in a dose dependent manner. Furthermore, 6,7,4′-trihydroxyisoflavone increased the GSK3β activity through inhibiting the phosphorylation at Ser9, which was caused by the enhancement of phosphatase activity. These effects of 6,7,4′-trihydroxyisoflavone led to inhibition of the nuclear translocation of β-catenin, and regulation of cell cycle related proteins, cyclinB and CDK2. Taken together, 6,7,4′-trihydroxyisoflavone regulated GSK3β/β-catenin signaling, and arrested at S and G2/M phase in MCF10DCIS.com human breast cancer cells, and it suggests that the hepatic metabolite of daidzein, 6,7,4′-trihydroxyisoflavone, may be a potent agent in inhibiting MCF10DCIS.com human breast cancer growth. Citation Format: Hyun-Chang Park, Cheng Bao, Jiwon Ko, Jaehoo Lee, Hong Jin Lee. 6,7,4-Trihydroxyisoflavone, a daidzein metabolites, regulated glycogen synthase kinase 3β/β-catenin signaling and inhibited cell proliferation in MCF10DCIS.com human breast cancer cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; A facile inhibitor screening of hepatitis C virus NS3 protein using nanoparticle-based RNA. PUMID/DOI：DOI:10.3390/bios2040427 Biosensors (Basel). 2012 Oct 24;2(4):427-32 Globally, over hundreds of million people are infected with the hepatitis C virus: the global rate of death as a direct result of the hepatitis C virus has increased remarkably. For this reason, the development of efficient drug treatments for the biological effects of the hepatitis C virus is highly necessary. We have previously shown that quantum dots (QDs)-conjugated RNA oligonucleotide can recognize the hepatitis C virus NS3 protein specifically and sensitively. In this study, we elucidated that this biochip can analyze inhibitors to the hepatitis C virus NS3 protein using a nanoparticle-based RNA oligonucleotide. Among the polyphenolic compounds examined, 7,8,4'-trihydroxyisoflavone and 6,7,4'-trihydroxyisoflavone demonstrated a remarkable inhibition activity on the hepatitis C virus NS3 protein. Both 7,8,4'-trihydroxyisoflavone and 6,7,4'-trihydroxyisoflavone attenuated the binding affinity in a concentrated manner as evidenced by QDs conjugated RNA oligonucleotide. At a concentration of 0.01 mug·mL-1, 7,8,4'-trihydroxyisoflavone and 6,7,4'-trihydroxyisoflavone showed more than a 30% inhibition activity of a nanoparticle-based RNA oligonucleotide biochip system. The Daidzein Metabolite, 6,7,4 '-Trihydroxyisoflavone, Is a Novel Inhibitor of PKC alpha in Suppressing Solar UV-Induced Matrix Metalloproteinase 1 PUMID/DOI：DOI:10.3390/ijms151121419 Int J Mol Sci. 2014 Nov 19;15(11):21419-32. Soy isoflavone is an attractive source of functional cosmetic materials with anti-wrinkle, whitening and skin hydration effects. After consumption, the majority of soy isoflavones are converted to their metabolites in the human gastrointestinal tract. To understand the physiological impact of soy isoflavone on the human body, it is necessary to evaluate and address the biological function of its metabolites. In this study, we investigated the effect of 6,7,4'-trihydroxyisoflavone (6,7,4'-THIF), a major metabolite of daidzein, against solar UV (sUV)-induced matrix metalloproteinases (MMPs) in normal human dermal fibroblasts. MMPs play a critical role in the degradation of collagen in skin, thereby accelerating the aging process of skin. The mitogen-activated protein/extracellular signal-regulated kinase (MEK)/extracellular signal-regulated kinase (ERK), mitogen-activated protein kinase (MKK) 3/6/p38 and MKK4/c-Jun N-terminal kinases (JNK) signaling pathways are known to modulate MMP-1 function, and their activation by sUV was significantly reduced by 6,7,4'-THIF pretreatment. Our results also indicated that the enzyme activity of protein kinase C (PKC)alpha, an upstream regulator of MKKs signaling, is suppressed by 6,7,4'-THIF using the in vitro kinase assay. Furthermore, the direct interaction between 6,7,4'-THIF and endogenous PKC alpha was confirmed using the pull-down assay. Not only sUV-induced MMP-1 expression, but also sUV-induced signaling pathway activation were decreased in PKC alpha knockdown cells. Overall, we elucidated the inhibitory effect of 6,7,4'-THIF on sUV-induced MMPs and suggest PKC alpha as its direct molecular target. Metabolism of the soyabean isoflavone daidzein by CYP1A2 and the extra-hepatic CYPs 1A1 and 1B1 affects biological activity. PUMID/DOI：DOI:10.1016 / j.bcp.2006.05.015 Biochem Pharmacol. 2006 Aug 28;72(5):624-31. Metabolism of the isoflavones daidzein and genistein, which may protect against some cancers, was studied using human liver microsomes and recombinant CYP isoforms. The detection of three, more polar metabolites of each isoflavone by RP-HPLC required NADPH, consistent with CYP-mediated metabolism. For different liver preparations, metabolite generation from daidzein showed a significant linear correlation with metabolite generation from genistein, indicating metabolism by the same CYP(s). The lowest rate of metabolism of both isoflavones was by the preparation with the lowest CYP1A2 activity. Metabolite peak areas were substantially and significantly reduced by the CYP1A2 inhibitor furafylline and to a lesser extent by the CYP2E1 inhibitor 4-methylpyrazole. Recombinant CYP1A2, but not CYP2E1, generated the metabolites of daidzein and genistein and recombinant CYP1A1 and CYP1B1, expressed at sites including the breast and prostate, were also active. The effects of two CYP-derived metabolites of daidzein, 6,7,4'-trihydroxyisoflavone and 7,3',4'-trihydroxyisoflavone, were studied in the MCF-7 human breast cancer cell line at a concentration (50 microM) at which daidzein induces an antiproliferative response. 7,3',4'-Trihydroxyisoflavone reduced total cell numbers to a greater extent than 6,7,4'-trihydroxyisoflavone or daidzein and increased cell death. Together, these data demonstrate proof of principle that CYP-mediated metabolism of daidzein can be an activation pathway. We conclude that CYP1A2 makes the major contribution to the hepatic metabolism of both daidzein and genistein and along with metabolism at sites of hormone-dependent tumours may enhance a cancer-protective effect of daidzein if sufficiently high concentrations are reached in target tissues 6,7,4'-Trihydroxyisoflavone inhibits HCT-116 human colon cancer cell proliferation by targeting CDK1 and CDK2 PUMID/DOI：DOI:10.1093/carcin/bgr008 Carcinogenesis. 2011 Apr;32(4):629-35. Colon cancer is a common epithelial malignancies worldwide. Epidemiologic evidence has shown that nutrition and dietary components are important environmental factors involved in the development of this disease. We investigated the biological activity of 6,7,4'-trihydroxyisoflavone (6,7,4'-THIF, a metabolite of daidzein) in in vitro and in vivo models of human colon cancer. 6,7,4'-THIF suppressed anchorage-dependent and -independent growth of HCT-116 and DLD1 human colon cancer cells more effectively than daidzein. In addition, 6,7,4'-THIF induced cell cycle arrest at the S and G(2)/M phases in HCT-116 human colon cancer cells. Western blot analysis revealed that 6,7,4'-THIF effectively suppressed the expression of cyclin-dependent kinase (CDK) 2, but had no effect on other S- or G(2)/M-phase regulatory proteins such as cyclin A, cyclin B1 or CDK1. Daidzein did not affect the expression of any of these proteins. In kinase and pull-down assays, 6,7,4'-THIF, but not daidzein, inhibited CDK1 and CDK2 activities in HCT-116 cells by directly interacting with CDK1 and CDK2. In a xenograft mouse model, 6,7,4'-THIF significantly decreased tumor growth, volume and weight of HCT-116 xenografts. 