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1                                              STAT (Sarcoidosis Treated with Anti-TNF) is a French ret
2                                              STAT proteins are a family of transcription factors that
3 n (12% decrease in DTN time, 95% CI 3%-20%), STAT stroke protocol (11% decrease in DTN time, 95% CI 1
4 n as PTPN2, as a negative regulator of IL-7R-STAT signaling in T cell progenitors, contributing to bo
5 24, 2015), 3 changes were implemented: (1) a STAT stroke protocol to prenotify the stroke team about
6 kines and growth hormones typically activate STATs and could therefore act as humoral transfer factor
7 Oylation, the protein inhibitor of activated STAT (PIAS) E3-ligases were initially described as trans
8           The protein inhibitor of activated STAT (PIAS) family of SUMO ligases is predominantly asso
9 phatases, and protein inhibitor of activated STAT (PIAS) proteins.
10 er of the Siz/protein inhibitor of activated STAT (PIAS) RING family of SUMO E3 ligases, as essential
11 rotein ligase protein inhibitor of activated STAT 4 (PIAS4) is a pivotal protein in regulating the TG
12 e SUMO ligase protein inhibitor of activated STAT 4 (PIAS4) is upregulated during HSV-1 infection and
13     The PIAS (protein inhibitor of activated STAT) family of SUMO (small ubiquitin-like modifier) lig
14 ases (JAKs) classically signal by activating STAT transcription factors but can also regulate gene ex
15  with other studies of constitutively active STAT mutants, provides insight into the pathogenesis and
16                                     Although STAT activation has been widely implicated in cancer, th
17 y or advanced stages of diabetes ameliorated STAT activity and resulted in reduced serum creatinine l
18  (CTLA-4), CD154 (CD40L), T-bet, GATA-3, and STAT-1.
19                           Activating JAK and STAT mutations were not sufficient to initiate leukemic
20 , blocked IFNG-induced signaling via JAK and STAT.
21 s from this patient exhibit reduced JAK1 and STAT phosphorylation following cytokine stimulations, re
22 ing-related loss in binding of NF-kappaB and STAT factors.
23 e factor 1alpha (HIF-1alpha), NF-kappaB, and STAT proteins, and are the targets for the interactions
24 esion through integrin alpha5beta1, MAPK and STAT activity, and initiation of pluripotency signalling
25 thways including Elk1/SRF, AP1, NFkappaB and STAT, and reduces EGFR expression in ovarian cancer cell
26 1 and regulated expression of IL-6, PDPN and STAT-1.
27                                     Smad and STAT proteins are critical signal transducers and transc
28 ate transcriptional activity of NFkappaB and STATs, we hypothesized that these kinases support RS cel
29  transcription factors, such as NFkappaB and STATs.
30 es as privileged structures for antagonizing STAT SH2 domains, and demonstrates that apoptosis can be
31 tional NF-kappaB, activator protein 1 (AP1), STAT, and Smad DBS in the TSLP promoter region.
32   These effects seem to be regulated by AP1, STAT-3 and NF-kappaB signaling pathways.
33 K293 or HEK293-STAT6 cells, and on the basal STAT activity in stably transfected L-428 and U-HO1 cHL
34 own the association and coordination between STATs and SMADs in mediating TGF-beta functions in hepat
35 on with AP-1 components (c-Fos or Jun), bind STAT-1 in a homodimer like complex (HDLC).
36                    Of interest, RvD1 blocked STAT-1 and its target inflammatory genes (i.e., CXCL9),
37 during the viral life cycle is controlled by STAT-5 and the kinase GSK3beta.
38                Under physiologic conditions, STAT signaling is stimulus dependent and tightly regulat
39                   Here we show that cytokine-STAT signalling promotes mycobacterial survival within m
40 isms of action of two families of endogenous STAT inhibitors, the SOCS and PIAS families, to potentia
41 ally, ticks lacking the transcription factor STAT, which signals downstream of IFNgamma, did not indu
42 evels found in the C26 CM was sufficient for STAT reporter activation and atrophy in myotubes.
43                               The heightened STAT signaling is critical to maintain the expression of
44 ns in hepatic cells, but it is not clear how STATs are activated under these circumstances.
