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Search results for: Proteasome

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#36472403   2022/12/06 To Up

A cross-sectional study of antibodies to ubiquitin proteasome system in different glomerulopathies.

Recently, evidence has emerged that the ubiquitin system, which is involved in extracellular protein degradation, is most susceptible to damage in podocytes in cases of podocytopathies. We studied anti-ubiquitin carboxyl-terminal hydrolase L1 (UCHL1) antibodies in glomerulopathies with proteinuria.
Natalia Chebotareva, Venzsin Cao, Anatoliy Vinogradov, Igor Alentov, Natalia Sergeeva, Alexey Kononikhin, Sergey Moiseev

1647 related Products with: A cross-sectional study of antibodies to ubiquitin proteasome system in different glomerulopathies.

100 μg100 μg100 μg100 μg100 μg2 Pieces/Box100 μg100.00 ug100 μg0.2 mg100.00 ug100 μg

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#36472010   // To Up

[Proteomics analysis of Astragalus polysaccharide on TLR4-activated lung cancer cell-derived exosomes].

Astragalus polysaccharide(APS), one of the main active components of Astragali Radix, plays an anti-tumor effect by regulating the inflammatory microenvironment of tumors. Exosomes are small extracellular vesicles with a diameter ranging from 50 to 200 nm and carry several biological components from parental cells such as nucleic acids and proteins. When combined with recipient cells, they play an important role in intercellular communication and immune response. In this study, exosomes released from H460 cells at the inflammatory state or with APS addition activated by Toll-like receptor 4(TLR4) were extracted by ultracentrifugation and characterized by Western blot, transmission electron microscopy, and nanoparticle tracking analysis. The exosomal proteins derived from H460 cells in the three groups were further analyzed by label-free proteomics, and 897, 800, and 911 proteins were identified in the three groups(Con, LPS, and APS groups), 88% of which belonged to the ExoCarta exosome protein database. Difference statistical analysis showed that the expression of 111 proteins was changed in the LPS group and the APS group(P<0.05). The biological information analysis of the differential proteins was carried out. The molecular functions, biological processes, and signaling pathways related to the differential proteins mainly involved viral processes, protein binding, and bacterial invasion of proteasome and epithelial cells. Key differential proteins mainly included plasminogen activator inhibitor-1, laminin α5, laminin α1, and CD44, indicating that tumor cells underwent systemic changes in different states and were reflected in exosomes in the inflammatory microenvironment. The analysis results also suggested that APS might affect the inflammatory microenvironment through the TLR4/MyD88/NF-κB signaling pathway or the regulation of the extracellular matrix. This study is conducive to a better understanding of the mechanism of tumor development in the inflammatory state and the exploration of the anti-inflammatory effect of APS at the exosome level.
Kang-Die Hu, Kai-Ge Yang, Cheddah Soumia, Ming-Yuan Wu, Chao Yan, Xin-Yan Li, Yan Wang

1547 related Products with: [Proteomics analysis of Astragalus polysaccharide on TLR4-activated lung cancer cell-derived exosomes].



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#36471805   2022/11/19 To Up

BRCA1 mediates protein homeostasis through the ubiquitination of PERK and IRE1.

Tumors with mutations have poor prognoses due to genomic instability. Yet this genomic instability has risks and BRCA1-deficient (def) cancer cells must develop pathways to mitigate these risks. One such risk is the accumulation of unfolded proteins in BRCA1-def cancers from increased mutations due to their loss of genomic integrity. Little is known about how BRCA1-def cancers survive their genomic instability. Here we show that BRCA1 is an E3 ligase in the endoplasmic reticulum (ER) that targets the unfolded protein response (UPR) stress sensors, Eukaryotic Translation Initiation Factor 2-alpha Kinase 3 (PERK) and Serine/Threonine-Protein Kinase/Endoribonuclease Inositol-Requiring Enzyme 1 (IRE1) for ubiquitination and subsequent proteasome-mediated degradation. When BRCA1 is mutated or depleted, both PERK and IRE1 protein levels are increased, resulting in a constitutively activated UPR. Furthermore, the inhibition of protein folding or UPR signaling markedly decreases the overall survival of BRCA1-def cancer cells. Our findings define a mechanism used by the BRCA1-def cancer cells to survive their increased unfolded protein burden which can be used to develop new therapeutic strategies to treat these cancers.
Robert Hromas, Gayathri Srinivasan, Ming Yang, Aruna Jaiswal, Taylor A Totterdale, Linda Phillips, Austin Kirby, Nazli Khodayari, Mark Brantley, Elizabeth A Williamson, Kimi Y Kong

1261 related Products with: BRCA1 mediates protein homeostasis through the ubiquitination of PERK and IRE1.

