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1 ent in cells (e.g., TIA-1) or induced (e.g., tristetraprolin).
2 d the non-ARE-containing RNAs GADD45beta and tristetraprolin.
3 otein HuA and the mRNA-destabilizing protein tristetraprolin.
4 or c-myc mRNA that were poorly recognized by tristetraprolin.
5 e activity of the mRNA-destabilizing protein tristetraprolin.
6 y changed and included the mRNA decay factor Tristetraprolin.
7 egulates meprin alpha expression by inducing tristetraprolin.
8 ta provoked an increase in the expression of tristetraprolin, a homeostatic zinc finger protein that
11 lly bound to ARE(TNF) mRNA and competed with tristetraprolin, a protein known to bind and destabilize
13 hat are targeted by the RNA-binding protein, tristetraprolin (also known as zinc finger protein 36 (Z
14 Nase binds both to mRNA cap structure and to tristetraprolin, an inducible host protein that sequeste
15 d by the phosphorylation and inactivation of tristetraprolin, an mRNA destabilizing protein that targ
17 se in expression and RNA binding activity of tristetraprolin, an mRNA-binding protein that destabiliz
19 f PMR1 with SGs under conditions which cause tristetraprolin and butyrate response factor 1, proteins
24 oup of RNA-binding proteins (including TIS11/tristetraprolin and TIS11D) that share characteristic ta
26 he activity of the mRNA-destabilizing factor tristetraprolin, and thereby inhibits the expression of
30 cytotoxic T lymphocyte function mediated by tristetraprolin, contributing to regulation of antitumou
33 IFN-gamma production by naive wild type and tristetraprolin-deficient CD8(+) T-cells is comparable.
35 rtantly, deletion of IL-27 receptor WSX-1 in tristetraprolin-deficient mice (WSX-1/tristetraprolin do
36 er, tumor growth is accelerated, not only in tristetraprolin-deficient mice after cytotoxic T lymphoc
40 ic T lymphocyte depletion, but also in WSX-1/tristetraprolin double knockout mice, with substantial r
41 X-1 in tristetraprolin-deficient mice (WSX-1/tristetraprolin double knockout) leads to a reduction in
43 d proteins and in vitro assays, we find that tristetraprolin engages CCR4-NOT through multiple intera
46 array data sets revealed that suppression of tristetraprolin expression is a negative prognostic indi
50 cripts contained potential binding sites for tristetraprolin family member proteins that were conserv
59 chanisms in macrophages, including p38 MAPK, tristetraprolin, IL-10, and binding of SMAD3 to the IL-2
61 formed to evaluate the expression of HuA and tristetraprolin in purified human T lymphocytes and to e
62 binds the destabilizing ARE-binding protein tristetraprolin induced following activation of HVS-tran
64 ooxygenase-2 transcript, and transfection of tristetraprolin into HCA-7 cells reduced the level of fu
66 modulation of the phosphorylation status of tristetraprolin is an important physiological mechanism
70 ripts following T lymphocyte activation, and tristetraprolin may subsequently mediate their degradati
72 east cancer, because patients with low tumor tristetraprolin mRNA levels were more likely to present
73 ematically dysregulated in cancers; however, tristetraprolin mRNA levels were significantly decreased
74 ell growth and confluence, the expression of tristetraprolin mRNA was inversely correlated with that
77 lves the association of ARE-binding proteins tristetraprolin or AUF1 and proteasome activity, of whic
79 cted cells, the mutant but not the wild-type tristetraprolin precluded the degradation of the AU-rich
83 lthough absent in resting cells, cytoplasmic tristetraprolin protein was detected 3-6 h following act
88 esulting from decreased activity of TTP, the tristetraprolin RNA-binding protein responsible for mRNA
94 shed TNF-alpha ARE-binding proteins, HuR and tristetraprolin, that shuttle between the nucleus and cy
95 th the exception of the destabilizing factor tristetraprolin, the identity and function of the protei
96 to AU-rich elements via its interaction with tristetraprolin, the RNase deadenylates and cleaves the
99 complex with the mRNA-destabilizing protein tristetraprolin (TTP) and a conserved adenylate-uridylat
100 nt evidence that in human cells the proteins Tristetraprolin (TTP) and BRF-1 deliver ARE-mRNAs to pro
101 ucleolytic decay, associate with the protein tristetraprolin (TTP) and its homolog BRF-1, which bind
103 sly, the Reg-2 transcript is destabilized by tristetraprolin (TTP) and Reg-1 through the AREs element
