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1 type of the latter compartment, known as the stress granule.
2 in involved in the recruitment of Syk to the stress granule.
3 e phosphorylation of proteins at or near the stress granule.
4 relocalization also of hEndoV to cytoplasmic stress granules.
5 icating that mutant VCP delayed clearance of stress granules.
6 ch as nucleoli, the nuclear pore complex and stress granules.
7 ct specific translation factors in cytosolic stress granules.
8 ave more than 50% of their mRNA molecules in stress granules.
9 e RhoA is implicated in the formation of RNA stress granules.
10 res similar in morphology to hypoxia-induced stress granules.
11 hat it is defective in inducing formation of stress granules.
12 visible RNA granules, including P bodies and stress granules.
13 cting partners also found to be recruited to stress granules.
14 te in the cytoplasm and form TDP-43 positive stress granules.
15 riggers aggregation of proteins and RNA into stress granules.
16 then inhibits TORC1 through sequestration at stress granules.
17 ncluding nucleoli, Cajal and PML bodies, and stress granules.
18 lular fraction highly enriched in starvation stress granules.
19 erties different from those of the canonical stress granules.
20 with ALS-linked proteins and inclusion into stress granules.
21 suggesting that these sites were not typical stress granules.
22 ucleoprotein complexes known as P bodies and stress granules.
23 associated with rapid induction of antiviral stress granules.
24 ery, ribonucleoprotein particles (RNPs), and stress granules.
25 ed that profilin 1 might also associate with stress granules.
26 rodegeneration and promotes the formation of stress granules.
27 DP-43 and ataxin-2, is that they localize to stress granules.
28 tive TRASH domain no longer redistributed to stress granules.
29 inhibit these proteins from aggregating into stress granules.
30 that resemble but are clearly distinct from stress granules.
31 ransport, and storage of specific mRNAs into stress granules.
32 R1(p150) is required for its localization to stress granules.
33 s a novel function for Rbfox2 in cytoplasmic stress granules.
34 tion of TAR DNA binding protein and FUS with stress granules.
35 orms inclusions that appear to correspond to stress granules.
36 to oxidative stress through the formation of stress granules.
37 ) is likewise sufficient for localization to stress granules.
38 s associated with messenger RNA-sequestering stress granules.
39 ositive foci, such as regulation of cellular stress granules.
40 hat affected the dynamics of P bodies and/or stress granules.
41 RNA-binding protein TIA1, a key component of stress granules.
42 (PTB4) also results in their localization to stress granules.
43 ration (i.e. Ataxin-2 and SMN) interact with stress granules.
44 , Hsp26, Hsp42, and some known components of stress granules.
45 G-ALS variants also lack the ability to form stress granules.
46 at early stages is differently localized in stress granules.
47 nelles involved in RNA metabolism, including stress granules.
48 protein is crucial for its localization into stress granules.
49 G-ALS variants also lack the ability to form stress granules.
50 ger coalescence of RNA-binding proteins into stress granules.
51 ved measurements of ACTB mRNA trafficking to stress granules.
52 these pathological inclusions are related to stress granules.
53 the cytoplasm and participate in assembly of stress granules.
54 d in foci that co-localize with P bodies and stress granules, a class that is enriched for mRNAs invo
55 nt TIA1 constructs caused a mild increase in stress granule abundance compared to wild type, and show
56 coincides with translational repression, and stress granules actively signal to mediate cell fate dec
61 Upon DNA damage, p53 mRNA is released from stress granules and associates with polyribosomes to inc
62 sion increases the association of dFMRP with stress granules and colocalizes with polyA binding prote
63 ss incorporation of hnRNPA2 and hnRNPA1 into stress granules and drive the formation of cytoplasmic i
64 ovides a mechanistic link between persistent stress granules and fibrillar protein pathology in disea
66 otein-protein interactions and links between stress granules and human diseases and identifies ATP-de
68 otein interaction, the recruitment of FUS to stress granules and interaction with PABP are RNA depend
70 a potential calcium signaling target within stress granules and other mRNPs that accumulate during f
72 ith YB-1, a translational regulator found in stress granules and P bodies, in intracytoplasmic foci.
