Search results for: Methyltransferase PRMT1 Assay Kit
#36883376 
2023/03/08
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RNA profiling of sEV (small extracellular vesicles)/exosomes reveals biomarkers and vascular endothelial dysplasia with moyamoya disease.
The association of exosomal RNA profiling and pathogenesis of moyamoya disease (MMD) and intracranial Atherosclerotic disease (ICAD) is unknown. In this study, we investigated the RNA profiles of sEV (small extracellular vesicles)/exosomes in patients with MMD and ICAD. Whole blood samples were collected from 30 individuals, including 10 patients with MMD, 10 patients with ICAD, and 10 healthy individuals. Whole transcriptome analysis was performed using the GeneChip WT Pico Reagent kit. Transcriptional correlation was verified using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The association between functional dysregulation and candidate RNAs was studied . In total, 1,486 downregulated and 2,405 upregulated RNAs differed significantly between patients with MMD and healthy controls. Differential expression of six circRNAs was detected using qPCR. Among these significantly differentially expressed RNAs, IPO11 and PRMT1 circRNAs were upregulated, whereas CACNA1F circRNA was downregulated. This is the first study showing that the differential expression of exosomal RNAs associated with MMD pathogenesis, such as overexpression of IPO11 and PRMT1 circRNAs, may be related to angiogenesis in MMD. The downregulation of CACNA1F circRNA may be related to vascular occlusion. These results propose the utility of exosomal RNAs as biological markers in MMD.Shihao He, Jianfeng Liang, Guifeng Xue, Yanru Wang, Yahui Zhao, Ziqi Liu, Xiaokuan Hao, Yanchang Wei, Xiaolin Chen, Hao Wang, Shuai Kang, Rong Wang, Yuanli Zhao, Xun Ye
1503 related Products with: RNA profiling of sEV (small extracellular vesicles)/exosomes reveals biomarkers and vascular endothelial dysplasia with moyamoya disease.
96T2ug2ug96 tests96 tests2ug1.00 flask2ug x 2096 tests5ug
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#35841066 2022/07/15
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MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1.
Pancreatic β-cell dysfunction is commonly observed in patients with type 2 diabetes mellitus. Protein arginine methyltransferase 1 (PRMT1) plays an important role in pancreatic β-cell dysfunction. However, the detailed mechanisms remain largely unknown.Lixia Lv, Xiumin Wang, Jinhua Shen, Ying Cao, Qin Zhang
2491 related Products with: MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1.
1KG1 mg1.00 flask96 tests400 ug96 assays96 assays400 ug1 mg1.00 flask5x5 ml50 ml
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#33552280 2020/12/31
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PRMT1 expression predicts sensitivity to platinum-based chemotherapy in patients with ovarian serous carcinoma.
Patients with ovarian serous carcinoma are generally diagnosed at an advanced disease stage. The standard treatment for these patients is maximal debulking surgery followed by platinum-taxane combination chemotherapy. Despite initially responding well, more than half of patients become refractory to first-line chemotherapy. Upregulation of protein arginine methyltransferase 1 (PRMT1) expression has been demonstrated to methylate apoptosis signal-regulated kinase 1 and inhibit its activity, thereby contributing to chemoresistance. The present study investigated the association between PRMT1 expression and sensitivity to platinum-based chemotherapy in 51 patients with ovarian serous carcinoma (International Federation of Gynecology and Obstetrics stages III and IV), and the effect of RNA interference-mediated downregulation of PRMT1 on the sensitivity of ovarian cancer cells to cisplatin and carboplatin . Immunohistochemistry of tumor specimens was used to compare the expression levels of PRMT1, a Cell Counting Kit-8 assay and small interfering RNA transfection were performed for chemosensitivity assays, and reverse transcription-quantitative PCR was used to examine PRMT1 mRNA expression. Patients were divided into platinum-sensitive (n=26) and platinum-resistant (n=25) groups. PRMT1 expression was significantly lower in the platinum-sensitive group than in the platinum-resistant group (P=0.019). When patients were categorized according to PRMT1 expression, those in the low PRMT1 expression group were more sensitive to platinum-based chemotherapy than those in the high PRMT1 expression group (P=0.01). Additionally, experiments revealed that suppression of PRMT1 expression by siRNA significantly increased the sensitivity of human ovarian serous carcinoma cells to cisplatin and carboplatin (P<0.05). In conclusion, PRMT1 expression could predict sensitivity to platinum-based chemotherapy in patients with ovarian serous carcinoma.Hiroaki Matsubara, Takeshi Fukuda, Yuichiro Awazu, Shigenori Nanno, Masahiro Shimomura, Yuta Inoue, Makoto Yamauchi, Tomoyo Yasui, Toshiyuki Sumi
2999 related Products with: PRMT1 expression predicts sensitivity to platinum-based chemotherapy in patients with ovarian serous carcinoma.
500 gm.1 kit 1 G
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#29383172 2017/12/14
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Novel prognostic marker PRMT1 regulates cell growth via downregulation of CDKN1A in HCC.
