更新于：2024-11-01

IP6K3

更新于：2024-11-01

基本信息

别名

IHPK3、inositol hexakisphosphate kinase 3、Inositol hexaphosphate kinase 3

+ [3]

简介

Converts inositol hexakisphosphate (InsP6) to diphosphoinositol pentakisphosphate (InsP7/PP-InsP5). Converts 1,3,4,5,6-pentakisphosphate (InsP5) to PP-InsP4.

关联

项与 IP6K3 相关的药物

SCO-006

靶点

IP6K1 x IP6K2 x IP6K3

作用机制

IP6K1抑制剂 [+2]

在研机构

SCOHIA PHARMA, Inc.初创企业

原研机构

Takeda Pharmaceutical Co., Ltd.

在研适应症

卵巢透明细胞癌

非在研适应症

高磷血症

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 IP6K3 相关的临床结果

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100 项与 IP6K3 相关的转化医学

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0 项与 IP6K3 相关的专利（医药）

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195

项与 IP6K3 相关的文献（医药）

2024-07-01·EFSA Journal

Safety evaluation of the food enzyme 3‐phytase from the non‐genetically modified Aspergillus niger strain PHY93‐08

Article

作者: Kovalkovicova, Natalia ; Chesson, Andrew ; Roos, Yrjo ; Gott, David Michael ; EFSA Panel on Food Contact Materials, Enzymes and Processing Aids ; Vernis, Laurence ; Crebelli, Riccardo ; Cocconcelli, Pier Sandro ; Bolognesi, Claudia ; Mengelers, Marcel ; Barat Baviera, Jose Manuel ; Glandorf, Boet ; Lampi, Evgenia ; Lambre, Claude ; Steffensen, Inger-Lise ; Lunardi, Simone ; Zorn, Holger ; Liu, Yi ; Van Loveren, Henk ; Andryszkiewicz, Magdalena ; Grob, Konrad ; Tlustos, Christina ; Riviere, Gilles ; Mortensen, Alicja

Abstract The food enzyme 3‐phytase (myo‐inositol‐hexakisphosphate 3‐phosphohydrolase EC 3.1.3.8) is produced with the non‐genetically modified Aspergillus niger strain PHY93‐08 by Shin Nihon Chemical Co., Ltd. The food enzyme is free from viable cells of the production organism. It is intended to be used in nine food manufacturing processes. Since residual amounts of food enzyme–total organic solids (TOS) are removed in two of the food manufacturing processes, dietary exposure was calculated only for the remaining seven processes. It was estimated to be up to 0.763 mg TOS/kg body weight (bw) per day in European populations. Genotoxicity tests did not raise safety concerns. The systemic toxicity was assessed by means of a repeated dose 90‐day oral toxicity study in rats. The Panel identified a no observed adverse effect level of 2560 mg TOS/kg bw per day, the highest dose tested, which when compared with the estimated dietary exposure, resulted in a margin of exposure of at least 3355. A search for the similarity of the amino acid sequence of the food enzyme to known allergens was made and no matches were found. The Panel considered that the risk of allergic reactions upon dietary exposure cannot be excluded, but the likelihood is low. Based on the data provided, the Panel concluded that this food enzyme does not give rise to safety concerns under the intended conditions of use.

2024-06-01·Zhongguo shi yan xue ye xue za zhi

[Whole Exome Sequencing Reveals Gene Mutation Characteristics of Primary Central Nervous System Lymphoma].

Article

作者: Zhang, Li-Tian ; Han, Ye ; Li, Cui-Cui ; Wu, Chong-Yang ; Jin, Qi-Qi ; Jiang, Hao-Yun

题目全外显子测序揭示原发中枢神经系统淋巴瘤的基因突变特征.目的对18例原发中枢神经系统淋巴瘤（PCNSL）患者肿瘤组织进行全外显子测序，探索PCNSL的基因突变特点。.方法收集2018年9月至2020年12月在兰州大学第二医院病理科确诊的18例免疫功能正常（无HIV及服用免疫抑制剂病史）、病理类型为弥漫大B细胞淋巴瘤的PCNSL患者肿瘤组织，进行基于高通量测序的全外显子测序，平均测序深度>100×。测序结果经数据处理及生物信息学分析，得到患者的基因突变全景及突变特征。.结果18例患者均检测到明显的体细胞突变，中位体细胞突变数目为321，以错义突变为主（约占90%），突变类型以C>T为主（占50.2%），反映了与年龄相关的突变模式；前15位高频突变基因中，PSD3、DUSP5、MAGEB16、TELO2、FMO2、TRMT13、AOC1、PIGZ、SVEP1、IP6K3、TIAM1为驱动基因。驱动基因通路富集结果显示，RTK-RAS、Wnt、NOTCH、Hippo、Cell-Cycle通路明显富集。各样本的肿瘤突变负荷在3.558 48/Mb-8.780 89/Mb之间，平均突变负荷4.953 32/Mb，与TCGA数据库中其他肿瘤的研究队列相比明显增高。.结论PCNSL频繁发生体细胞的错义突变，以点突变为主，突变类型主要为C>T。驱动基因主要参与RTK-RAS、Wnt、NOTCH、Hippo通路信号传导，表明以上通路可能与PCNSL发病机制相关。PCNSL有显著的高肿瘤突变负荷，这或许是PD-1抑制剂治疗PCNSL有效的原因之一。.

2024-04-01·Journal of Lipid Research

Cholesterol trafficking to the ER leads to the activation of CaMKII/JNK/NLRP3 and promotes atherosclerosis

Article

作者: Tall, Alan R ; Westerterp, Marit ; Yalcinkaya, Mustafa ; Wang, Nan ; Xiao, Tong ; Liu, Wenli ; Abramowicz, Sandra ; Wang, Ranran

The deposition of cholesterol-rich lipoproteins in the arterial wall triggers macrophage inflammatory responses, which promote atherosclerosis. The NLRP3 inflammasome aggravates atherosclerosis; however, cellular mechanisms connecting macrophage cholesterol accumulation to inflammasome activation are poorly understood. We investigated the mechanisms of NLRP3 inflammasome activation in cholesterol-loaded macrophages and in atherosclerosis-prone Ldlr^-/- mice with defects in macrophage cholesterol efflux. We found that accumulation of cholesterol in macrophages treated with modified LDL or cholesterol crystals, or in macrophages defective in the cholesterol efflux promoting transporters ABCA1 and ABCG1, leads to activation of NLRP3 inflammasomes as a result of increased cholesterol trafficking from the plasma membrane to the ER, via Aster-B. In turn, the accumulation of cholesterol in the ER activates the inositol triphosphate-3 receptor, CaMKII/JNK, and induces NLRP3 deubiquitylation by BRCC3. An NLRP3 deubiquitylation inhibitor or deficiency of Abro1, an essential scaffolding protein in the BRCC3-containing cytosolic complex, suppressed inflammasome activation, neutrophil extracellular trap formation (NETosis), and atherosclerosis in vivo. These results identify a link between the trafficking of cholesterol to the ER, NLRP3 deubiquitylation, inflammasome activation, and atherosclerosis.