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#34129878   2021/06/12 To Up

Beta2-microglobulin(B2M) in cancer immunotherapies: Biological function, resistance and remedy.

Cancer immunotherapies have made much headway during the past decades. Techniques including the immune checkpoint inhibition (ICI) and adoptive cell therapy (ACT) have harvested impressive efficacy and provided far-reaching tools for treating cancer patients. However, due to inadequate priming of the immune system, a certain subgroup of patients remains resistant to cancer immunotherapies during or after the treatment. β2-microglobulin (B2M) is an important subunit of major histocompatibility complex (MHC) class I which exerts substantive biological functions in tumorigensis and immune control. Accumulating evidence have shown that alterations of B2M gene and B2M proteins contribute to poor reaction to cancer immunotherapies by dampening antigen presentation. Here, we discuss the basic biological functions of B2M, its distribution in a spectrum of cancers, and current understanding of its role in ICI, cancer vaccines, CAR-T therapies. Furthermore, we summarize some promising therapeutic strategies to improve the efficacy inhibited by B2M defects.
Hanbing Wang, Baorui Liu, Jia Wei

1382 related Products with: Beta2-microglobulin(B2M) in cancer immunotherapies: Biological function, resistance and remedy.

100ul

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#34129824   // To Up

STAG2 loss rewires oncogenic and developmental programs to promote metastasis in Ewing sarcoma.

The core cohesin subunit STAG2 is recurrently mutated in Ewing sarcoma but its biological role is less clear. Here, we demonstrate that cohesin complexes containing STAG2 occupy enhancer and polycomb repressive complex (PRC2)-marked regulatory regions. Genetic suppression of STAG2 leads to a compensatory increase in cohesin-STAG1 complexes, but not in enhancer-rich regions, and results in reprogramming of cis-chromatin interactions. Strikingly, in STAG2 knockout cells the oncogenic genetic program driven by the fusion transcription factor EWS/FLI1 was highly perturbed, in part due to altered enhancer-promoter contacts. Moreover, loss of STAG2 also disrupted PRC2-mediated regulation of gene expression. Combined, these transcriptional changes converged to modulate EWS/FLI1, migratory, and neurodevelopmental programs. Finally, consistent with clinical observations, functional studies revealed that loss of STAG2 enhances the metastatic potential of Ewing sarcoma xenografts. Our findings demonstrate that STAG2 mutations can alter chromatin architecture and transcriptional programs to promote an aggressive cancer phenotype.
Biniam Adane, Gabriela Alexe, Bo Kyung A Seong, Diana Lu, Elizabeth E Hwang, Denes Hnisz, Caleb A Lareau, Linda Ross, Shan Lin, Filemon S Dela Cruz, Melissa Richardson, Abraham S Weintraub, Sarah Wang, Amanda Balboni Iniguez, Neekesh V Dharia, Amy Saur Conway, Amanda L Robichaud, Benjamin Tanenbaum, John M Krill-Burger, Francisca Vazquez, Monica Schenone, Jason N Berman, Andrew L Kung, Steven A Carr, Martin J Aryee, Richard A Young, Brian D Crompton, Kimberly Stegmaier

1926 related Products with: STAG2 loss rewires oncogenic and developmental programs to promote metastasis in Ewing sarcoma.

250ul96 wells (1 kit)100 1 kit1 mg

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#34129355   2021/06/15 To Up

First report of causing root and crown rot on maize in Italy.