106 We have identified the RNA-binding protein Tristetraprolin (TTP) as a negative regulator of NLRP3 i
107 RNA-binding proteins Hu antigen R (HuR) and tristetraprolin (TTP) bind AU-rich elements in the 3' un
114 lacenta- and yolk sac-specific member of the tristetraprolin (TTP) family of CCCH tandem zinc finger
119 g Ifnb1 mRNA destabilization mediated by the tristetraprolin (TTP) family of RNA-binding proteins and
120 protein 36-like 1 (Zfp36L1), a member of the tristetraprolin (TTP) family of tandem CCCH finger prote
121 sponse factor 1 (TIS11b/BRF1) belongs to the tristetraprolin (TTP) family of zinc-finger proteins, wh
122 c AU-rich motifs are regulated by binding of tristetraprolin (TTP) family tandem zinc finger proteins
125 d uridine-rich element (ARE)-binding protein tristetraprolin (TTP) in influencing mRNA stability of I
126 or T-cell intracellular antigen-1 (TIA-1) or tristetraprolin (TTP) initially do not colocalize with t
132 es diverse antiproliferative activities, and tristetraprolin (TTP) is a mitogen-induced RNA-binding p
138 ere, we report that the destabilizing factor tristetraprolin (TTP) is also ubiquitously expressed in
146 yeloid cells, the mRNA-destabilizing protein tristetraprolin (TTP) is induced and extensively phospho
147 Expression of the immediate early protein tristetraprolin (TTP) is induced by numerous stimuli, in
149 lowing TNF treatment, the mRNA decay protein tristetraprolin (TTP) is Lys-63-polyubiquitinated by TNF
154 Furthermore, IFN-gamma enhances LPS-induced tristetraprolin (TTP) mRNA expression and protein produc
155 studied the role that Hu antigen R (HuR) and tristetraprolin (TTP) play in regulating the expression
157 of being a negative regulator, we found that tristetraprolin (TTP) positively correlates with HIF-1 t
158 c conditions, the mRNA-destabilizing protein tristetraprolin (TTP) regulates apoptosis and the number
161 We hypothesized that the ARE-binding protein tristetraprolin (TTP) regulates T lymphocyte IL-2 mRNA d
162 TNF-alpha mRNA stability via the binding of tristetraprolin (TTP) to the adenosine/uridine-rich elem
164 o impacts on the anti-inflammatory protein - tristetraprolin (TTP), a destabilizing RNA binding prote
166 e degradation of the E47 mRNA and found that tristetraprolin (TTP), a physiological regulator of mRNA
170 In the case of one member of this family, tristetraprolin (TTP), absence of the protein in knockou
175 ein, Zfp36l2, like its better-known relative tristetraprolin (TTP), can decrease the stability of AU-
178 ities and show that the RNA-binding protein, tristetraprolin (TTP), interacts with these elements.
179 ne encoding the putative zinc finger protein tristetraprolin (TTP), is rapidly induced in fibroblasts
180 Here we show that a key destabilizing AUBP, tristetraprolin (TTP), is repressed by the p38 mitogen-a
181 mRNA coding for tumor necrosis factor (TNF), tristetraprolin (TTP), suppressor of cytokine signaling-
188 nduced expression of the ARE-binding protein tristetraprolin (TTP), which colocalized to P bodies.
189 transcriptionally by the RNA-binding protein tristetraprolin (TTP), which destabilizes IL-10 mRNA in
190 he latter is regulated, at least in part, by tristetraprolin (TTP), which is increased in aged B cell
193 owever, bone marrow-derived macrophages from tristetraprolin (TTP)-deficient mice were less sensitive
204 When coexpressed with the prototypic ARE-BP tristetraprolin (TTP, ZFP36) that mainly destabilizes it
205 nt with its role in moderating inflammation, tristetraprolin (TTP, ZFP36) was among the most highly e
208 ly, Myc directly suppresses transcription of Tristetraprolin (TTP/ZFP36), an mRNA-destabilizing AUBP,
209 in AU-rich cis-elements (AREs) recognized by tristetraprolin (TTP/Zfp36), an RNA-binding protein prev
212 We find that the fission yeast homologues of Tristetraprolin/TTP and Pumilio/Puf (Zfs1 and Puf3) inte
213 gulation/activity of HuR and inactivation of tristetraprolin, two AU-rich element-binding proteins.
214 Interestingly, the RNA destabilizing protein tristetraprolin was induced following IgE cross-linkage
217 n inhibitory transcription factor, and ZFP36/Tristetraprolin, which binds to AU-rich elements within
218 nactivation of the mRNA-destabilizing factor tristetraprolin, which we show is able to target the IFN
219 estabilizing protein Tis11b, a member of the tristetraprolin/ZFP36 family, and thereby, decreases MR
222 rated roles for three of the family members, tristetraprolin, ZFP36L1, and ZFP36L2, in inflammation,