45 ymal/CSCs have a significantly repressed IFN/STAT gene expression signature and an enhanced ability t
46 ansducer and activator of transcription (IFN/STAT) gene signature and are often enriched for cancer s
47 hages through TLR2, associated with impaired STATs signaling pathway.
48 tivation of transcription factors, including STATs, is known to promote tumor initiation and progress
49                   Moreover, mTOR-independent STAT-5 signaling contributed to improved NK-cell functio
50  JAK2 inhibitors also blocked C26 CM-induced STAT reporter activation, STAT3 phosphorylation, and atr
51 y epithelial cells inhibits cytokine-induced STAT activation.
52 Mycobacterium marinum, mycobacterium-induced STAT activity triggered by unpaired-family cytokines red
53       Additionally, NBQX treatment inhibited STAT-3 phosphorylation, but not astrogliosis or transcri
54              Whether this signaling involves STAT activation, epigenetic modification of chromatin, o
55 vival and fate, specifically PDGFR, ERK, JAK STAT, MAPK, and TCR/NF-kappaB signaling; epigenetic regu
56                                          JAK-STAT signaling mediates the actions of numerous cytokine
57                                          JAK-STAT signaling was critical for TA-CA1 LTD as inhibition
58 TAT) signaling pathway by ruxolitinib, a JAK-STAT-specific inhibitor.
59 f genes involved in RNAi, Toll, Imd, and JAK-STAT pathways, but the majority of differentially expres
60     Complete and conserved Toll, IMD and JAK-STAT signaling pathways were found in P. xylostella.
61   Thus CRYs link the circadian clock and JAK-STAT signaling through control of STAT5B phosphorylation
62 p-dependent protein translation, blocked JAK-STAT signaling, and markedly attenuated NFkappaB-depende
63  IFN-stimulated genes (ISGs) by blocking Jak-STAT signaling; however, this occurs by different mechan
64 ells, and their expression was driven by JAK-STAT and NFkappaB activity.
65 indicate an essential role for canonical JAK-STAT signaling in activity-dependent LTD at TA-CA1 synap
66                                Canonical JAK-STAT signaling is pivotal for long-term depression at ad
67 elation analysis links PinT to host cell JAK-STAT signalling, and we identify infection-specific alte
68                   However, unlike common JAK-STAT pathway inhibitors, BRD0476 inhibits JAK-STAT signa
69 driver mutations leading to constitutive JAK-STAT activation, the cellular and molecular biology of m
70  II receptor families and the downstream JAK-STAT pathway along with its key negative regulators.
71 ythropoietin stimulation, and heightened JAK-STAT activation.
72 )) and used pathway analysis to identify JAK-STAT/IL12/IL27 signalling and cytokine-cytokine pathways
73        Here we review recent advances in Jak-STAT biology, focusing on immune cell function, disease
74 inked to differential gene expression in JAK-STAT signaling, NADPH oxidation, and other cancer-relate
75 ons in key signaling pathways, including JAK-STAT, NOTCH and NF-kappaB, have also been defined, the s
76       This was associated with increased JAK-STAT signaling in NK cells in which Cish was deleted.
77 enotype is mediated by Nol3(-/-)-induced JAK-STAT activation and downstream activation of cyclin-depe
78 hrough inhibiting the interferon-induced JAK-STAT signaling pathway, a key antiviral pathway involved
79 TAT pathway inhibitors, BRD0476 inhibits JAK-STAT signaling without suppressing the kinase activity o
80 at LTD at adult TA-CA1 synapses involves JAK-STAT signaling, but unlike SC-CA1 synapses, requires rap
81 (TLR), mitogen-activated protein kinase, Jak-STAT, and the nucleotide oligomerization domain-like rec
82 nt, and these mutations all activate MPL-JAK-STAT signaling in MPN stem cells.
83 /HPCs were associated with inhibition of JAK-STAT activity, leading to the induction of apoptosis.
84 y of 24 is supported by demonstration of JAK-STAT and HDAC pathway blockade in hematological cell lin
85 potency is supported by demonstration of JAK-STAT and HDAC pathway blockade in several hematological
86 urages further discussion on the role of JAK-STAT signaling in the various stem cell niches of the ha
87 s, indicating a general sensitization of JAK-STAT signaling in this leukemia subset.