Maize (Zea mays L.) is a cereal crop of great economic importance in Italy; production is currently of 62,587,469 t, with an area that covers 628,801 ha, concentrated in northern Italy (ISTAT 2020). Fusarium species are associated with root and crown rot causing failures in crop establishment under high soil moisture. In 2019 maize seedlings collected in a farm located in San Zenone degli Ezzelini (VI, Italy) showed root and crown rot symptoms with browning of the stem tissues, wilting of the seedling, and collapsing due to the rotting tissues at the base of the stem. The incidence of diseased plants was approximately 15%. Seedlings were cleaned thoroughly from soil residues under tap water. Portions (about 3-5 mm) of tissue from roots and crowns of the diseased plants were cut and surface disinfected with a water solution of NaClO at 0.5% for 2 minutes and rinsed in sterile H20. The tissue fragments were plated on Potato Dextrose Agar (PDA) amended with 50 mg/l of streptomycin sulfate and incubated for 48-72 hours at 25oC. Over the 80 tissue fragments plated, 5% were identified as Fusarium verticillioides, 60% as Fusarium spp., 35% developed saprophytes. Fusarium spp. isolates that showed morphological characteristics not belonging to known pathogenic species on maize were selected and used for further investigation while species belonging to F. oxysporum were discarded. Single conidia of the Fusarium spp. colonies were cultured on PDA and Carnation Leaf Agar (CLA) for pathogenicity tests, morphological and molecular identification. The colonies showed white to pink, abundant, densely floccose to fluffy aerial mycelium. Colony reverse showed light violet pigmentation, in rings on PDA. On CLA the isolates produced slightly curved macronidia with 3 septa 28.1 - 65.5 µm long and 2.8-6.3 µm wide (n=50). Microconidia were cylindrical, aseptate, 4.5 -14.0 µm long and 1.5-3.9 µm wide (n=50). Spherical clamydospores were 8.8 ± 2.5 µm size (n=30), produced singly or in pairs on the mycelium, according to the description by Skovgaard et al. (2003) for F. commune. The identity of two single-conidia strains was confirmed by sequence comparison of the translation elongation factor-1α (tef-1α), and RNA polymerase II subunit (rpb2) gene fragments (O'Donnell et al. 2010). BLASTn searches of GenBank, and Fusarium-ID database, using the partial tef-1α (MW419921, MW419922) and rpb2 (MW419923, MW419924) sequences of representative isolate DB19lug07 and DB19lug20, revealed 99% identity for tef-1α and 100% identity to F. commune NRRL 28387(AF246832, AF250560). Pathogenicity tests were carried out by suspending conidia from a 10-days old culture on PDA in sterile H2O to 5×104 CFU/ml. Fifty seeds were immersed in 50 ml of the conidial suspension of each isolate for 24 hours and in sterile water (Koch et al. 2020). The seeds were drained, dried at room temperature, and sown in trays filled with a steamed mix of white peat and perlite, 80:20 v/v, and maintained at 25°C and RH of 80-85% for 14 days with 12 hours photoperiod. Seedlings were extracted from the substrate, washed under tap water, and observed for the presence of root and crown rots like the symptoms observed on the seedlings collected in the field. Control seedlings were healthy and F. commune was reisolated from the symptomatic ones and identified by resequencing of tef-1α gene. F. commune has been already reported on maize (Xi et al. 2019) and other plant species, like soybean (Ellis et al. 2013), sugarcane (Wang et al. 2018), potato (Osawa et al. 2020), indicating that some attention must be paid in crop rotation and residue management strategies. To our knowledge this is the first report of F. commune as a pathogen of maize in Italy. References Ellis M L et al. 2013. Plant Disease, 97, doi: 10.1094/PDIS-07-12-0644-PDN. ISTAT. 2020. http://dati.istat.it/Index.aspx?QueryId=33702. Accessed December 28, 2020. Koch, E. et al. 2020. Journal of Plant Diseases and Protection. 127, 883-893 doi: 10.1007/s41348-020-00350-w O'Donnell K et al. 2010. J. Clin. Microbiol. 48:3708. https://doi.org/10.1128/JCM.00989-10 Osawa H et al. 2020. Journal of General Plant Pathology, doi.org/10.1007/s10327-020-00969-5. Skovgaard K 2003. Mycologia, 95:4, 630-636, DOI: 10.1080/15572536.2004.11833067. Wang J et al. 2018. Plant Disease, 102, doi/10.1094/PDIS-07-17-1011-PDN Xi K et al. 2019. Plant Disease, 103, doi/10.1094/PDIS-09-18-1674-PDN.
Monica Mezzalama, Vladimiro Guarnaccia, Ilaria Martino, Giulia Tabome, Maria Lodovica Gullino

2593 related Products with: First report of causing root and crown rot on maize in Italy.