6,7,4'-THIF bound directly to CDK1 and CDK2 in vivo, resulting in the suppression of CDK1 and CDK2 activity in tumors corresponding with our in vitro results. Collectively, these results suggest that CDK1 and CDK2 are potential molecular targets of 6,7,4'-THIF to suppress HCT-116 cell proliferation in vitro and in vivo. These findings provide insight into the biological actions of 6,7,4'-THIF and might establish a molecular basis for the development of new cancer therapeutic agents. Novel tempeh (fermented soyabean) isoflavones inhibit in vivo angiogenesis in the chicken chorioallantoic membrane assay. PUMID/DOI：DOI:10.1079 / BJN20041330 Br J Nutr. 2005 Mar;93(3):317-23. Anti-angiogenic strategies are emerging as an important tool for the treatment of cancer and inflammatory diseases. In the present investigation we isolated several isoflavones from a tempeh (fermented soyabean) extract. The isolated isoflavones were identified as 5,7,4'-trihydroxyisoflavone (genistein), 7,4'-dihydroxyisoflavone (daidzein), 6,7,4'-trihydroxyisoflavone (factor 2), 7,8,4'-trihydroxyisoflavone (7,8,4'-TriOH) and 5,7,3',4'-tetrahydroxyisoflavone (orobol). The effects on angiogenesis of these isoflavones were evaluated in the chicken chorioallantoic membrane assay; their capacity to inhibit vascular endothelial growth factor-induced endothelial cell proliferation and expression of the Ets 1 transcription factor, known to be implicated in the regulation of new blood vessel formation, were also investigated. We found that all isoflavones inhibited angiogenesis, albeit with different potencies. Compared with negative controls, which slightly inhibited in vivo angiogenesis by 6.30 %, genistein reduced angiogenesis by 75.09 %, followed by orobol (67.96 %), factor 2 (56.77 %), daidzein (48.98 %) and 7,8,4'-TriOH (24.42 %). These compounds also inhibited endothelial cell proliferation, with orobol causing the greatest inhibition at lower concentrations. The isoflavones also inhibited Ets 1 expression, providing some insight into the molecular mechanisms of their action. Furthermore, the chemical structure of the different isoflavones suggests a structure-activity relationship. Our present findings suggest that the new isoflavones might be added to the list of low molecular mass therapeutic agents for the inhibition of angiogenesis. The relationship between structure and in vitro antibacterial activity of selected isoflavones and their metabolites with special focus on antistaphylococcal effect of demethyltexasin PUMID/DOI：DOI: 10.1111/lam.12361 Lett Appl Microbiol. 2015 Mar;60(3):242-7. In this study, we tested 15 naturally occurring isoflavones and their metabolites for their possible antibacterial properties against nine Gram-positive and Gram-negative bacteria. The in vitro antibacterial activity was determined using the broth microdilution method, and the results were expressed as minimum inhibitory concentrations (MICs). 6,7,4-trihydroxyisoflavone (demethyltexasin), 7,3,4-trihydroxyisoflavone (hydroxydaidzein), 5,7-dihydroxy-4-methoxyisoflavone (biochanin A), 7,8,4-trihydroxyisoflavone (demethylretusin) and 5,7,4-trihydroxyisoflavone (genistein) produced significant antibacterial activity (MICs16gml(-1)). The most effective compound, demethyltexasin, was subsequently tested for its growth-inhibitory effect against Staphylococcus aureus, and it exhibited significant antistaphylococcal effects against various standard strains and clinical isolates, including methicillin and tetracycline resistant ones with the MICs ranging from 16 to 128gml(-1). The Prolyl Isomerase Pin1 Is a Novel Target of 6,7,4 '-Trihydroxyisoflavone for Suppressing Esophageal Cancer Growth PUMID/DOI：DOI: 10.1158/1940-6207.CAPR-16-0318 Cancer Prev Res (Phila). 