88        We propose that overactivation of JAK-STAT signaling is part of the mechanism underlying disea
89 d for mutant CALR-mediated activation of JAK-STAT signaling.
90 K2 or EPOR rearrangements (12.4%), other JAK-STAT sequence mutations (7.2%), other kinase alterations
91 ns in 8.8%, alterations activating other JAK-STAT signaling genes (IL7R, SH2B3, JAK1) in 6.3% or othe
92 nterferon (IFN-I) response by preventing JAK-STAT signaling, suggesting that suppression of this path
93 alysis of the 17-gene signature revealed Jak-STAT signaling pathway as the most significantly represe
94                Our findings suggest that JAK-STAT pathway inhibition may represent a therapeutic stra
95 LF2(+) group identified mutations in the JAK-STAT and Ras pathway in 85% of patients, and 20% had a C
96 itant genomic alterations activating the JAK-STAT pathway (JAK1, JAK2, IL7R) identified in 63 patient
97 esis that using these drugs to block the JAK-STAT pathway would prevent autoimmune diabetes.
98 rine and paracrine signaling through the JAK-STAT pathway, leading to the transcriptional induction o
99 eptor (IL-7R), via its activation of the JAK-STAT pathway, promotes gene programs that change dynamic
100 tural proteins 1 and/or 2 perturbing the Jak-STAT signaling pathway, with concomitant reduced express
101 plication of CSFV through inhibiting the JAK-STAT signaling pathway.
102 eporters, demonstrating that it uses the JAK-STAT signaling pathway.
103 ficant increase in the expression of the JAK-STAT target gene Pim1 and muscles from 2-day and 3-week
104 ceptor gene CSF3R, which signals through JAK-STAT proteins.
105  cell antigens to CD4(+) T cells through Jak-STAT signal transduction.
106 th EPOR rearrangements were sensitive to JAK-STAT inhibition, suggesting a therapeutic option in high
107 ansducer and activator of transcription (JAK-STAT) pathways, or indirectly via changes in the tumor m
108 ansducer and activator of transcription (JAK-STAT) signaling pathway by ruxolitinib, a JAK-STAT-speci
109 al pathways, such as IL-6 signalling via JAK-STAT pathway.
110           However, it is unclear whether JAK-STAT signaling also regulates excitatory synaptic functi
111                                          Jak/STAT research has not only impacted basic science, parti
112 esults suggest that LNK suppresses IL-7R/JAK/STAT signaling to restrict pro-/pre-B progenitor expansi
113 brid synthekine ligands that dimerized a JAK/STAT cytokine receptor with a receptor tyrosine kinase (
114 IL-2 induced IL-36R gene expression in a JAK/STAT-dependent manner.
115                           While aberrant JAK/STAT signaling is crucial to the development of gastric
116 s of CRLF2, JAK2, and EPOR that activate JAK/STAT signaling.
117 h-like ALL) is associated with activated JAK/STAT, Abelson kinase (ABL), and/or phosphatidylinositol
118 ccumulate additional mutations affecting JAK/STAT signaling, protein translation, and epigenetic cont
119 ndent processes, apical delamination and JAK/STAT activation, are concurrently required for the initi
120 tor of the Rho family small GTPases, and JAK/STAT is activated ectopically in these coldspot nTSG-def
121 igate the possible role of TNF-alpha and JAK/STAT pathway on de novo lipogenesis and PCSK9 expression
122 cross-coupling between the CREB/CRTC and JAK/STAT pathways contributes to BM homeostasis.
123      Pharmacologic inhibition of ERK and JAK/STAT pathways reversed miR-194-driven phenotypes.
124 included components of the Toll, Imd and JAK/STAT pathways, consistent with interactions between the
125 iurnal rhythmicity of insulin action and JAK/STAT signaling in adipose tissue.
126 teral diffusion in lipid nanodomains and JAK/STAT signaling in patient cells, whereas adding galectin
127 iac factors along with canonical Wnt and JAK/STAT signaling reprogrammed adult mouse cardiac, lung, a
128  factors involved in B-cell receptor and JAK/STAT signaling, the nonclassical NF-kappaB pathway, cell
129 (MTGNB) along with activation of Wnt and JAK/STAT signaling.