1000 TESTS/0.65ml100 U100ug1mg100ul100ug1021mg10100 μg1mg

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#36470859   2022/12/05 To Up

Proteogenomic characterization of MiT family translocation renal cell carcinoma.

Microphthalmia transcription factor (MiT) family translocation renal cell carcinoma (tRCC) is a rare type of kidney cancer, which is not well characterized. Here we show the comprehensive proteogenomic analysis of tRCC tumors and normal adjacent tissues to elucidate the molecular landscape of this disease. Our study reveals that defective DNA repair plays an important role in tRCC carcinogenesis and progression. Metabolic processes are markedly dysregulated at both the mRNA and protein levels. Proteomic and phosphoproteome data identify mTOR signaling pathway as a potential therapeutic target. Moreover, molecular subtyping and immune infiltration analysis characterize the inter-tumoral heterogeneity of tRCC. Multi-omic integration reveals the dysregulation of cellular processes affected by genomic alterations, including oxidative phosphorylation, autophagy, transcription factor activity, and proteasome function. This study represents a comprehensive proteogenomic analysis of tRCC, providing valuable insights into its biological mechanisms, disease diagnosis, and prognostication.
Yuanyuan Qu, Xiaohui Wu, Aihetaimujiang Anwaier, Jinwen Feng, Wenhao Xu, Xiaoru Pei, Yu Zhu, Yang Liu, Lin Bai, Guojian Yang, Xi Tian, Jiaqi Su, Guo-Hai Shi, Da-Long Cao, Fujiang Xu, Yue Wang, Hua-Lei Gan, Shujuan Ni, Meng-Hong Sun, Jian-Yuan Zhao, Hailiang Zhang, Dingwei Ye, Chen Ding

1232 related Products with: Proteogenomic characterization of MiT family translocation renal cell carcinoma.

100ug1 kit

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#36469307   2022/12/05 To Up

miR-210-3p promotes obesity-induced adipose tissue inflammation and insulin resistance by targeting SOCS1 mediated NF-κB pathway.

Under the condition of chronic obesity, an increased level of free fatty acids along with low oxygen tension in the adipose tissue creates a pathophysiological adipose tissue microenvironment (ATenv) leading to the impairment of adipocyte function and insulin resistance. Here, we found the synergistic effect of hypoxia and lipid (HL) surge in fostering adipose tissue macrophages(ATMs) inflammation and its polarization. ATenv significantly increased miR-210-3p expression in ATMs which promotes NF-ĸB activation-dependent proinflammatory cytokines expressions along with the downregulation of anti-inflammatory cytokines expression. Interestingly, delivery of miR-210-3p mimic significantly increased the macrophage inflammation in absence of HL co-stimulation; while miR-210-3p inhibitor notably compromised HL-induced macrophage inflammation through increased production of SOCS1 (suppressor of cytokine signalling 1), a negative regulator of NF-ĸB inflammatory signalling pathway. Mechanistically, miR-210 directly binds to 3' UTR of SOCS1 mRNA and silenced its expression and thus preventing proteasomal degradation of NF-ĸB p65. Direct delivery of anti-miR-210-3p LNA in the ATenv markedly rescued mice from obesity-induced adipose tissue inflammation and insulin resistance. Thus, miR-210-3p inhibition in ATMs could serve as a novel therapeutic strategy for managing obesity-induced type 2 diabetes.
Debarun Patra, Soumyajit Roy, Leena Arora, Shaheen Wasil Kabeer, Satpal Singh, Upalabdha Dey, Dipanjan Banerjee, Archana Sinha, Suman Dasgupta, Kulbhusan Tikoo, Aditya Kumar, Durba Pal

2671 related Products with: miR-210-3p promotes obesity-induced adipose tissue inflammation and insulin resistance by targeting SOCS1 mediated NF-κB pathway.

