This product is isolated and purified from the heartwood of Podocarpus macrophyllus
3H-3,10b-Ethanonaphtho[1,2-c]-1,2-dioxin-7-carboxylic acid, 5,6,6a,7,8,9,10,10a-octahydro-7,10a-dimethyl-3-(1-methylethyl)-, (3R,6aR,10aS,10bR)-/3H-3,10b-Ethanonaphtho[1,2-c]-1,2-dioxin-7-carboxylic acid, 5,6,6a,7,8,9,10,10a-octahydro-7,10a-dimethyl-3-(1-methylethyl)-, (3S,6aR,7R,10aS,10bS)-/(1R,2S,7R,12R)-12-Isopropyl-2,6-dimethyl-13,14-dioxatetracyclo[10.2.2.0.0]hexadec-10-ene-6-carboxylic acid/(1S,2S,6R,7R,12S)-12-Isopropyl-2,6-dimethyl-13,14-dioxatetracyclo[10.2.2.0.0]hexadec-10-ene-6-carboxylic acid
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
437.9±45.0 °C at 760 mmHg
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Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
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Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and highly aggressive leukemia for which knowledge on disease mechanisms and effective therapies are currently lacking. Only a handful of recurring genetic mutations have been identified and none is specific to BPDCN. In this study, through molecular cloning in an index case that presented a balanced t(3;5)(q21;q31) and molecular cytogenetic analyses in a further 46 cases, we identify monoallelic deletion of NR3C1 (5q31), encoding the glucocorticoid receptor (GCR), in 13 of 47 (28%) BPDCN patients. Targeted deep sequencing in 36 BPDCN cases, including 10 with NR3C1 deletion, did not reveal NR3C1 point mutations or indels. Haploinsufficiency for NR3C1 defined a subset of BPDCN with lowered GCR expression and extremely poor overall survival (P = .0006). Consistent with a role for GCR in tumor suppression, functional analyses coupled with gene expression profiling identified corticoresistance and loss-of-EZH2 function as major downstream consequences of NR3C1 deletion in BPDCN. Subsequently, more detailed analyses of the t(3;5)(q21;q31) revealed fusion of NR3C1 to a long noncoding RNA (lncRNA) gene (lincRNA-3q) that encodes a novel, nuclear, noncoding RNA involved in the regulation of leukemia stem cell programs and G1/S transition, via E2F. Overexpression of lincRNA-3q was a consistent feature of malignant cells and could be abrogated by bromodomain and extraterminal domain (BET) protein inhibition. Taken together, this work points to NR3C1 as a haploinsufficient tumor suppressor in a subset of BPDCN and identifies BET inhibition, acting at least partially via lncRNA blockade, as a novel treatment option in BPDCN.
NR3C1 haploinsufficiency is found in patients with a plasmacytoid dendritic cell neoplasm characterized by very poor clinical outcome. Overexpression of lincRNA-3q is a consistent feature of malignant cells in these patients and can be abrogated by BET protein inhibition.
Haploinsufficiency for NR3C1, the gene encoding the glucocorticoid receptor, in blastic plasmacytoid dendritic cell neoplasms
2016 Jun 16
2016 Jun 16
The genetic causes of oocyte meiotic deficiency (OMD), a form of primary infertility characterised by the production of immature oocytes, remain largely unexplored. Using whole exome sequencing, we found that 26% of a cohort of 23 subjects with OMD harboured the same homozygous nonsense pathogenic mutation in PATL2, a gene encoding a putative RNA‐binding protein. Using Patl2 knockout mice, we confirmed that PATL2 deficiency disturbs oocyte maturation, since oocytes and zygotes exhibit morphological and developmental defects, respectively. PATL2’s amphibian orthologue is involved in the regulation of oocyte mRNA as a partner of CPEB. However, Patl2’s expression profile throughout oocyte development in mice, alongside colocalisation experiments with Cpeb1, Msy2 and Ddx6 (three oocyte RNA regulators) suggest an original role for Patl2 in mammals. Accordingly, transcriptomic analysis of oocytes from WT and Patl2 −/− animals demonstrated that in the absence of Patl2, expression levels of a select number of highly relevant genes involved in oocyte maturation and early embryonic development are deregulated. In conclusion, PATL2 is a novel actor of mammalian oocyte maturation whose invalidation causes OMD in humans.