Hepatocellular carcinoma (HCC) is a major type of liver cancer caused by the hepatitis B and C viruses, alcohol and exposure to aflatoxin. For HCC treatment, anticancer drugs have been widely used, but drug resistance in advanced HCC is an important problem, resulting in a continuous need for novel therapeutic targets. Therefore, in this study, we established a screening pipeline based on RNA-seq to screen novel therapeutic/prognostic targets in HCC and identified PRMT1 (Protein Arginine Methyltransferase 1). In the prognostic analysis, the overexpression of PRMT1 was clearly associated with poor prognosis in a number of HCC patient cohorts. Moreover, after PRMT1 knockdown, HCC cell lines exhibited cell growth and spheroid formation suppression, an increase in Sub-G1 cells by FACS analysis, and enrichment of the cell cycle pathway via functional enrichment analysis. With these results, we demonstrated that PRMT1 could be a novel prognostic marker and therapeutic target for HCC therapy.Jea-Woon Ryu, Seon-Kyu Kim, Mi-Young Son, Su-Jin Jeon, Jung-Hwa Oh, Jung Hwa Lim, Sunwha Cho, Cho-Rok Jung, Ryuji Hamamoto, Dae-Soo Kim, Hyun-Soo Cho
1796 related Products with: Novel prognostic marker PRMT1 regulates cell growth via downregulation of CDKN1A in HCC.
20ug2 Pieces/Box50096 samples100ug Lyophilized1x10e7 cells1 mL
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#29128891 2017/11/11
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PRMT1 promotes hyperglycemia in a FoxO1-dependent manner, affecting glucose metabolism, during hypobaric hypoxia exposure, in rat model.
High-altitude (HA) environment causes changes in cellular metabolism among unacclimatized humans. Previous studies have revealed that insulin-dependent activation of protein kinase B (Akt) regulates metabolic processes via discrete transcriptional effectors. Moreover, protein arginine methyltransferase (PRMT)1-dependent arginine modification of forkhead box other (FoxO)1 protein interferes with Akt-dependent phosphorylation. The present study was undertaken to test the involvement of PRMT1 on FoxO1 activation during hypobaric hypoxia (HH) exposure in rat model.Susovon Bayen, Supriya Saini, Priya Gaur, Arul Joseph Duraisamy, Alpesh Kumar Sharma, Karan Pal, Praveen Vats, Shashi Bala Singh
1369 related Products with: PRMT1 promotes hyperglycemia in a FoxO1-dependent manner, affecting glucose metabolism, during hypobaric hypoxia exposure, in rat model.
100 UG1 Set18 kgs100 μg1 Set1 Set1 Set1 Set96 assays2 Pieces/Box100ug Lyophilized
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#28978671 2017/10/04
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Transcriptional memory of cells of origin overrides β-catenin requirement of MLL cancer stem cells.
While β-catenin has been demonstrated as an essential molecule and therapeutic target for various cancer stem cells (CSCs) including those driven by MLL fusions, here we show that transcriptional memory from cells of origin predicts AML patient survival and allows β-catenin-independent transformation in MLL-CSCs derived from hematopoietic stem cell (HSC)-enriched LSK population but not myeloid-granulocyte progenitors. Mechanistically, β-catenin regulates expression of downstream targets of a key transcriptional memory gene, that is highly enriched in LSK-derived MLL-CSCs and helps sustain leukemic self-renewal. Suppression of sensitizes LSK-derived MLL-CSCs to β-catenin inhibition resulting in abolishment of CSC transcriptional program and transformation ability. In addition, further molecular and functional analyses identified Prmt1 as a key common downstream mediator for β-catenin/ functions in LSK-derived MLL-CSCs. Together, these findings not only uncover an unexpectedly important role of cells of origin transcriptional memory in regulating CSC self-renewal, but also reveal a novel molecular network mediated by β-catenin/Hoxa9/Prmt1 in governing leukemic self-renewal.Teerapong Siriboonpiputtana, Bernd B Zeisig, Magdalena Zarowiecki, Tsz Kan Fung, Maria Mallardo, Chiou-Tsun Tsai, Priscilla Nga Ieng Lau, Quoc Chinh Hoang, Pedro Veiga, Jo Barnes, Claire Lynn, Amanda Wilson, Boris Lenhard, Chi Wai Eric So
1760 related Products with: Transcriptional memory of cells of origin overrides β-catenin requirement of MLL cancer stem cells.
5 x 10A5 cells/vial1 mg10 ug1 x 10^6 cells/vial96T1 5 G1.00 flask1x10e7 cells100ml21 mL
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#24927133 //
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A sensitive luminescent assay for the histone methyltransferase NSD1 and other SAM-dependent enzymes.
A major focus of our pediatric cancer research is the discovery of chemical probes to further our understanding of the biology of leukemia harboring fusion proteins arising from chromosomal rearrangements, and to develop novel specifically targeted therapies. The NUP98-NSD1 fusion protein occurs in a highly aggressive subtype of acute myeloid leukemia after rearrangement of the genes NUP98 and NSD1. The methyltransferase activity of NSD1 is retained in the fusion, and it gives rise to abnormally high levels of methylation at lysine 36 on histone 3, enforcing oncogene activation. Therefore, inhibition of the methyltransferase activity of NUP98-NSD1 may be considered a viable therapeutic strategy. Here, we report the development and validation of a highly sensitive and robust luminescence-based assay for NSD1 and other methyltransferases that use S-adenosylmethionine (SAM) as a methyl donor. The assay quantifies S-adenosylhomocysteine (SAH), which is produced during methyl transfer from SAM. SAH is converted enzymatically to adenosine monophosphate (AMP); in the process, adenosine triphosphate (ATP) is consumed and the amount of ATP remaining is measured using a luminescent assay kit. The assay was validated by pilot high-throughput screening (HTS), dose-response confirmation of hits, and elimination of artifacts through counterscreening against SAH detection in the absence of NSD1. The known methyltransferase inhibitor suramin was identified, and profiled for selectivity against the histone methyltransferases EZH2, SETD7, and PRMT1. HTS using the luminescent NSD1 assay described here has the potential to deliver selective NSD1 inhibitors that may serve as leads in the development of targeted therapies for NUP98-NSD1-driven leukemias.Katherine M Drake, Venita G Watson, Anne Kisielewski, Rebecca Glynn, Andrew D Napper