2017 May;10(5):308-318 Intake of soy isoflavones is inversely associated with the risk of esophageal cancer. Numerous experimental results have supported the anticancer activity of soy isoflavones. This study aimed to determine the anti-esophageal cancer activity of 6,7,4'-trihydroxyisoflavone (6,7,4'-THIF), a major metabolite of daidzein, which is readily metabolized in the human body. Notably, 6,7,4'-THIF inhibited proliferation and increased apoptosis of esophageal cancer cells. On the basis of a virtual screening analysis, Pin1 was identified as a target protein of 6,7,4'-THIF. Pull-down assay results using 6,7,4'-THIF Sepharose 4B beads showed a direct interaction between 6,7,4'-THIF and the Pin1 protein. Pin1 is a critical therapeutic and preventive target in esophageal cancer because of its positive regulation of beta-catenin and cyclin D1. The 6,7,4'-THIF compound simultaneously reduced Pin1 isomerase activity and the downstream activation targets of Pin1. The specific inhibitory activity of 6,7,4'-THIF was analyzed using Neu/Pin1 wild-type (WT) and Neu/Pin1 knockout (KO) MEFs. 6,7,4'-THIF effected Neu/Pin1 WT MEFs, but not Neu/Pin1 KO MEFs. Furthermore, the results of a xenograft assay using Neu/Pin1 WT and KO MEFs were similar to those obtained from the in vitro assay. Overall, we found that 6,7,4'-THIF specifically reduced Pin1 activity in esophageal cancer models. Importantly, 6,7,4'-THIF directly bound to Pin1 but not FKBP or cyclophilin A, the same family of proteins. Because Pin1 acts like an oncogene by modulating various carcinogenesis-related proteins, this study might at least partially explain the underlying mechanism(s) of the anti-esophageal cancer effects of soy isoflavones. (C) 2017 AACR. Inhibitory Effect of Flavonoids on 26S Proteasome Activity PUMID/DOI：DOI: 10.1021/jf9017492 J Agric Food Chem. 2009 Oct 28;57(20):9706-15. Inhibiting proteasomal degradation has been shown to induce apoptosis in tumor cells. Utilization of proteasome inhibition is therefore one approach to anticancer therapy. Some of the flavonoids can induce cell apoptosis via inhibiting proteasome 26S activity. In this study, the inhibition of 26S proteasome from pig red blood cells was analyzed on 12 flavones, 5 flavanones, and 9 isoflavones by using a proteolysis assay. Several flavonoids such as apigenin-6-hydroxy-7-O-beta-D-glucoside, quercetin, rutin, 6-hydroxyapigenin, 5,6,4'-trihydroxy-7,3'-dimethoxyflavone, 5,6,3',4'-tetrahydroxy-7-methoxyflavone, glycitecin, and 6,7,4'-trihydroxyisoflavone inhibited the chymotrypsin-like, caspase-like, or trypsin-like activity of 26S proteasome when Suc-LLVY-AMC, Z-LLE-AMC, and Ac-RLR-AMC were used as substrates. Three peptidase activities of flavonoids were found to be significantly correlated with one another. Flavones had significantly stronger inhibitory effects on chymotrypsin-like and caspase-like activities than flavanones and isoflavones. 5,6,3',4'-Tetrahydroxy-7-methoxyflavone, 5,6,4'-trihydroxy-7,3'-dimethoxyflavone, and quercetin displayed a mixed type inhibition of 26S by Lineweaver-Burk plots analysis. Furthermore, 5,6,3',4'-tetrahydroxy-7-methoxyflavone is found to have a higher inhibitory effect on 26S proteasome activities and is the only flavonoid to inhibit all three peptidase activities, whereas the inhibition of flavonoids was not affected by ubiquitin-induced stimulation of the three peptidase activities of 26S proteasome; 5,6,3,4'-tetrahydroxy-7-methoxyflavone inhibited 75% casein degradation. These results suggest that both the 6-hydroxy and 7-methoxy positions of the flavone may play an important role in targeting 26S activity.