female sterility, oocyte developmental competence, oocyte maturation arrest, oocyte maturation failure, Patl2
PATL2 is a key actor of oocyte maturation whose invalidation causes infertility in women and mice
Marie Christou‐Kent, 1 Zine‐Eddine Kherraf, 1 Amir Amiri‐Yekta, 1 , 2 , 3 Emilie Le Blevec, 1 Thomas Karaouzene, 1 Beatrice Conne, 4 Jessica Escoffier, 1 Said Assou, 5 Audrey Guttin, 6 Emeline Lambert, 1 Guillaume Martinez, 1 , 2 , 7 Magalie Boguenet, 1 Selima Fourati Ben Mustapha, 8 Isabelle Cedrin Durnerin, 9 Lazhar Halouani, 8 Ouafi Marrakchi, 8 Mounir Makni, 8 Habib Latrous, 8 Mahmoud Kharouf, 8 Charles Coutton, 1 , 2 , 7 Nicolas Thierry‐Mieg, 10 Serge Nef, 4 Serge P Bottari, 1 Raoudha Zouari, 8 Jean Paul Issartel, 6 Pierre F Ray, 1 , 2 , † and Christophe Arnoultcorresponding author 1 , †
Chronic myelomonocytic leukemia (CMML) is a myeloid hematological malignancy with overlapping features of myelodysplastic syndromes (MDSs) and myeloproliferative neoplasms (MPNs). The knowledge of the role of the tumor microenvironment (TME), particularly mesenchymal stromal cells (MSCs), in MDS pathogenesis is increasing. Generally, cancer is associated with a procoagulant state participating in tumor development. Monocytes release procoagulant, tissue factor (TF)-bearing microparticles. We hypothesized that MSCs and clonal monocytes release procoagulant extracellular vesicles (EVs) within the CMML TME, inducing a procoagulant state that could modify hematopoietic stem cell (HSC) homeostasis. We isolated and cultured MSCs and monocytes from CMML patients and MSCs from healthy donors (HDs). Their medium EVs and small EVs (sEVs) were collected after iterative ultracentrifugations and characterized by nanoparticle tracking analysis. Their impact on hemostasis was studied with a thrombin generation assay and fibrinography. CMML or HD HSCs were exposed to sEVs from either CMML or HD MSCs. CMML MSC sEVs increased HD HSC procoagulant activity, suggesting a transfer of TF from the CMML TME to HD HSCs. The presence of TF on sEVs was shown by electron microscopy and western blot. Moreover, CMML monocyte EVs conferred a procoagulant activity to HD MSCs, which was reversed by an anti-TF antibody, suggesting the presence of TF on the EVs. Our findings revealed a procoagulant “climate” within the CMML environment related to TF-bearing sEVs secreted by CMML MSCs and monocytes.
We revealed a procoagulant climate within the CMML microenvironment related to TF-bearing sEVs secreted by CMML MSCs and monocytes.
Tumor microenvironment and clonal monocytes from chronic myelomonocytic leukemia induce a procoagulant climate
Johanna Zannoni,1,* Natacha Mauz,1,2,* Landry Seyve,3,4 Mathieu Meunier,1,2 Karin Pernet-Gallay,5 Julie Brault,3,6 Claire Jouzier,1,2 David Laurin,1,7 Mylene Pezet,8 Martine Pernollet,9 Jean-Yves Cahn,2 Fabrice Cognasse,10,11 Benoît Polack,3,4 and Sophie Parkcorresponding author1,2
2019 Jun 25