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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
57                          Surprisingly, yeast stress granules adopt a different material state, which
58        In addition, hnRNPA1 was recruited to stress granules after treatment of cells with quercetin
59       RNA immunoprecipitation with the known stress granule aggregates TIAR and G3BP1 was performed o
60            Unexpectedly, deletion of several stress granule and processing body genes, including pbp1
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
65                               The ability of stress granules and G3BP1 to activate PKR and other inna
66 otein-protein interactions and links between stress granules and human diseases and identifies ATP-de
67 adaptation to ER stress through induction of stress granules and inhibition of translation.
68 otein interaction, the recruitment of FUS to stress granules and interaction with PABP are RNA depend
69 HNRNPs) and the response to cellular stress (stress granules and ND10 bodies).
70  a potential calcium signaling target within stress granules and other mRNPs that accumulate during f
71                                              Stress granules and P bodies are conserved cytoplasmic a
72 ith YB-1, a translational regulator found in stress granules and P bodies, in intracytoplasmic foci.
73                         RNA granules such as stress granules and processing bodies (PBs) contain tran
74 Unlike other cytoplasmic structures, such as stress granules and processing bodies, inclusion bodies
75                                 Finally, RNA stress granules and smaller dendritic trees were also ob
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
84 granules, while RIG-I associates with TRIM25/stress granules and with mitochondrial MAVS.
85 oma 1 is the target of Rbfox2 in cytoplasmic stress granules, and Rbfox2 regulates the retinoblastoma
86                                              Stress granules appear during virus infection, and their
87         These data provide evidence that RNA stress granules are a novel form of epigenetic regulatio
88         Furthermore, these data suggest that stress granules are active in signaling to the translati
89                                              Stress granules are cytoplasmic inclusions that repress
90                                              Stress granules are important in the stress response and
91 to refine a longstanding paradigm indicating stress granules are inert structures and explains why G3
92                                              Stress granules are large messenger ribonucleoprotein (m
93                                              Stress granules are membrane-less organelles composed of
94                                              Stress granules are mRNA-protein assemblies formed from
95                                              Stress granules are mRNA-protein granules that form when
96                                              Stress granules are non-membrane bound RNA-protein (RNP)
97                                              Stress granules are small RNA-protein granules that modi
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.
103                          ATP is required for stress granule assembly and dynamics.
104 he first insight on how caliciviruses impair stress granule assembly by targeting the nucleating fact
105                 The virus itself can prevent stress granule assembly from these complexes, but this i
106 creen was employed to identify regulators of stress granule assembly in quiescent cells.
107 roteins in vitro have the opposite effect on stress granule assembly in vivo.
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
111 slation, and block a cellular process called stress granule assembly.
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
114                                    In vitro, stress-granule-associated proteins can demix to form liq
115 es, suggesting that calcium is necessary for stress granule association.
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
120  By mass spectrometry we have identified 463 stress granule candidate proteins.
121                                    Moreover, stress granule clearance in mammalian cells is reduced b
122                               Tia1/Pub1 is a stress granule component carrying a Q/N-rich prion domai
123 wn ALS genetic risk factor and ataxin 2 is a stress granule component in mammalian cells.
124 n flies, and TDP-43 interacts with a central stress granule component, polyA-binding protein (PABP).
125 ys through the activity of G3BP1, a critical stress granule component.
126 utamine aggregates specifically recruit some stress granule components, revealing a possible mechanis
127 elicases and protein remodelers as conserved stress granule components.
128                Our observations suggest that stress granules contain a stable core structure surround
129                       Human astrocytoma cell stress granules contain mRNAs that are known to be invol
130 -stimulated gene translation is inhibited in stress granule-containing HCV-infected cells.
131 NA-sequencing (RNA-seq) analysis of purified stress granule cores and single-molecule fluorescence in
132                        Proteomic analysis of stress granule cores reveals a dense network of protein-
133                         mRNA accumulation in stress granules correlates with longer coding and UTR re
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
136                                              Stress granule disassembly is also a stepwise process wi
137 the cell signals for renewed translation and stress granule disassembly.
138 ess, indicating a possible role for hYVH1 in stress granule disassembly.
