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Altered expression of stromal interaction molecule(STIM)-calcium release-activated calcium channel protein(ORAI) and inositol1,4,5-trisphosphate receptors(IP_3Rs)in cancer:will they become a new battlefield for oncotherapy? 被引量:3
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作者 Jing Wen Ying-Cheng Huang +2 位作者 Huan-Huan Xiu Zhi-Ming Shan Kang-Qing Xu 《Chinese Journal of Cancer》 SCIE CAS CSCD 2016年第5期214-222,共9页
The stromal interaction molecule(STIM)-calcium release-activated calcium channel protein(ORAI) and inositol1,4,5-trisphosphate receptors(IP_3Rs) play pivotal roles in the modulation of Ca^(2+)-regulated pathways from ... The stromal interaction molecule(STIM)-calcium release-activated calcium channel protein(ORAI) and inositol1,4,5-trisphosphate receptors(IP_3Rs) play pivotal roles in the modulation of Ca^(2+)-regulated pathways from gene transcription to cell apoptosis by driving calcium-dependent signaling processes.Increasing evidence has implicated the dysregulation of STIM-ORAI and IP_3Rs in tumorigenesis and tumor progression.By controlling the activities,structure,and/or expression levels of these Ca^(2+)-transporting proteins,malignant cancer cells can hijack them to drive essential biological functions for tumor development.However,the molecular mechanisms underlying the participation of STIM-ORAI and IP_3Rs in the biological behavior of cancer remain elusive.In this review,we summarize recent advances regarding STIM-ORAI and IP_3Rs and discuss how they promote cell proliferation,apoptosis evasion,and cell migration through temporal and spatial rearrangements in certain types of malignant cells.An understanding of the essential roles of STIM-ORAI and IP_3Rs may provide new pharmacologic targets that achieve a better therapeutic effect by inhibiting their actions in key intracellular signaling pathways. 展开更多
关键词 STROMAL interaction MOLECULE (STIM) CALCIUM release-activated CALCIUM channel protein (ORAI) Inositol 1 4 5-trisphosphate receptors (ip3Rs) Ca2+ Tumorigenesis
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Inositol 1,4,5-trisphosphate 3-kinases:functions and regulations 被引量:1
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作者 HuiJunXIA GuangYANG 《Cell Research》 SCIE CAS CSCD 2005年第2期83-91,共9页
Inositol 1,4,5-trisphosphate 3-kinase (IP3 3-kinase/IP3K) plays an important role in signal transduction in animal cellsby phosphorylating inositol 1,4,5-trisphosphate (IP3) to inositol 1,3,4,5-tetrakisphosphate (IP4)... Inositol 1,4,5-trisphosphate 3-kinase (IP3 3-kinase/IP3K) plays an important role in signal transduction in animal cellsby phosphorylating inositol 1,4,5-trisphosphate (IP3) to inositol 1,3,4,5-tetrakisphosphate (IP4). Both IP3 and IP4 arecritical second messengers which regulate calcium (Ca2+) homeostasis. Mammalian IP3Ks are involved in many biologicalprocesses, including brain development, memory, learning and so on. It is widely reported that Ca2+ is a canonicalsecond messenger in higher plants. Therefore, plant IP3K should also play a crucial role in plant development. Recently,we reported the identification of plant IP3K gene (AtIpk2β/AtIP3K) from Arabidopsis thaliana and its characterization.Here, we summarize the molecular cloning, biochemical properties and biological functions of IP3Ks from animal, yeastand plant. This review also discusses potential functions of IP3Ks in signaling crosstalk, inositol phosphate metabolism,gene transcriptional control and so on. 展开更多
关键词 inositol 1 4 5-trisphosphate 3-kinase (ip3 3-kinase/ip3K) inositol polyphosphate kinase (ipk) inositol phos-phate multikinase (ipmk) calcium (Ca^(2+)) signal transduction
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ERp44 C160S/C212S mutants regulate IP_(3)R_(1) channel activity
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作者 Congyan Pan Ji Zheng +5 位作者 Yanyun Wu Yingxiao Chen Likun Wang Zhansong Zhou Wenxuan Yin Guangju Ji 《Protein & Cell》 SCIE CSCD 2011年第12期990-996,共7页
Previous studies have indicated that ERp44 inhibits inositol 1,4,5-trisphosphate(IP3)-induced Ca2+release(IICR)via IP3R1,but the mechanism remains largely unexplored.Using extracellular ATP to induce intracellular cal... Previous studies have indicated that ERp44 inhibits inositol 1,4,5-trisphosphate(IP3)-induced Ca2+release(IICR)via IP3R1,but the mechanism remains largely unexplored.Using extracellular ATP to induce intracellular calcium transient as an IICR model,Ca2+image,pull down assay,and Western blotting experiments were carried out in the present study.We found that extracellular ATP induced calcium transient via IP3Rs(IICR)and the IICR were markedly decreased in ERp44 overexpressed Hela cells.The inhibitory effect of C160S/C212S but not C29S/T396A/ΔT(331–377)mutants of ERp44 on IICR were significantly decreased compared with ERp44.However,the binding capacity of ERp44 to L3V domain of IP3R1(1L3V)was enhanced by ERp44 C160S/C212S mutation.Taken together,these results suggest that the mutants of ERp44,C160/C212,can more tightly bind to IP3R1 but exhibit a weak inhibition of IP3R1 channel activity in Hela cells. 展开更多
关键词 ERp44 MUTANTS ATP inositol1 4 5-trisphosphate(ip3)receptors calciumtransient
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