2 Pieces/Box100 μg2 Pieces/Box2 Pieces/Box50 ug

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#36468454   2022/12/05 To Up

Chemokine signaling synchronizes angioblast proliferation and differentiation during pharyngeal arch artery vasculogenesis.

Developmentally, the great vessels of the heart originate from the pharyngeal arch arteries (PAAs). During PAA vasculogenesis, PAA precursors undergo sequential cell fate decisions that are accompanied by proliferative expansion. However, how these two processes are synchronized remains poorly understood. Here, we find that the zebrafish chemokine receptor Cxcr4a is expressed in PAA precursors, and genetic ablation of either cxcr4a or the ligand gene cxcl12b causes PAA stenosis. Cxcr4a is required for the activation of the downstream PI3K/AKT cascade, which promotes not only PAA angioblast proliferation, but also differentiation. AKT has a well-known role in accelerating cell-cycle progression through the activation of cyclin-dependent kinases. Despite this, we demonstrate that AKT phosphorylates Etv2 and Scl, the key regulators of angioblast commitment, on conserved serine residues, thereby protecting them from ubiquitin-mediated proteasomal degradation. Altogether, our study reveals a central role for chemokine signaling in PAA vasculogenesis through orchestrating angioblast proliferation and differentiation.
Jie Liu, Mingming Zhang, Haojian Dong, Jingwen Liu, Aihua Mao, Guozhu Ning, Yu Cao, Yiyue Zhang, Qiang Wang

1038 related Products with: Chemokine signaling synchronizes angioblast proliferation and differentiation during pharyngeal arch artery vasculogenesis.

50 ug5 x 50 ug2 Pieces/Box25 mg100.00 ug100ug Lyophilized0.5 mg 5 G16-22 Sample Kit100ug Lyophilized

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#36467842   2022/08/31 To Up

Impact of ixazomib-lenalidomide-dexamethasone therapy on overall survival in multiple myeloma patients: Analysis of the emerging-markets subgroup of the TOURMALINE-MM1 trial.

Ixazomib-lenalidomide-dexamethasone (ixazomib-Rd) showed clinical efficacy over placebo-Rd in patients with relapsed/refractory multiple myeloma (MM) in the TOURMALINE-MM1 trial. Over a median follow-up of ∼85 months, as patients showed disease progression, they received subsequent novel therapies that confounded the overall survival (OS) benefit. Here, we conducted a post hoc analysis in 148 patients from seven countries defined as emerging markets, with limited access to novel therapies for MM during the trial period, to describe the impact of these therapies on OS. Patients were randomised to ixazomib-Rd ( = 71) or placebo-Rd ( = 77). The median progression-free survival (PFS) was 18.7 versus 10.2 months, with ixazomib-Rd versus placebo-Rd (hazard ratio [HR], 0.504; = 0.008) demonstrating a statistically significant improvement as observed in the primary trial. The median OS improved by 32.6 months with ixazomib-Rd over placebo-Rd (63.5 vs. 30.9 months; HR, 0.794; = 0.261); however, the statistically significant benefit seen in PFS was not observed for OS. Improvement with ixazomib-Rd over placebo-Rd was observed in overall response (81.7% vs. 64.9%; odds ratio [OR], 2.38; = 0.019) and complete response (22.5% vs. 3.9%; OR, 7.57; < 0.001). Patient-reported quality of life and use of subsequent therapies were similar across treatment groups. No new safety concerns were identified. Compared with the main cohort, median OS was 10 months longer with ixazomib-Rd and 21 months shorter with placebo-Rd in this subgroup, indicating a clinically meaningful survival benefit of ixazomib-Rd treatment in this patient population with limited access to subsequent novel therapies.
Andrew Spencer, Olga Samoilova, Wee-Joo Chng, Richard Labotka, Cong Li, Kwang-Wei Wu, Nakul Saxena, Xu Yan, Jae Hoon Lee, Meral Beksac

1238 related Products with: Impact of ixazomib-lenalidomide-dexamethasone therapy on overall survival in multiple myeloma patients: Analysis of the emerging-markets subgroup of the TOURMALINE-MM1 trial.

