|1.||Foskett, J Kevin: 4 articles (10/2015 - 06/2008)|
|2.||Mikoshiba, Katsuhiko: 4 articles (01/2015 - 09/2003)|
|3.||Mak, Don-On Daniel: 3 articles (10/2015 - 01/2010)|
|4.||Cheung, King-Ho: 3 articles (10/2015 - 06/2008)|
|5.||Liu, Pei: 3 articles (01/2011 - 10/2004)|
|6.||Boehning, Darren: 2 articles (03/2015 - 05/2008)|
|7.||Müller, Marioly: 2 articles (05/2014 - 06/2008)|
|8.||Subramanian, Manivannan: 2 articles (05/2013 - 01/2013)|
|9.||Hasan, Gaiti: 2 articles (05/2013 - 01/2013)|
|10.||Singleton, Andrew: 2 articles (05/2011 - 05/2010)|
12/01/2008 - "Hypoxia differently modulates gene expression of inositol 1,4,5-trisphosphate receptors in mouse kidney and HEK 293 cell line."
10/15/2003 - "We propose that NO-mediated modification of the IP3 receptor during hypoxia may lead to increased intranuclear Ca2+, resulting in altered transcription of apoptotic genes and activation of cascades of hypoxia-induced programmed neuronal death."
10/15/2003 - "Because NNLA inhibits NOS and prevents generation of NO, we conclude that the mechanism of hypoxia-induced modification of the neuronal nuclear membrane IP3 receptor is NO mediated. "
10/15/2003 - "Furthermore, the data demonstrate that administration of NNLA prior to hypoxia prevents the hypoxia-induced modification of the IP3 receptor in neuronal nuclei of newborn piglets. "
10/15/2003 - "The results show that hypoxia results in increased Bmax and Kd values for the IP3 receptor. "
|2.||Breast Neoplasms (Breast Cancer)
11/01/2013 - "Studies from our laboratory have shown that type 3 IP3 receptor (IP3R3) and voltage- and Ca(2+)-dependent K(+) channels BKCa channels are involved in human breast cancer cell proliferation. "
11/01/2013 - "Molecular interaction and functional coupling between type 3 inositol 1,4,5-trisphosphate receptor and BKCa channel stimulate breast cancer cell proliferation."
07/01/2005 - "The aim of this study was to establish the type(s) of inositol 1,4,5-trisphosphate receptors (IP3Rs) in T47D breast cancer cells that regulate intracellular calcium (Ca2+) and whether they interact with cyclin (Cy), an important regulator of cyclin-dependent kinases (cdk), during cell cycle progression. "
12/01/2013 - "Actein alters the activity of the ER IP3 receptor and Na,K-ATPase, induces calcium release and modulates the NF-κB and MEK pathways and may be worthwhile to explore to prevent and treat breast cancer."
10/15/2004 - "The cDNA-oligoarray analysis and reverse transcription-PCR verification indicated common changes in gene expression in methionine-dependent cell lines to include up-regulation/induction of cyclin D1, mitotic arrest deficient (MAD)1, p21, growth arrest and DNA-damage-inducible (GADD)45 alpha, GADD45 gamma, GADD34, breast cancer (BRCA)1, 14-3-3sigma, B-cell CLL/lymphoma (BCL)1, transforming growth factor (TGF)-beta, TGF-beta-induced early response (TIEG), SMAD5, SMAD7, SMAD2, insulin-like growth factor binding protein (IGFBP7), IGF-R2, vascular endothelial growth factor (VEGF), TNF-related apoptosis-inducing ligand (TRAIL), TNF-alpha converting enzyme (TACE), TRAIL receptor (TRAIL-R)2, TNFR-related death receptor (DR)6, TRAF interacting protein (I-TRAF), IL-6, MDA7, IL-1B convertase (ICE)-gamma, delta and epsilon, IRF1, IRF5, IRF7, interferon (IFN)-gamma and receptor components, ISG15, p65-NF-kappaB, JUN-B, positive cofactor (PC)4, C/ERB-beta, inositol triphosphate receptor I, and methionine adenosyltransferase II. On the other hand, cyclins A1, A2, B1 and B2, cell division cycle (CDC)2 and its kinase, CDC25 A and B, budding uninhibited by benzimidazoles (BUB)1 and 3, MAD2, CDC28 protein kinase (CKS)1 and 2, neuroepithelial cell transforming gene (NET)1, activator of S-phase kinase (ASK), CDC14B phosphatase, BCL2, TGF-beta activated kinase (TAK)1, TAB1, c-FOS, DNA topoisomerase II, DNA polymerase alpha, dihydrofolate reductase, thymidine kinase, stathmin, and MAP4 were down-regulated. "
