2014
Reticulon 4 Is Necessary for Endoplasmic Reticulum Tubulation, STIM1-Orai1 Coupling, and Store-operated Calcium Entry
Jozsef L, Tashiro K, Kuo A, Park EJ, Skoura A, Albinsson S, Rivera-Molina F, Harrison KD, Iwakiri Y, Toomre D, Sessa WC. Reticulon 4 Is Necessary for Endoplasmic Reticulum Tubulation, STIM1-Orai1 Coupling, and Store-operated Calcium Entry. Journal Of Biological Chemistry 2014, 289: 9380-9395. PMID: 24558039, PMCID: PMC3969502, DOI: 10.1074/jbc.m114.548602.Peer-Reviewed Original ResearchConceptsSTIM1-Orai1 couplingER morphologyRedistribution of STIM1Store-operated calcium entryER tubulationER sheetsElevated cytoplasmicReticulon 4Functional consequencesRTN4SOCETubulationCalcium entryRecent advancesFundamental questionsSTIM1CytoplasmicHomeostasisApoptosisRegulationMechanisticallyFirst timeCellsMorphology
2013
Absence of Nogo-B (Reticulon 4B) Facilitates Hepatic Stellate Cell Apoptosis and Diminishes Hepatic Fibrosis in Mice
Tashiro K, Satoh A, Utsumi T, Chung C, Iwakiri Y. Absence of Nogo-B (Reticulon 4B) Facilitates Hepatic Stellate Cell Apoptosis and Diminishes Hepatic Fibrosis in Mice. American Journal Of Pathology 2013, 182: 786-795. PMID: 23313137, PMCID: PMC3586693, DOI: 10.1016/j.ajpath.2012.11.032.Peer-Reviewed Original ResearchConceptsHepatic stellate cell apoptosisMF-HSCsStellate cell apoptosisHepatic fibrosisKO miceCell apoptosisHuman hepatic stellate cellsRole of NogoCarbon tetrachloride inhalationCaspase-3B knockout miceHepatic stellate cellsPotential therapeutic strategyApoptosis of HSCsWT miceFibrotic areasLiver fibrosisSelective blockadeExperimental cirrhosisLX2 cellsCirrhotic liverStellate cellsTherapeutic strategiesKnockout miceFibrosis
2010
The type III inositol 1,4,5-trisphosphate receptor is associated with aggressiveness of colorectal carcinoma
Shibao K, Fiedler MJ, Nagata J, Minagawa N, Hirata K, Nakayama Y, Iwakiri Y, Nathanson MH, Yamaguchi K. The type III inositol 1,4,5-trisphosphate receptor is associated with aggressiveness of colorectal carcinoma. Cell Calcium 2010, 48: 315-323. PMID: 21075448, PMCID: PMC3572849, DOI: 10.1016/j.ceca.2010.09.005.Peer-Reviewed Original ResearchConceptsTrisphosphate receptorCaco-2 colon cancer cellsGain of expressionColorectal cancerColorectal carcinomaColon cancer cellsColon cancerType IIICellular functionsInhibition of apoptosisType III inositolLymph node metastasisDepth of invasionNormal colorectal mucosaShRNA knockdownMargin of tumorDevelopment of diseaseExpression levelsLiver metastasesCell proliferationNode metastasisTNM stageApoptosisColorectal mucosaIsoforms
2007
Loss of Akt1 Leads to Severe Atherosclerosis and Occlusive Coronary Artery Disease
Fernández-Hernando C, Ackah E, Yu J, Suárez Y, Murata T, Iwakiri Y, Prendergast J, Miao RQ, Birnbaum MJ, Sessa WC. Loss of Akt1 Leads to Severe Atherosclerosis and Occlusive Coronary Artery Disease. Cell Metabolism 2007, 6: 446-457. PMID: 18054314, PMCID: PMC3621848, DOI: 10.1016/j.cmet.2007.10.007.Peer-Reviewed Original ResearchMeSH KeywordsAcute Coronary SyndromeAnimalsApolipoproteins EApoptosisAtherosclerosisBone Marrow TransplantationCoronary OcclusionDisease Models, AnimalEndothelial CellsFemaleHumansInflammation MediatorsMacrophagesMaleMiceMice, KnockoutNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIProto-Oncogene Proteins c-aktConceptsLoss of Akt1Apolipoprotein E knockout backgroundOcclusive coronary artery diseaseBone marrow transfer experimentsAcute coronary syndromeCoronary artery diseaseLesion expansionCoronary syndromeCoronary atherosclerosisSevere atherosclerosisArtery diseaseInflammatory mediatorsCoronary lesionsVascular protectionVascular originProinflammatory genesENOS phosphorylationCardiovascular systemLesion formationGenetic ablationEndothelial cellsAtherogenesisEnhanced expressionKnockout backgroundVessel wall