96 wells100ug196 tests100ug Lyophilized500 ml100ug100 μg100ug100 μg

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#34129205   2021/06/15 To Up

Losartan Protects Podocytes against High Glucose-induced Injury by Inhibiting B7-1 Expression.

The role of B7-1 in podocyte injury has received increasing attention. The aim of this study was to investigate whether losartan protects podocytes of patients with diabetic kidney disease (DKD) by regulating B7-1 and the underlying mechanisms. Rats with streptozotocin-induced DKD were treated with losartan for 8 weeks. Biochemical changes in blood and urine were analyzed. Kidneys were isolated for electron microscopy, immunofluorescence, real-time quantitative PCR (RT-PCR), and Western blot analysis. Immortalized mouse podocyte cells were cultured in normal or high glucose medium in the presence or absence of losartan for 48 h, and then the cells were collected for immunofluorescence, PCR, Western blotting and monolayer permeability detection. The phosphatidylinositol 3-kinase (PI3K) 110α subunit and angiotensin II type 1 receptor (AT1R) plasmids were transfected into podocytes, respectively, and then Western blotting was performed to assess the expression of B7-1 protein. The results showed that losartan ameliorated podocyte structure and function in the rat model of DKD, and reduced the expression of B7-1 protein. Overexpression of PI3K 110a subunit in podocytes attenuated the inhibitory effect of losartan on B7-1 expression in high glucose-stimulated podocytes. The expression of B7-1 was significantly increased by overexpression of AT1R and significantly reduced by blocking PI3K 110a subunit. We conclude that losartan protects podocytes against high glucose-induced injury by inhibiting AT1R-mediated B7-1 expression. This effect is dependent on the AT1R-PI3K 110a subunit pathway.
Hui Gao, Wen-Yan Du, Jing Lin, Shi-Liang Han, Yun-Jing Zhang, Xi-Feng Sun

1960 related Products with: Losartan Protects Podocytes against High Glucose-induced Injury by Inhibiting B7-1 Expression.

1 G100ug Lyophilized1000 assays10x96, 2.0ml cultures 1060 ml 100ug Lyophilized100ug 1 G100ug Lyophilized 1000 ml 100ug Lyophilized

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#34129030   2021/06/15 To Up

Cantil: a previously unreported organ in wild-type Arabidopsis regulated by FT, ERECTA and heterotrimeric G proteins.

We describe a previously unreported macroscopic Arabidopsis organ, the cantil, named for its 'cantilever' function of holding the pedicel at a distance from the stem. Cantil development is strongest at the first nodes after the vegetative to reproductive inflorescence transition; cantil magnitude and frequency decrease acropetally. Cantils develop in wild-type Arabidopsis accessions (e.g. Col-0, Ws and Di-G) as a consequence of delayed flowering in short days; cantil formation is observed in long days when flowering is delayed by null mutation of the floral regulator FLOWERING LOCUS T. The receptor-like kinase ERECTA is a global positive regulator of cantil formation; therefore, cantils never form in the Arabidopsis strain Ler. ERECTA functions genetically upstream of heterotrimeric G proteins. Cantil expressivity is repressed by the specific heterotrimeric complex subunits GPA1, AGB1 and AGG3, which also play independent roles: GPA1 suppresses distal spurs at cantil termini, while AGB1 and AGG3 suppress ectopic epidermal rippling. These G protein mutant traits are recapitulated in long-day flowering gpa1-3 ft-10 plants, demonstrating that cantils, spurs and ectopic rippling occur as a function of delayed phase transition, rather than as a function of photoperiod per se.
Timothy E Gookin, Sarah M Assmann

2087 related Products with: Cantil: a previously unreported organ in wild-type Arabidopsis regulated by FT, ERECTA and heterotrimeric G proteins.