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
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In this work we demonstrate efficient quality control of a variety of gasoline and ethanol (gasohol) blends using a multimode interference (MMI) fiber sensor. The operational principle relies on the fact that the addition of ethanol to the gasohol blend reduces the refractive index (RI) of the gasoline. Since MMI sensors are capable of detecting small RI changes, the ethanol content of the gasohol blend is easily determined by tracking the MMI peak wavelength response. Gasohol blends with ethanol contents ranging from 0% to 50% has been clearly identified using this device, which provides a linear response with a maximum sensitivity of 0.270 nm/% EtOH. The sensor can also distinguish when water incorporated in the blend has exceeded the maximum volume tolerated by the gasohol blend, which is responsible for phase separation of the ethanol and gasoline and could cause serious engine failures. Since the MMI sensor is straightforward to fabricate and does not require any special coating it is a cost effective solution for real time and in-situ monitoring of the quality of gasohol blends.
optical fiber sensor, multimode interference, MMI, gasohol, gasoline, ethanol
Gasohol Quality Control for Real Time Applications by Means of a Multimode Interference Fiber Sensor
Adolfo J. Rodriguez Rodriguez,1 Oscar Baldovino-Pantaleon,1 Rene F. Dominguez Cruz,1 Carlos R. ZamarreNo,2 Ignacio R. Matias,2 and Daniel A. May-Arrioja1,*
The human pathogenic bacterium Clostridium perfringens secretes an enterotoxin (CpE) that targets claudins through its C-terminal receptor-binding domain (cCpE). Isoform-specific binding by CpE causes dissociation of claudins and tight junctions (TJs), resulting in cytotoxicity and breakdown of the gut epithelial barrier. Here, we present crystal structures of human claudin-9 (hCLDN-9) in complex with cCpE at 3.2 and 3.3 a. We show that hCLDN-9 is a high-affinity CpE receptor and that hCLDN-9-expressing cells undergo cell death when treated with CpE but not cCpE, which lacks its cytotoxic domain. Structures reveal cCpE-induced alterations to 2 epitopes known to enable claudin self-assembly and expose high-affinity interactions between hCLDN-9 and cCpE that explain isoform-specific recognition. These findings elucidate the molecular bases for hCLDN-9 selective ion permeability and binding by CpE, and provide mechanisms for how CpE disrupts gut homeostasis by dissociating claudins and TJs to affect epithelial adhesion and intercellular transport.
claudin, tight junction, membrane protein, X-ray structure, toxin
Claudin-9 structures reveal mechanism for toxin-induced gut barrier breakdown
Alex J. Vecchioa,1 and Robert M. Strouda,2
2019 Sep 3;
The apocritan Hymenoptera show extraordinary features in mitochondrial genomes, but no complete sequence has been reported for the basal lineage, Evanioidea. Here, we sequenced the complete mitochondrial genome of Evania appendigaster. This genome is 17,817 bp long; with low A+T content, 77.8%, compared with other hymenopteran species. Four tRNA genes were rearranged, among which remote inversion is the dominant gene rearrangement event. Gene shuffling is caused by tandem duplication-random loss while remote inversion is best explained by recombination. The start codon of nad1 was found as TTG, which might be common across Hymenoptera. trnS2 and trnK use abnormal anticodons TCT and TTT, respectively, and the D-stem pairings in trnS2 are absent. The secondary structure of two rRNA genes are predicted and compared with those in other insects. Five long intergenic spacers were present, including a long intergenic spacer between atp8 and atp6, where these two genes overlap in the previously reported animal genomes. A conserved motif was found between trnS1 and nad1, which is proposed to be associated with mtTERM. The A+T-rich region is 2,325 bp long, among the longest in insects, and contains a tandem repeat region.
Intergenic spacer, Gene rearrangement, Recombination, Tandem repeat, Secondary structure
The complete mitochondrial genome of Evania appendigaster (Hymenoptera: Evaniidae) has low A+T content and a long intergenic spacer between atp8 and atp6
Shu-jun Wei, Pu Tang, Li-hua Zheng, Min Shi, and Xue-xin Chencorresponding author