Inositol 1,4,5-Trisphosphate

Intracellular messenger formed by the action of phospholipase C on phosphatidylinositol 4,5-bisphosphate, which is one of the phospholipids that make up the cell membrane. Inositol 1,4,5-trisphosphate is released into the cytoplasm where it releases calcium ions from internal stores within the cell's endoplasmic reticulum. These calcium ions stimulate the activity of B kinase or calmodulin.

Also Known As:

Networked: 247 relevant articles (2 outcomes, 22 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	De Smedt, H: 4 articles (01/2013 - 11/2001)
2.	Parys, J B: 4 articles (01/2013 - 11/2001)
3.	Missiaen, L: 4 articles (01/2013 - 11/2001)
4.	Jarius, S: 3 articles (01/2015 - 01/2015)
5.	Wildemann, B: 3 articles (01/2015 - 01/2015)
6.	Ehrlich, Barbara E: 3 articles (09/2014 - 03/2005)
7.	Wojcikiewicz, Richard J H: 2 articles (05/2015 - 08/2003)
8.	Distelhorst, Clark W: 2 articles (10/2014 - 04/2008)
9.	Monaco, G: 2 articles (01/2013 - 02/2012)
10.	Akl, H: 2 articles (01/2013 - 02/2012)

Related Diseases

1.	Ischemia 01/01/1992 - "In the dentate molecular layer, [3H]inositol 1,4,5-trisphosphate binding also showed significant reduction during recirculation except for a slight recovery 48 h and seven days after ischemia. " 01/01/1992 - "In contrast, [3H]inositol 1,4,5-trisphosphate binding showed significant reduction in the selectively vulnerable regions 1-24 h after ischemia. " 01/01/2008 - "Ischemia/reperfusion induce renal tubule apoptosis by inositol 1,4,5-trisphosphate receptor and L-type Ca2+ channel opening." 01/01/2001 - "We have further shown that the subcellular distribution of inositol 1,4,5-trisphosphate receptor phosphorylation in neurons is regulated by excitatory neurotransmission, as well as excitotoxic insult and neuronal ischemia-reperfusion. " 01/01/1999 - "We examined the effect of ischemia on inositol 1,4,5-trisphosphate receptor-induced Ca2+ release by functional and morphological approaches, using the gerbil model after 6-h unilateral occlusion of the common carotid artery. "
2.	Anoxia (Hypoxia) 05/01/1999 - "Endogenous levels of inositol 1,4,5-trisphosphate were unaltered by hypoxia. " 03/01/1999 - "Effect of chronic hypoxia on alpha-1 adrenoceptor-mediated inositol 1,4,5-trisphosphate signaling in ovine uterine artery." 02/01/1994 - "Hypoxia increased the basal level of inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) to 190% (P < 0.01), while NE-stimulated Ins(1,4,5)P3 production was significantly suppressed. " 03/01/1999 - "The present study examined the effect of chronic hypoxia on coupling efficiency of alpha-1 adrenoceptors to inositol 1,4,5-trisphosphate (InsP3) signaling in ovine uterine artery. " 02/01/1997 - "To test the hypothesis that hypoxia-induced developmental and vessel specific cerebral artery contractility changes are mediated, in part, by changes in alpha1-adrenergic receptor (alpha1-AR) density and/or NE-induced inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] responses, we performed the following study. "
3.	Neuroblastoma 01/15/1990 - "This study reports increased intracellular Ca2+ and inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] in response to muscarinic-cholinergic stimulation of human neuroblastoma (SH-SY5Y) cells. " 12/01/2015 - "Here, we evaluated several fluorescent Ca(2+) indicators in the context of local Ca(2+) signals (puffs) evoked by inositol 1,4,5-trisphosphate (IP3) in cultured human neuroblastoma SH-SY5Y cells, using high-speed video-microscopy. " 11/01/2001 - "Hormonal stimulation of SH-SY5Y neuroblastoma cells and HeLa cells for several hours downregulated inositol 1,4,5-trisphosphate expression and concomitantly altered the properties of the Ca(2+) puffs. " 01/01/1992 - "The ability of two enantiomeric fluoro-analogues of D-myo-inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] to mobilize intracellular Ca2+ stores in SH-SY5Y neuroblastoma cells has been investigated. " 11/25/1991 - "Chronic muscarinic stimulation of SH-SY5Y neuroblastoma cells suppresses inositol 1,4,5-trisphosphate action. "
4.	Neoplasms (Cancer) 10/01/2014 - "Bcl-2 regulation of the inositol 1,4,5-trisphosphate receptor and calcium signaling in normal and malignant lymphocytes: potential new target for cancer treatment." 10/01/2012 - "The decrease in diacylglycerol (DAG) and inositol 1,4,5-triphosphate (IP₃) due to inhibition of PLC(γ)1, leads to the downregulation of Ca²⁺-dependent processes within the cell and also inhibits the formation of tumors. " 02/19/2010 - "Inositol 1,4,5-trisphosphate 3-kinase-A is a new cell motility-promoting protein that increases the metastatic potential of tumor cells by two functional activities." 09/01/2009 - "Moreover, POP has also been proposed as a regulator of inositol 1,4,5-triphosphate signaling and several other functions such as cell proliferation and differentiation, as well as signal transduction in the central nervous system, and it is suspected to be involved in pathological conditions such as Parkinson's and Alzheimer's diseases and cancer. " 07/01/1992 - "An attempt was made to identify a specific binding of inositol 1,4,5-trisphosphate (IP3) to human chromaffin cell tumors. "
5.	Spinocerebellar Ataxias (Spinocerebellar Ataxia) 01/01/2014 - "A suite of models was developed to study the role of inositol 1,4,5-trisphosphate receptor 1 (IP3R1) in spinocerebellar ataxias (SCAs). " 10/15/2010 - "The purpose of this study was to characterise a novel family with very slowly progressive pure spinocerebellar ataxia (SCA) caused by a deletion in the inositol 1,4,5-triphosphate receptor 1 (ITPR1) gene on chromosome 3. This is a detailed clinical, genetic, and radiological description of the genotype. " 01/01/2014 - "Integration of modeling with experimental and clinical findings synthesizes and refines the central role of inositol 1,4,5-trisphosphate receptor 1 in spinocerebellar ataxia." 09/12/2012 - "Chronic suppression of inositol 1,4,5-triphosphate receptor-mediated calcium signaling in cerebellar purkinje cells alleviates pathological phenotype in spinocerebellar ataxia 2 mice." 05/01/2015 - "Mutations in the inositol 1,4,5-triphosphate receptor type 1 gene (ITPR1) have been identified in families with early-onset spinocerebellar ataxia type 29 (SCA29) and late-onset SCA15, but have not been found in sporadic infantile-onset cerebellar ataxia. "

Related Drugs and Biologics

1.	Acetylcholine (Acetylcholine Chloride)
2.	Glucose (Dextrose)
3.	Calcium
4.	Inositol 1,4,5-Trisphosphate Receptors (Inositol Triphosphate Receptor)
5.	Calcium Channels (Calcium Channel)
6.	Adenosine Triphosphate (ATP)
7.	Phosphotransferases (Kinase)
8.	Ryanodine Receptor Calcium Release Channel (Ryanodine Receptor)
9.	Ankyrins
10.	Carrier Proteins (Binding Protein)

Related Therapies and Procedures

1.	Injections
2.	Electrodes (Electrode)