74 Unlike other cytoplasmic structures, such as stress granules and processing bodies, inclusion bodies
76 ding protein (G3BP) overexpression to induce stress granules and study their assembly process and sig
77 bulk mRNA molecules accumulate in mammalian stress granules and that only 185 genes have more than 5
78 evidence suggests a link between persistent stress granules and the accumulation of pathological inc
79 ng the interplay between TDP-43 aggregation, stress granules and the effect of ALS-associated TDP-43
80 inverse correlation between the presence of stress granules and the induction of IFN-stimulated prot
81 mediated LLPS contributes to the assembly of stress granules and their liquid properties and provides
82 toplasmic ribonucleoprotein granules such as stress granules and those seeded by the aggregation of s
83 The ATP stores inside a cell do not overlay stress granules and we suggest that hEndoV is redistribu
85 oma 1 is the target of Rbfox2 in cytoplasmic stress granules, and Rbfox2 regulates the retinoblastoma
91 to refine a longstanding paradigm indicating stress granules are inert structures and explains why G3
98 xpectedly, we found that genes that modulate stress granules are strong modifiers of TDP-43 toxicity
99 d we suggest that hEndoV is redistributed to stress granules as a strategy to create a local environm
100 on of eIF2alpha and concomitant formation of stress granules, as well as promotion of autophagy and a
101 aken together, these observations argue that stress granules assemble through a multistep process ini
102 ed role and mechanism of SIRT6 in regulating stress granule assembly and cellular stress resistance.
104 he first insight on how caliciviruses impair stress granule assembly by targeting the nucleating fact
108 inine-rich DPRs in cells induced spontaneous stress granule assembly that required both eIF2alpha pho
109 149, which regulates G3BP1 oligomerization, stress granule assembly, and RNase activity intrinsic to
110 differently, with the CCT complex inhibiting stress granule assembly, while the MCM and RVB complexes
112 -2 (Atx2) are triplet expansion disease- and stress granule-associated proteins implicated in neurona
113 n 1 and related protein profilin 2 are novel stress granule-associated proteins in mouse primary cort
116 as knocking down hYVH1 expression attenuated stress granule breakdown during recovery from arsenite s
117 We found that assembly of large G3BP-induced stress granules, but not small granules, precedes phosph
118 s on HeLa cells, including quantification of stress granules by high content analysis and fluorescenc
119 cluding CDC48 alleles, provide evidence that stress granules can be targeted to the vacuole by autoph
124 n flies, and TDP-43 interacts with a central stress granule component, polyA-binding protein (PABP).
126 utamine aggregates specifically recruit some stress granule components, revealing a possible mechanis
131 NA-sequencing (RNA-seq) analysis of purified stress granule cores and single-molecule fluorescence in
134 to a corresponding increase in formation of stress granules, cytoplasmic protein/RNA complexes that
135 oreover, multiple ATP-driven machines affect stress granules differently, with the CCT complex inhibi
139 e poly(A) binding protein and accumulates in stress granules during arsenite treatment of human cells
140 etic interaction and recent evidence linking stress granule dynamics to ALS pathogenesis, we hypothes
142 hat ALS-linked mutations in profilin 1 alter stress granule dynamics, providing further evidence for
146 ulates abnormally, suggesting that prolonged stress granule dysfunction may contribute to pathogenesi
147 Endogenous WDR62 and MAPKBP1 co-localize to stress granules following arsenite treatment, but not du
150 s trigger phosphorylated-eIF2alpha-dependent stress granule formation and global translational suppre
151 microRNA biogenesis under stress, involving stress granule formation and re-organization of DICER an
153 recursor model" which presents the idea that stress granule formation contributes to a TDP-43 aggrega
155 was both necessary and sufficient to prevent stress granule formation in response to eIF2alpha phosph
157 that the treatment of cells with inducers of stress granule formation leads to the recruitment of Syk
158 te that the dysfunction induced by prolonged stress granule formation might contribute directly to AL
161 , decreased number of processing bodies, and stress granule formation, implying global translational
162 es that TDP-43 aggregation is independent of stress granule formation, in contrast to the "precursor
163 toplasmic MTDH was associated with increased stress granule formation, reduced survival in response t
168 ation of autophagosomes and the clearance of stress granules from the cell once the stress is relieve
171 ubsequent analysis revealed that astrocytoma stress granules harbor unique mRNAs for various cellular
173 Recent work connecting TDP-43 and FUS to stress granules has suggested how this cellular pathway,
176 e the authors find that p53 mRNA, present in stress granules in activated B lymphocytes, is released
178 ng the relationship between viruses and mRNA stress granules in animal cells and will discuss importa
179 wn that ADAR1(p150) localized to cytoplasmic stress granules in HeLa cells following either oxidative
189 ctures, the processing body (P body) and the stress granule, in the yeast Saccharomyces cerevisiae.
191 ge response.Sequestering mRNA in cytoplasmic stress granules is a mechanism for translational repress
192 s flexible and that the solid state of yeast stress granules is an adaptation to extreme environments
193 studies have suggested that the assembly of stress granules is central in orchestrating stress and a
195 ote Ssd1-mRNA interactions with P-bodies and stress granules, leading to translational repression.