1 mL

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#34128684   2021/06/15 To Up

A Synthetic Route to The Core Structure of (-)-Retigeranic Acid A.

Retigeranic acid A is a uniquely structured pentacyclic sesterterpene bearing eight stereogenic centers. We report a concise route to the core structure of (-)-retigeranic acid A. The stereochemistry of its six chiral centers and three quaternary carbon centers was well-controlled. This route features two intramolecular Pauson-Khand reactions (IMPKRs): the first forged the D and E rings to deliver the triquinane subunit, and the second constructed the A and B rings and diastereoselectively installed the quaternary C center.
Xiao Wang, Dian Li, Junlin Zhang, Jianxian Gong, Junkai Fu, Zhen Yang

1102 related Products with: A Synthetic Route to The Core Structure of (-)-Retigeranic Acid A.

1 G 500 G430 tests 100 G430 Tests / Kit100

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#34128214   2021/06/14 To Up

Haplotypes of the genes (GCK and G6PC2) underlying the glucose/glucose-6-phosphate cycle are associated with pancreatic beta cell glucose sensitivity in patients with newly diagnosed type 2 diabetes from the VNDS study (VNDS 11).

Elevated fasting plasma glucose has been associated with increased risk for development of type 2 diabetes (T2D). The balance between glucokinase (GCK) and glucose-6-phosphate catalytic subunit 2 (G6PC2) activity are involved in glucose homeostasis through glycolytic flux, and subsequent insulin secretion.
C Zusi, E Rinaldi, S Bonetti, M L Boselli, E Trabetti, G Malerba, E Bonora, R C Bonadonna, M Trombetta

2682 related Products with: Haplotypes of the genes (GCK and G6PC2) underlying the glucose/glucose-6-phosphate cycle are associated with pancreatic beta cell glucose sensitivity in patients with newly diagnosed type 2 diabetes from the VNDS study (VNDS 11).

200ul1250ul200ul96 assays 1 G200ul100 assays 1 G1

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#34128175   2021/06/10 To Up

The ER membrane protein complex subunit Emc3 controls angiogenesis via the FZD4/WNT signaling axis.

The endoplasmic reticulum (ER) membrane protein complex (EMC) regulates the synthesis and quality control of membrane proteins with multiple transmembrane domains. One of the membrane spanning subunits, EMC3, is a core member of the EMC complex that provides essential hydrophilic vestibule for substrate insertion. Here, we show that the EMC subunit Emc3 plays critical roles in the retinal vascular angiogenesis by regulating Norrin/Wnt signaling. Postnatal endothelial cell (EC)-specific deletion of Emc3 led to retarded retinal vascular development with a hyperpruned vascular network, the appearance of blunt-ended, aneurysm-like tip endothelial cells (ECs) with reduced numbers of filopodia and leakage of erythrocytes at the vascular front. Diminished tube formation and cell proliferation were also observed in EMC3 depleted human retinal endothelial cells (HRECs). We then discovered a critical role for EMC3 in expression of FZD4 receptor of β-catenin signaling using RNA sequencing, real-time quantitative PCR (RT-qPCR) and luciferase reporter assay. Moreover, augmentation of Wnt activity via lithium chloride (LiCl) treatment remarkably enhanced β-catenin signaling and cell proliferation of HRECs. Additionally, LiCl partially reversed the angiogenesis defects in Emc3-cKO mice. Our data reveal that Emc3 plays essential roles in angiogenesis through direct control of FZD4 expression and Norrin/β-catenin signaling.
Mu Yang, Shujin Li, Wenjing Liu, Xiao Li, Yunqi He, Yeming Yang, Kuanxiang Sun, Lin Zhang, Wanli Tian, Lixin Duan, Huafu Chen, Dezhong Yao, Zhenglin Yang, Xianjun Zhu

1914 related Products with: The ER membrane protein complex subunit Emc3 controls angiogenesis via the FZD4/WNT signaling axis.

100 U1mg102100μg100μg4 Membranes/Box1 Set500 Units100 ul1 mg

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