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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
16 se in expression and RNA binding activity of tristetraprolin, an mRNA-binding protein that destabiliz
18 f PMR1 with SGs under conditions which cause tristetraprolin and butyrate response factor 1, proteins
23 oup of RNA-binding proteins (including TIS11/tristetraprolin and TIS11D) that share characteristic ta
25 he activity of the mRNA-destabilizing factor tristetraprolin, and thereby inhibits the expression of
29 cytotoxic T lymphocyte function mediated by tristetraprolin, contributing to regulation of antitumou
32 IFN-gamma production by naive wild type and tristetraprolin-deficient CD8(+) T-cells is comparable.
34 rtantly, deletion of IL-27 receptor WSX-1 in tristetraprolin-deficient mice (WSX-1/tristetraprolin do
35 er, tumor growth is accelerated, not only in tristetraprolin-deficient mice after cytotoxic T lymphoc
38 ic T lymphocyte depletion, but also in WSX-1/tristetraprolin double knockout mice, with substantial r
39 X-1 in tristetraprolin-deficient mice (WSX-1/tristetraprolin double knockout) leads to a reduction in
43 array data sets revealed that suppression of tristetraprolin expression is a negative prognostic indi
47 cripts contained potential binding sites for tristetraprolin family member proteins that were conserv
56 formed to evaluate the expression of HuA and tristetraprolin in purified human T lymphocytes and to e
57 binds the destabilizing ARE-binding protein tristetraprolin induced following activation of HVS-tran
58 ooxygenase-2 transcript, and transfection of tristetraprolin into HCA-7 cells reduced the level of fu
60 modulation of the phosphorylation status of tristetraprolin is an important physiological mechanism
64 ripts following T lymphocyte activation, and tristetraprolin may subsequently mediate their degradati
66 east cancer, because patients with low tumor tristetraprolin mRNA levels were more likely to present
67 ematically dysregulated in cancers; however, tristetraprolin mRNA levels were significantly decreased
68 ell growth and confluence, the expression of tristetraprolin mRNA was inversely correlated with that
71 lves the association of ARE-binding proteins tristetraprolin or AUF1 and proteasome activity, of whic
73 cted cells, the mutant but not the wild-type tristetraprolin precluded the degradation of the AU-rich
76 lthough absent in resting cells, cytoplasmic tristetraprolin protein was detected 3-6 h following act
81 esulting from decreased activity of TTP, the tristetraprolin RNA-binding protein responsible for mRNA
86 shed TNF-alpha ARE-binding proteins, HuR and tristetraprolin, that shuttle between the nucleus and cy
87 th the exception of the destabilizing factor tristetraprolin, the identity and function of the protei
88 to AU-rich elements via its interaction with tristetraprolin, the RNase deadenylates and cleaves the
91 complex with the mRNA-destabilizing protein tristetraprolin (TTP) and a conserved adenylate-uridylat
92 nt evidence that in human cells the proteins Tristetraprolin (TTP) and BRF-1 deliver ARE-mRNAs to pro
93 ucleolytic decay, associate with the protein tristetraprolin (TTP) and its homolog BRF-1, which bind
97 We have identified the RNA-binding protein Tristetraprolin (TTP) as a negative regulator of NLRP3 i
98 RNA-binding proteins Hu antigen R (HuR) and tristetraprolin (TTP) bind AU-rich elements in the 3' un
105 lacenta- and yolk sac-specific member of the tristetraprolin (TTP) family of CCCH tandem zinc finger
110 protein 36-like 1 (Zfp36L1), a member of the tristetraprolin (TTP) family of tandem CCCH finger prote
111 sponse factor 1 (TIS11b/BRF1) belongs to the tristetraprolin (TTP) family of zinc-finger proteins, wh
113 d uridine-rich element (ARE)-binding protein tristetraprolin (TTP) in influencing mRNA stability of I
114 or T-cell intracellular antigen-1 (TIA-1) or tristetraprolin (TTP) initially do not colocalize with t
119 es diverse antiproliferative activities, and tristetraprolin (TTP) is a mitogen-induced RNA-binding p
125 ere, we report that the destabilizing factor tristetraprolin (TTP) is also ubiquitously expressed in
130 yeloid cells, the mRNA-destabilizing protein tristetraprolin (TTP) is induced and extensively phospho
131 Expression of the immediate early protein tristetraprolin (TTP) is induced by numerous stimuli, in
133 lowing TNF treatment, the mRNA decay protein tristetraprolin (TTP) is Lys-63-polyubiquitinated by TNF
138 Furthermore, IFN-gamma enhances LPS-induced tristetraprolin (TTP) mRNA expression and protein produc
139 studied the role that Hu antigen R (HuR) and tristetraprolin (TTP) play in regulating the expression
141 of being a negative regulator, we found that tristetraprolin (TTP) positively correlates with HIF-1 t
142 c conditions, the mRNA-destabilizing protein tristetraprolin (TTP) regulates apoptosis and the number
145 We hypothesized that the ARE-binding protein tristetraprolin (TTP) regulates T lymphocyte IL-2 mRNA d
146 TNF-alpha mRNA stability via the binding of tristetraprolin (TTP) to the adenosine/uridine-rich elem
148 o impacts on the anti-inflammatory protein - tristetraprolin (TTP), a destabilizing RNA binding prote
150 e degradation of the E47 mRNA and found that tristetraprolin (TTP), a physiological regulator of mRNA
154 In the case of one member of this family, tristetraprolin (TTP), absence of the protein in knockou
158 ein, Zfp36l2, like its better-known relative tristetraprolin (TTP), can decrease the stability of AU-
160 ities and show that the RNA-binding protein, tristetraprolin (TTP), interacts with these elements.
161 ne encoding the putative zinc finger protein tristetraprolin (TTP), is rapidly induced in fibroblasts
162 Here we show that a key destabilizing AUBP, tristetraprolin (TTP), is repressed by the p38 mitogen-a
163 mRNA coding for tumor necrosis factor (TNF), tristetraprolin (TTP), suppressor of cytokine signaling-
170 nduced expression of the ARE-binding protein tristetraprolin (TTP), which colocalized to P bodies.
171 transcriptionally by the RNA-binding protein tristetraprolin (TTP), which destabilizes IL-10 mRNA in
172 he latter is regulated, at least in part, by tristetraprolin (TTP), which is increased in aged B cell
174 owever, bone marrow-derived macrophages from tristetraprolin (TTP)-deficient mice were less sensitive
182 nt with its role in moderating inflammation, tristetraprolin (TTP, ZFP36) was among the most highly e
185 ly, Myc directly suppresses transcription of Tristetraprolin (TTP/ZFP36), an mRNA-destabilizing AUBP,
186 in AU-rich cis-elements (AREs) recognized by tristetraprolin (TTP/Zfp36), an RNA-binding protein prev
187 gulation/activity of HuR and inactivation of tristetraprolin, two AU-rich element-binding proteins.
188 Interestingly, the RNA destabilizing protein tristetraprolin was induced following IgE cross-linkage
191 n inhibitory transcription factor, and ZFP36/Tristetraprolin, which binds to AU-rich elements within
192 nactivation of the mRNA-destabilizing factor tristetraprolin, which we show is able to target the IFN
193 estabilizing protein Tis11b, a member of the tristetraprolin/ZFP36 family, and thereby, decreases MR
195 rated roles for three of the family members, tristetraprolin, ZFP36L1, and ZFP36L2, in inflammation,
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