5 G

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#36467498   2022/11/23 To Up

MSC Senescence-Related Genes Are Associated with Myeloma Prognosis and Lipid Metabolism-Mediated Resistance to Proteasome Inhibitors.

Complex carcinogenic mechanisms and the existence of tumour heterogeneity in multiple myeloma (MM) prevent the most commonly used staging system from effectively interpreting the prognosis of patients. Since the microenvironment plays an important role in driving tumour development and MM occurs most often in middle-aged and elderly patients, we hypothesize that ageing of bone marrow mesenchymal stem cells (BM-MSCs) may be associated with the progression of MM.
Yang-Jia Cao, Yan-Hua Zheng, Qing Li, Jin Zheng, Li-Tian Ma, Can-Jun Zhao, Tian Li

2737 related Products with: MSC Senescence-Related Genes Are Associated with Myeloma Prognosis and Lipid Metabolism-Mediated Resistance to Proteasome Inhibitors.

480/kit6ml 25 G430 Tests / Kit10 mg25 0.05 mg1 module100 ug100 mg

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#36464247   2022/12/04 To Up

Erythrocyte type 1 equilibrative nucleoside transporter expression in sickle cell disease and sickle cell trait.

Hypoxia-mediated red blood cell (RBC) sickling is central to the pathophysiology of sickle cell disease (SCD). The signalling nucleoside adenosine is thought to play a significant role in this process. This study investigated expression of the erythrocyte type 1 equilibrative nucleoside transporter (ENT1), a key regulator of plasma adenosine, in adult patients with SCD and carriers of sickle cell trait (SCT). Relative quantitative expression analysis of erythrocyte ENT1 was carried out by Western blot and flow cytometry. Patients with SCD with steady state conditions, either with SS or SC genotype, untreated or under hydroxycarbamide (HC) treatment, exhibited a relatively high variability of erythrocyte ENT1, but with levels not significantly different from normal controls. Most strikingly, expression of erythrocyte ENT1 was found to be significantly decreased in patients with SCD undergoing painful vaso-occlusive episode and, unexpectedly, also in healthy SCT carriers. Promoting hypoxia-induced adenosine signalling, the reduced expression of erythrocyte ENT1 might contribute to the pathophysiology of SCD and to the susceptibility of SCT individuals to altitude hypoxia or exercise to exhaustion.
Bérengère Koehl, Livia Claude, Karen Reminy, Vanessa Tarer, Véronique Baccini, Marc Romana, Yves Colin-Aronovicz, Vijaya L Damaraju, Michael Sawyer, Thierry Peyrard, Maryse Etienne-Julan, Caroline Le Van Kim, Slim Azouzi, Luc Reininger

2295 related Products with: Erythrocyte type 1 equilibrative nucleoside transporter expression in sickle cell disease and sickle cell trait.

100ug Lyophilized100ug Lyophilized100ug Lyophilized1x10e7 cells100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized1x10e7 cells100ug Lyophilized100ug Lyophilized

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#36463561   2022/12/04 To Up

The MODIFY Study Protocol: An Open-Label, Single-Arm, Multicenter, Prospective Pragmatic Study of Ixazomib-Based Triple-Drug Therapy in Chinese Patients with Multiple Myeloma.

Although the bortezomib-based triple-drug therapy is considered as a front-line therapy for multiple myeloma (MM) in Chinese patients, increased level of toxicity leads to treatment dissatisfaction. Treatment with ixazomib, an oral proteasome inhibitor, has demonstrated better efficacy and safety profile without increasing the toxicity. In this study, we investigate the safety and clinical outcomes of Chinese patients with newly diagnosed MM (NDMM) who transitioned from a bortezomib-based triple-drug therapy to an ixazomib-based triple-drug therapy in a real-world clinical setting.
Wenming Chen, Aijun Liu, Lin Li

2835 related Products with: The MODIFY Study Protocol: An Open-Label, Single-Arm, Multicenter, Prospective Pragmatic Study of Ixazomib-Based Triple-Drug Therapy in Chinese Patients with Multiple Myeloma.

16 Arrays/Slide

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