197 ese results illustrate that HCV exploits the stress granule machinery at least two ways: by inducing
198 by the colocalization of CML38 with the mRNP stress granule marker RNA Binding Protein 47 (RBP47) upo
199 1 or Hrb98DE protein in association with the stress granule marker ROX8 and additional endogenous RNA
200 ements in oxidated proteins but observed the stress granule markers RasGAP SH3-binding protein and ph
205 ot differentially sequestered in cytoplasmic stress granules nor did they induce a systemic antiviral
208 PARP13 and two of its functional partners in stress granules: PARP12/ARTD12, and PARP15/BAL3/ARTD7.
209 her mutant VCP triggers dysregulation of the stress granule pathway in vivo, we analyzed skeletal mus
212 rotein (Pab1 in yeast), a defining marker of stress granules, phase separates and forms hydrogels in
213 ribosomal subunit proteins L10a and S6, the stress granule protein G3BP1, and a subset of translatio
214 find that m(6)A disrupts RNA binding by the stress granule proteins G3BP1/2, USP10, CAPRIN1, and RBM
215 NA) knockdown experiments, we found that the stress granule proteins T-cell-restricted intracellular
218 ion of the TORC1 complex in cytoplasmic mRNP stress granules provides a negative regulatory mechanism
221 s work suggests that autophagic clearance of stress granule related and pathogenic RNP granules that
225 lling while preserving the effect of nsP3 on stress granule responses and co-localisation with GTPase
226 , a target of TDP-43, is required for normal stress granule (SG) assembly, but the functional consequ
228 Moreover, PABPN1 rescues the dysregulated stress granule (SG) dynamics and facilitates the removal
229 n effective antiviral strategy that leads to stress granule (SG) formation and translational arrest m
230 s exhibit an increased propensity to trigger stress granule (SG) formation resulting in global transl
235 ther to daughter cells for translation or to stress granules (SGs) and P-bodies (PBs) for mRNA storag
236 er ribonucleoprotein (mRNP) complexes called stress granules (SGs) and processing bodies (PBs), sites
248 induced granules appear to be similar to the stress granules (SGs) generated in cells triggered by he
250 nsider the assembly and dissociation of mRNA stress granules (SGs) in hypertonic-stressed cells and t
251 show that EBOV does not induce formation of stress granules (SGs) in infected cells and is therefore
252 ell stress efficiently triggers formation of stress granules (SGs) in proliferating, quiescent, and d
253 SV-2) are disrupted in their ability to form stress granules (SGs) in response to oxidative stress an
254 nditions, many mammalian mRNAs accumulate in stress granules (SGs) together with numerous RNA-binding
257 protein synthesis and subsequent assembly of stress granules (SGs), cytoplasmic aggregates that conta
258 lation initiation and induce the assembly of stress granules (SGs), cytoplasmic ribonucleoprotein com
260 RNAs in ribonucleoprotein complexes known as stress granules (SGs), which contain translationally sil
261 Natural WNV strain infections do not induce stress granules (SGs), while W956IC (a lineage 2/1 chime
275 to oxidative stress, PARP12 is recruited to stress-granules (SGs), known sites of mRNA translational
277 al protein synthesis and/or formation of RNA stress granules suggested diminished ribosome recruitmen
278 and co-localized with DNAJB6 at sarcoplasmic stress granules suggesting that these proteins maybe nov
280 ular stress, PABPC1 relocates to cytoplasmic stress granules that are multimolecular aggregates of st
282 pon cell activation with mitogens, including stress granules that contain the RNA binding protein Tia
283 noncoding RNAs (ncRNAs), can be targeted to stress granules, the targeting efficiency varies from <1
284 Rbfox2 is a novel constituent of cytoplasmic stress granules, the translational silencing machinery a
286 D1 caused a cell type-dependent induction of stress granules, translational arrest, and growth impair
290 from breast cancer patients, Grp78-positive stress granules were observed, consistent with the likel
292 bition of AurkB results in fewer and smaller stress granules when analyzed using high-throughput fluo
293 ve stress recruits mutant FUS to cytoplasmic stress granules where it is able to bind and sequester w
294 ptionally induced and localized to cytosolic stress granules, where nuclear factors dock to compensat
295 nducible ADAR1 proteins induced formation of stress granules, whereas neither wild-type (WT) nor Adar
296 ribonucleoprotein (mRNP) complexes including stress granules, which are known to accumulate as messen
297 ncipal types of cytoplasmic RNA granules are stress granules, which contain stalled translation initi
298 RNA-protein granules, processing bodies and stress granules, which contain translationally repressed
299 ibuted into cytoplasmic dots associated with stress granules, while RIG-I associates with TRIM25/stre
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