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
141 sport, DNA damage repair, pre-mRNA splicing, stress granule dynamics, and others.
142 hat ALS-linked mutations in profilin 1 alter stress granule dynamics, providing further evidence for
143 n were implicated in protein translation and stress granule dynamics.
144 nt pathomechanism probably involving altered stress granule dynamics.
145  we show that casein kinase 2 (CK2) promotes stress granule dynamics.
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
148                                              Stress granules form in response to particular environme
149                                  Finally, as stress granule formation and dendritic loss occur early
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
152                                              Stress granule formation coincides with translational re
153 recursor model" which presents the idea that stress granule formation contributes to a TDP-43 aggrega
154                  PKR autophosphorylation and stress granule formation correlated with the timing of d
155 was both necessary and sufficient to prevent stress granule formation in response to eIF2alpha phosph
156              Consistent with these findings, stress granule formation is known to regulate mRNA trans
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
159 ation of protein synthesis by downregulating stress granule formation through G3BP1.
160                 Significantly, we found that stress granule formation was inhibited in MDBK cells inf
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
164 modulate mRNA translation and participate in stress granule formation.
165 endent lipid production leads to upregulated stress granule formation.
166  mechanism was associated with disruption of stress granule formation.
167  where they can regulate translation through stress granule formation.
168 ation of autophagosomes and the clearance of stress granules from the cell once the stress is relieve
169                 Current dogma indicates that stress granules function as inert storage depots for tra
170 ence and resistance to diverse environmental stresses, granule genesis is poorly understood.
171 ubsequent analysis revealed that astrocytoma stress granules harbor unique mRNAs for various cellular
172                     Functional impairment of stress granules has been implicated in amyotrophic later
173     Recent work connecting TDP-43 and FUS to stress granules has suggested how this cellular pathway,
174                        Finally, we show that stress granules have different properties in mammalian c
175                                   Defects in stress granule homeostasis constitute a cornerstone of A
176 e the authors find that p53 mRNA, present in stress granules in activated B lymphocytes, is released
177 g further evidence for the potential role of stress granules in ALS pathogenesis.
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
180 and Aurora kinase B (AurkB) are localized to stress granules in human astrocytoma cells.
181  synthesis, and reversed the accumulation of stress granules in infected cells.
182 nts disrupt the processing of nuclear TDP-43 stress granules in mammalian cells.
183  neuronal survival and the ability to induce stress granules in neuronal cell lines.
184  neuronal survival and the ability to induce stress granules in neuronal cell lines.
185  and fragile X mental retardation protein on stress granules in response to arsenic treatment.
186 ted gene silencing, and possibly shuttles to stress granules in stressed cells.
187    TDP-43 was also found to co-localize with stress granules in the cytosolic compartment.
188 ragments ability to trigger the formation of Stress Granules in vivo.
189 ctures, the processing body (P body) and the stress granule, in the yeast Saccharomyces cerevisiae.
190            Localization of ORF112 protein in stress granules induced in Cyprinid herpesvirus 3-infect
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
194  role for DNAJB6b in Z-disc organization and stress granule kinetics.
195 ote Ssd1-mRNA interactions with P-bodies and stress granules, leading to translational repression.
196 that Z-RNA or Z-DNA binding is important for stress granule localization.
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
201 toplasmic TDP-43 aggregates co-localize with stress granule markers.
202 mber and size of granules co-localizing with stress granule markers.
203                   These results suggest that stress granules may not represent a specific biological
204  a large set of proteins involved in RNA and stress granule metabolism.
205 ot differentially sequestered in cytoplasmic stress granules nor did they induce a systemic antiviral
206                                              Stress granules, on the other hand, were not assembled u
207 ormation does not depend on the formation of stress granules or processing bodies.
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
210  muscle but were insufficient to disrupt the stress granule pathway.
211 bly, while the MCM and RVB complexes promote stress granule persistence.
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
216 clear periphery that recruit both P-body and stress granule proteins, as well as mRNAs.
217  critical for phase separation of ALS-linked stress granule proteins.
218 ion of the TORC1 complex in cytoplasmic mRNP stress granules provides a negative regulatory mechanism
219 P1 was not identified, leaving a key step in stress granule regulation uncharacterized.
220 hat function in translational repression and stress granule regulation.
