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Endoplasmic reticulum ( ER ) stress(passive) caused byEndoplasmic reticulum ( ER ) stress
ER stress and induction of the UPRcausesER stress and induction of the UPR
chemically induced ER stress(passive) caused bychemically induced ER stress
ER stress as evidenced by BiP and CHOPtriggeredER stress as evidenced by BiP and CHOP
ER stress by inhibition of N - linked glycosylation ( Supplementary FigcausesER stress by inhibition of N - linked glycosylation ( Supplementary Fig
induction of a variety of ER stress markers ( data not shown ) , including the immediate early gene Atf3 , which was induced prior to the maximal repression of Sort1 ( Figure 4Bcausedinduction of a variety of ER stress markers ( data not shown ) , including the immediate early gene Atf3 , which was induced prior to the maximal repression of Sort1 ( Figure 4B
BiP , a major marker of ER stress in mammalian cells(passive) triggered byBiP , a major marker of ER stress in mammalian cells
to ER stress via the accumulation of misfolded proteins in the ERleadsto ER stress via the accumulation of misfolded proteins in the ER
ER stress and capillary degeneration in vivo , both of which were inhibited by resveratrolcausedER stress and capillary degeneration in vivo , both of which were inhibited by resveratrol
a development - dependent UPR in the mouse braincauseda development - dependent UPR in the mouse brain
accumulation of misfolded proteins in the ER ... a treatment used to induce ER stresscausesaccumulation of misfolded proteins in the ER ... a treatment used to induce ER stress
ER stress ( Nakagawa et al . , 2000 ; Nakagawa and Yuan , 2000causingER stress ( Nakagawa et al . , 2000 ; Nakagawa and Yuan , 2000
ER stress , markedly upregulated Grp78 , and activated autophagy without impairing the autophagic fluxtriggeredER stress , markedly upregulated Grp78 , and activated autophagy without impairing the autophagic flux
transcriptional upregulation of a stress - regulated proteintriggerstranscriptional upregulation of a stress - regulated protein
Pubmed]Photoreceptor - specific degeneration(passive) caused byPubmed]Photoreceptor - specific degeneration
glycosylation of newly synthesized proteins in the ERpreventsglycosylation of newly synthesized proteins in the ER
accumulation of unfolded proteins in the ER lumencausesaccumulation of unfolded proteins in the ER lumen
unfolded protein stress in the endoplasmic reticulum by inhibiting N - linked glycosylation , homozygous Ppp1r15atm1Dron mice and cultured cells derived from themcausesunfolded protein stress in the endoplasmic reticulum by inhibiting N - linked glycosylation , homozygous Ppp1r15atm1Dron mice and cultured cells derived from them
with walking letter Edition to achieve on the frame and awareness of biochemical Humans 'sleadwith walking letter Edition to achieve on the frame and awareness of biochemical Humans 's
protein glycosylationpreventsprotein glycosylation
more neuronal death in immature brain than mature braincausedmore neuronal death in immature brain than mature brain
Nrf2 activation in the absence of increased levels of ROS Protein folding occurring in the ER drives the production of reactive oxygen species ( ROS ) , which , in turn , can cause ER stress and trigger the UPR , one of the several pathogenetic mechanisms of prostate cancer initiation and progression [ 23–24causesNrf2 activation in the absence of increased levels of ROS Protein folding occurring in the ER drives the production of reactive oxygen species ( ROS ) , which , in turn , can cause ER stress and trigger the UPR , one of the several pathogenetic mechanisms of prostate cancer initiation and progression [ 23–24
the first step of N‐linked glycosylation of proteins in the ERpreventsthe first step of N‐linked glycosylation of proteins in the ER
dose - dependent decreases in hepatocyte CD1d , inhibited hepatocyte activation of CD1d - restricted T - cell responsescauseddose - dependent decreases in hepatocyte CD1d , inhibited hepatocyte activation of CD1d - restricted T - cell responses
a form of cell stress known to require Ca2 + ionsleadsa form of cell stress known to require Ca2 + ions
cellular dysfunction and apoptosis(passive) caused bycellular dysfunction and apoptosis
TRAIL - induced apoptosis(passive) caused byTRAIL - induced apoptosis
GLUT1 trafficking and autophagy induction(passive) caused byGLUT1 trafficking and autophagy induction
accumulation of unfolded proteins in cell endoplasmic reticulum ( ERcausesaccumulation of unfolded proteins in cell endoplasmic reticulum ( ER
pronounced endoplasmatic reticulum stress and apoptosis through activation of protein kinase RNA - like endoplasmic reticulum kinase ( PERK ) and activation of the gene encoding CCAAT - enhancer - binding protein homologous protein ( CHOPcausedpronounced endoplasmatic reticulum stress and apoptosis through activation of protein kinase RNA - like endoplasmic reticulum kinase ( PERK ) and activation of the gene encoding CCAAT - enhancer - binding protein homologous protein ( CHOP
to apoptosis in RPTC ( Fig . 2ledto apoptosis in RPTC ( Fig . 2
cells to undergo the unfolded protein responsecausescells to undergo the unfolded protein response
the vessel development in Matrigel(TMpreventedthe vessel development in Matrigel(TM
cleavage of Rtn1–GFP in the vacuole through Atg7-independent autophagycausescleavage of Rtn1–GFP in the vacuole through Atg7-independent autophagy
the unfolded protein response ( UPR ... and therefore act as a misfolding agent when used at high concentrations or long incubation times [ 40may ... triggerthe unfolded protein response ( UPR ... and therefore act as a misfolding agent when used at high concentrations or long incubation times [ 40
to a reduction of the apparent molecular mass for WT BARPledto a reduction of the apparent molecular mass for WT BARP
autophagy ... suggesting that it may serve as a compensatory effect to proteasomal degradation [ 68triggeredautophagy ... suggesting that it may serve as a compensatory effect to proteasomal degradation [ 68
to a significant increase in UPR gene expression ( P<0.05ledto a significant increase in UPR gene expression ( P<0.05
to the formation of so - called " colloid droplets " which were immunopositive and of which the ultrastructural correlates appeared to be product - filled dilatations of the rough endoplasmic reticulum [ 17ledto the formation of so - called " colloid droplets " which were immunopositive and of which the ultrastructural correlates appeared to be product - filled dilatations of the rough endoplasmic reticulum [ 17
to a marked increase in apoptosis in CD68-positive macrophages , as well as other cellsledto a marked increase in apoptosis in CD68-positive macrophages , as well as other cells