TDAG51 is induced by homocysteine, promotes detachment-mediated programmed cell death, and contributes to the cevelopment of atherosclerosis in hyperhomocysteinemia.
about
A novel HSF1-mediated death pathway that is suppressed by heat shock proteinsEndoplasmic Reticulum Stress and Associated ROSThe Role of Endoplasmic Reticulum Stress and Unfolded Protein Response in AtherosclerosisProtein kinase R-like ER kinase and its role in endoplasmic reticulum stress-decided cell fateThe role of glucosamine-induced ER stress in diabetic atherogenesisProtective mechanisms against homocysteine toxicity: the role of bleomycin hydrolase.A review about biomarkers for the investigation of vascular function and impairment in diabetes mellitusER chaperones in mammalian development and human diseasesPleckstrin homology-like domain, family A, member 1 (PHLDA1) and cancer.Signal transducer and activator of transcription-1 is critical for apoptosis in macrophages subjected to endoplasmic reticulum stress in vitro and in advanced atherosclerotic lesions in vivo.Valproate attenuates accelerated atherosclerosis in hyperglycemic apoE-deficient mice: evidence in support of a role for endoplasmic reticulum stress and glycogen synthase kinase-3 in lesion development and hepatic steatosis.Reduced apoptosis and plaque necrosis in advanced atherosclerotic lesions of Apoe-/- and Ldlr-/- mice lacking CHOP.Phosphatidylinositol 3-kinase signaling in proliferating cells maintains an anti-apoptotic transcriptional program mediated by inhibition of FOXO and non-canonical activation of NFkappaB transcription factorsTDAG51 is an ERK signaling target that opposes ERK-mediated HME16C mammary epithelial cell transformation.Molecular targeting of proteins by L-homocysteine: mechanistic implications for vascular disease.The role of endoplasmic reticulum stress in the progression of atherosclerosis.Small-molecule screen identifies modulators of EWS/FLI1 target gene expression and cell survival in Ewing's sarcoma.Endoplasmic reticulum stress and endothelial dysfunction.TDAG51 mediates the effects of insulin-like growth factor I (IGF-I) on cell survival.A reporter for tracking the UPR in vivo reveals patterns of temporal and cellular stress during atherosclerotic progression.Trypanosoma cruzi infection induces a global host cell response in cardiomyocytesGene Expression Analyses during Spontaneous Reversal of Cardiomyopathy in Mice with Repressed Nuclear CUG-BP, Elav-Like Family (CELF) Activity in Heart Muscle.Integrated stress response modulates cellular redox state via induction of cystathionine γ-lyase: cross-talk between integrated stress response and thiol metabolism.Role of hyperhomocysteinemia in endothelial dysfunction and atherothrombotic disease.Correlation of decreased expression of PHLDA1 protein with malignant phenotype of gastric adenocarcinoma.Endothelial NOTCH1 is suppressed by circulating lipids and antagonizes inflammation during atherosclerosis.Cystathionine β-synthase regulates endothelial function via protein S-sulfhydration.Homocysteine induces cell death in H9C2 cardiomyocytes through the generation of peroxynitrite.Genistein attenuates vascular endothelial impairment in ovariectomized hyperhomocysteinemic rats.Loss of TDAG51 results in mature-onset obesity, hepatic steatosis, and insulin resistance by regulating lipogenesis.Comparison of the effects of Leishmania major or Leishmania donovani infection on macrophage gene expression.Mechanisms linking diabetes mellitus to the development of atherosclerosis: a role for endoplasmic reticulum stress and glycogen synthase kinase-3.Characterization of the metastatic phenotype of a panel of established osteosarcoma cells.Hyperhomocysteinemia promotes insulin resistance by inducing endoplasmic reticulum stress in adipose tissueForkhead transcription factors (FoxOs) promote apoptosis of insulin-resistant macrophages during cholesterol-induced endoplasmic reticulum stress.Homocysteine activates T cells by enhancing endoplasmic reticulum-mitochondria coupling and increasing mitochondrial respiration.Methods and models for monitoring UPR-associated macrophage death during advanced atherosclerosisMouse models of cystathionine beta-synthase deficiency reveal significant threshold effects of hyperhomocysteinemia.TDAG51 deficiency promotes oxidative stress-induced apoptosis through the generation of reactive oxygen species in mouse embryonic fibroblasts.Distinct endothelial phenotypes evoked by arterial waveforms derived from atherosclerosis-susceptible and -resistant regions of human vasculature.
P2860
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P2860
TDAG51 is induced by homocysteine, promotes detachment-mediated programmed cell death, and contributes to the cevelopment of atherosclerosis in hyperhomocysteinemia.
description
2003 nî lūn-bûn
@nan
2003 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2003 թվականի մայիսին հրատարակված գիտական հոդված
@hy
2003年の論文
@ja
2003年論文
@yue
2003年論文
@zh-hant
2003年論文
@zh-hk
2003年論文
@zh-mo
2003年論文
@zh-tw
2003年论文
@wuu
name
TDAG51 is induced by homocyste ...... rosis in hyperhomocysteinemia.
@ast
TDAG51 is induced by homocyste ...... rosis in hyperhomocysteinemia.
@en
type
label
TDAG51 is induced by homocyste ...... rosis in hyperhomocysteinemia.
@ast
TDAG51 is induced by homocyste ...... rosis in hyperhomocysteinemia.
@en
prefLabel
TDAG51 is induced by homocyste ...... rosis in hyperhomocysteinemia.
@ast
TDAG51 is induced by homocyste ...... rosis in hyperhomocysteinemia.
@en
P2093
P356
P1476
TDAG51 is induced by homocyste ...... rosis in hyperhomocysteinemia.
@en
P2093
A B Lawrence de Koning
Donald W Jacobsen
Dongcheng Wu
Erling Falk
Gazi S Hossain
Geoff H Werstuck
Jeffrey G Dickhout
Johannes V van Thienen
P304
30317-30327
P356
10.1074/JBC.M212897200
P407
P577
2003-05-08T00:00:00Z