221 s work suggests that autophagic clearance of stress granule related and pathogenic RNP granules that
222                                 Furthermore, stress granule resolution was impaired on differentiated
223  nor Adar2(-/-) cells displayed a comparable stress granule response following IFN treatment.
224            Thus, reduced BMPR2 can subvert a stress granule response, heighten GM-CSF mRNA translatio
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
227        In live cells, TIA1 mutations delayed stress granule (SG) disassembly and promoted the accumul
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
231            eIF2alpha phosphorylation-induced stress granule (SG) formation was blocked by ISRIB.
232 GT in IBs was associated with suppression of stress granule (SG) formation.
233 LS patients are consistently co-labeled with stress granule (SG) marker proteins.
234                                              Stress granules (SG) are membrane-less organelles that a
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
237                                              Stress granules (SGs) are an important component of cell
238                                              Stress granules (SGs) are cytoplasmic condensates of sta
239                                              Stress granules (SGs) are cytoplasmic ribonucleoprotein
240                                              Stress granules (SGs) are cytoplasmic storage sites cont
241                                              Stress granules (SGs) are cytoplasmic structures that ar
242                                              Stress granules (SGs) are cytosolic ribonucleoprotein ag
243                                              Stress granules (SGs) are large cytoplasmic ribonucleopr
244                                              Stress granules (SGs) are large macromolecular aggregate
245                                              Stress granules (SGs) are transient cytoplasmic structur
246                                    Mammalian stress granules (SGs) contain stalled translation preini
247                     Dynamic, mRNA-containing stress granules (SGs) form in the cytoplasm of cells und
248 induced granules appear to be similar to the stress granules (SGs) generated in cells triggered by he
249                                              Stress granules (SGs) harbour translationally stalled me
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
255                    Eukaryotic cells assemble stress granules (SGs) when translation initiation is inh
256                                 Formation of stress granules (SGs), cytoplasmic aggregates of stalled
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
259             Here we investigated the role of stress granules (SGs), ribonucleoprotein complexes that
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
262 g mRNAs away in cellular compartments called stress granules (SGs).
263 g translation initiation and the assembly of stress granules (SGs).
264 RNAs accumulate in cytoplasmic foci known as stress granules (SGs).
265 ckle-like cytoplasmic structures shown to be stress granules (SGs).
266 ation initiation, and induce the assembly of stress granules (SGs).
267 g in reduced PB movement and cross talk with stress granules (SGs).
268 isible cytoplasmic foci, referred to as UBP1 stress granules (SGs).
269 asmic mislocalization and incorporation into stress granules (SGs).
270 -binding proteins to form inclusions, termed stress granules (SGs).
271 aining translationally silenced mRNPs termed stress granules (SGs).
272 n of discrete cytoplasmic inclusions, termed stress granules (SGs).
273 of cytoplasmic mRNA and protein foci, termed stress granules (SGs).
274 omplexes (PICs) mediates the condensation of stress granules (SGs).
275  to oxidative stress, PARP12 is recruited to stress-granules (SGs), known sites of mRNA translational
276          These data indicate that increasing stress granule size is associated with a threshold or sw
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
279            Although the field has focused on stress granules, TDP-43 also forms other types of RNA gr
280 ular stress, PABPC1 relocates to cytoplasmic stress granules that are multimolecular aggregates of st
281  substructures, referred to as cores, within stress granules that can be purified.
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
285                        Here, we describe the stress granule transcriptome of yeast and mammalian cell
286 D1 caused a cell type-dependent induction of stress granules, translational arrest, and growth impair
287                   Interestingly, the loss of stress granules was correlated with a decrease in the lo
288                 In contrast, the assembly of stress granules was not affected by changes in either PK
289         To investigate the role of Rbfox2 in stress granules we used RNA-immunoprecipitation sequenci
290  from breast cancer patients, Grp78-positive stress granules were observed, consistent with the likel
291                Interestingly, hYVH1-positive stress granules were significantly smaller, whereas knoc
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
300                      Our work links cellular stress granules with activation of PKR and other innate

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