Human PRPS1 blocking peptide (CDBP0499)

Synthetic Human PRPS1 blocking peptide for BL

Product Overview
ARTS ( N - term ) peptide ( human )
Species Reactivity
0.2 mg/ml
50 μg
PBS with 0.1% BSA 0.02% sodium azide pH7.2
0.02% Sodium Azide
Upon receipt - Keep as concentrated solution. Aliquot and store at -20℃ or below. Avoid freeze-thaw cycles.
UniProt ID
Antigen Description
This gene encodes an enzyme that catalyzes the phosphoribosylation of ribose 5-phosphate to 5-phosphoribosyl-1-pyrophosphate, which is necessary for purine metabolism and nucleotide biosynthesis. Defects in this gene are a cause of phosphoribosylpyrophosphate synthetase superactivity, Charcot-Marie-Tooth disease X-linked recessive type 5 and Arts Syndrome. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Feb 2011]
ATP binding; kinase activity; magnesium ion binding; nucleotide binding; protein homodimerization activity; ribose phosphate diphosphokinase activity; ribose phosphate diphosphokinase activity; ribose phosphate diphosphokinase activity; transferase activi
PRPS1; phosphoribosyl pyrophosphate synthetase 1; deafness, X linked 2, perceptive, congenital , DFN2; ribose-phosphate pyrophosphokinase 1; CMTX5; DFNX1; PRS I; ribose phosphate diphosphokinase 1; deafness 2, perceptive, congenital; ribose-phosphate diphosphokinase 1; phosphoribosyl pyrophosphate synthase I; deafness, X-linked 2, perceptive, congenital; dJ1070B1.2 (phosphoribosyl pyrophosphate synthetase 1); ARTS; DFN2; PRSI; PRS-I; PPRibP; KIAA0967;


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High expression of PRPS1 induces an anti-apoptotic effect in B-ALL cell lines and predicts an adverse prognosis in Chinese children with B-ALL


Authors: Ma, Yimei; An, Xizhou; Guan, Xianmin; Kong, Qinglin; Wang, Yanzhen; Li, Pengfei; Meng, Yan; Cui, Yinghui; Wen, Xianhao; Guo, Yuxia; Shen, Yali; Yu, Jie

Phosphoribosyl pyrophosphate synthetase 1 (PRPS1) is closely associated with a number of diseases; however, its influence in B-cell acute lymphoblastic leukemia (B-ALL) and the potential molecular mechanisms involved remain unclear. The present study aimed to evaluate the expression of PRPS1 in Chinese children with B-ALL and to investigate the mechanism of action of PRPS1 in this disease. A Cell Counting Kit-8 (CCK-8) assay was performed to examine the proliferation of B-ALL Sup-B15 and Raji cells, and flow cytometric analysis was conducted to determine the cell cycle distribution and rate of apoptosis. The mRNA and protein expression levels of PRPS1, MYC proto-oncogene, bHLH transcription factor, cyclin E1, B-cell lymphoma-2 (Bcl-2), cyclin dependent kinase 2 and caspase-3 were detected by reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Elevated PRPS1 expression was associated with a high-risk stratification and poor prognosis in patients with B-ALL. Furthermore, overexpression of PRPS1 accelerated the growth of and inhibited apoptosis in Sup-B15 and Raji cells as well as increasing the expression of Bcl-2 to induce an anti-apoptotic effect in B-ALL cell lines. The results of the present study indicate that PRPS1 regulates multiple processes in B-ALL and may be an attractive therapeutic target.

Down-expression of miR-154 suppresses tumourigenesis in CD133(+) glioblastoma stem cells


Authors: Yang, Liang; Yan, Zhongjie; Wang, Yuanyu; Ma, Wandong; Li, Chen

Glioblastoma multiforme (GBM) is the most common and aggressive form of brain cancer. Evidences have suggested that CD133 is a marker for a subset of glioblastoma cancer stem cells. However, whether miRNA plays a critical role in CD133(+) GBM is poorly understood. Here, we identified that miR-154 was upregulated in CD133(+) GBM cell lines. Knockdown of miR-154 remarkably suppressed proliferation and migration of CD133(+) GBM cells. Further study found that PRPS1 was a direct target of miR-154 in CD133(+) GBM cells. Overexpression of PRPS1 exhibited similar effects as miR-154 knockdown in CD133(+) GBMs. Our study identified miR-154 as a previously unrecognized positive regulator of proliferation and migration in CD133(+) GBM cells and a potentially therapeutic target of GBMs. Copyright (C) 2016 John Wiley & Sons, Ltd.

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