|3.||Alzheimer Disease (Alzheimer's Disease)
06/15/1998 - "Several studies have shown severe deficits in both IP3 receptor levels and PKC levels and activity in Alzheimer's disease brain, although the relationship of these changes to disease pathology is poorly understood. "
04/01/2005 - "Despite the strong negative effect of the presenilin2 and Alzheimer's-disease-linked presenilin2 variants on agonist-induced TRPC6 activation, conformational coupling between inositol 1,4,5-trisphosphate receptor type 3 (IP(3)R3) and TRPC6 was unaffected. "
06/15/1998 - "These findings suggest that reduced IP3 receptor and PKC levels in the entorhinal cortex/hippocampal formation reflect and may be important for the progression of Alzheimer's disease neurofibrillary pathology. "
10/01/2015 - "Analyzing and Quantifying the Gain-of-Function Enhancement of IP3 Receptor Gating by Familial Alzheimer's Disease-Causing Mutants in Presenilins."
05/14/2014 - "Suppression of InsP3 receptor-mediated Ca2+ signaling alleviates mutant presenilin-linked familial Alzheimer's disease pathogenesis."
04/05/1993 - "Polymerase chain reaction analysis of first-strand cDNAs from both mouse T-lymphoma cells and rat brain tissues reveals that the IP3 receptor transcript in mouse T-lymphoma cells belongs to the short form (non-neuronal form) and not the long form (neuronal form) detected in rat brain tissue. "
03/31/1995 - "Furthermore, this peptide competes effectively for ankyrin binding to IP3 receptor-containing vesicles and/or purified IP3 receptor, and it blocks ankyrin-induced inhibitory effects on IP3 binding and IP3-mediated internal Ca2+ release in mouse T-lymphoma cells. "
12/01/1993 - "This is in contrast to the brain and T-lymphoma cells in which the IP3 receptor is attached to ankyrin (L. "
03/31/1995 - "In this study we have used several complementary techniques to explore the interaction between the membrane linker molecule, ankyrin, and the inositol 1,4,5-trisphosphate (IP3) receptor in mouse T-lymphoma cells. "
11/01/2002 - "Here, we report that the calcium ionophore ionomycin induces a massive Ca2+-dependent apoptosis in wildtype DT-40 chicken B lymphoma cells, as well as in BTK-deficient, PLCgamma2-deficient and IP3 receptor-deficient DT-40 cells, but not in LYN- or SYK-deficient DT-40 cells. "
04/01/2000 - "Reduced [3H]IP3 binding but unchanged IP3 receptor levels in the rat hippocampus CA1 region following transient global ischemia and tolerance induction."
07/01/1993 - "These findings suggest that the selective alteration of IP3 receptor binding in the hippocampus CA1 may be closely associated with the selective vulnerability of this region to ischemia."
04/01/2000 - "We found that the IP3 receptor mRNA levels were decreased after damage-inducing ischemia (9 min) in the hippocampus CA1 and CA3 regions. "
04/01/2000 - "We used the 4-vessel occlusion model in rat brain to investigate the effect of transient ischemia insults on the IP3 receptor mRNA level, the IP3 receptor protein level and [3H]IP3 binding. "
01/01/1999 - "Such selective inhibition of inositol 1,4,5-trisphosphate receptor-induced Ca2+ release and the loss of type 1 inositol 1,4,5-trisphosphate receptor in the CA1 region of the hippocampus in cerebral ischemia may be associated with its region-specific vulnerability to ischemia."
|4.||Messenger RNA (mRNA)
|8.||Cyclin-Dependent Kinases (cdk Proteins)
|9.||Proteins (Proteins, Gene)
|10.||Phosphopyruvate Hydratase (Enolase)