130  of main immune pathways (Toll, Imd, and JAK/STAT), and immune effectors in P. xylostella in response
131 ing with Glide/Gcm: Notch, Hedgehog, and JAK/STAT, which all involve feedback loops.
132 ng pathways, including PI3K/Akt/mTOR and JAK/STAT.
133 aling pathways AKT, NFkappaB, ERK1/2 and JAK/STAT.
134 re is indirect positive feedback between JAK/STAT and insulin signaling in the muscles.
135                       Surprisingly, both JAK/STAT pathway activation and ruxolitinib efficacy were in
136 e onset of pupariation, is controlled by JAK/STAT signaling in early regenerating discs.
137 The HEL cell line, in which constitutive JAK/STAT pathway activation is caused by JAK2V617F, was used
138         JAK3 mutants induce constitutive JAK/STAT signaling and cause leukemia when expressed in the
139 the molecular basis of this constitutive JAK/STAT signaling in cHL has not been completely understood
140                             Constitutive JAK/STAT signaling is crucial for survival and proliferation
141 nd docking sites for required downstream JAK/STAT proteins.
142 d as strong inhibitors of the Drosophila JAK/STAT pathway, an effect conserved to human cells.
143 with high MPL expression showed enhanced JAK/STAT signaling and proliferation in response to THPO in
144 ose patients most likely to benefit from JAK/STAT targeted chemotherapies.
145 tified correlates of severity, including JAK/STAT, prolactin, and interleukin 9 signaling.
146 erferon-gamma- and interleukin-4-induced JAK/STAT activity in HEK293 or HEK293-STAT6 cells, and on th
147 ssion in CML LTHSCs reduced THPO-induced JAK/STAT signaling and leukemogenic potential.
148 y an application to data for Epo-induced JAK/STAT signaling.
149 l for the inhibition of cytokine-induced JAK/STAT signalling activation in DF-1.
150 e contraction, focal adhesion, integrin, JAK/STAT, MAPK, growth factor, and p53 signaling pathways we
151 t body through the cytokine Upd3 and its JAK/STAT-coupled receptor, Domeless.
152 genetic protein (BMP), Jun kinase (JNK), JAK/STAT, Notch, Insulin, and Wnt, revealed that many ligand
153 vation or reduced expression of negative JAK/STAT regulators such as silencer of cell signaling 1 (SO
154 sion along with suppression of NFkappaB, JAK/STAT and PI3K pathways.
155 ncreatic cancer to examine the effect of Jak/STAT and MAPK pathway inhibition in vitro.
156 xpression in HNC cells in the context of JAK/STAT pathway activation, Th1 inflammation, and HPV statu
157 cacy were independent of the presence of JAK/STAT pathway mutations, raising the possibility that the
158 t PTP1BDelta6 is a positive regulator of JAK/STAT signaling in cHL.
159 l studies underscore the central role of JAK/STAT signaling in myeloproliferative neoplasms (MPNs).
160             Specifically, stimulation of JAK/STAT signaling in the muscles can rescue the deficient i
161  cytokine Upd3, leading to activation of JAK/STAT signaling, differentiation of cells that form the p
162 s facilitated by HER2/HER3 activation of JAK/STAT signaling.
163 3, leading to constitutive activation of JAK/STAT signaling.
164 rs were used to disentangle the roles of JAK/STAT, MAPK, and PI3K signaling pathways.
165 hypothesize that ETP-ALL is dependent on JAK/STAT signaling.
166  cutaneous T-cell lymphoma pathogenesis, JAK/STAT signaling, we used conditional gene targeting to de
167 hich results in cell cycle perturbation, JAK/STAT signal activation, and differential regulation of N
168           These include B-cell receptor, JAK/STAT, NF-kappaB, NOTCH, and Toll-like receptor signaling
169 ring ISCs non-autonomously by regulating JAK/STAT signaling.
170 cancer pathways such as Ras/ERK1/2, Src, JAK/STAT, JNK, NF-kappaB, and PTEN/PI3K/AKT.
171 perimental CP, suggesting that targeting Jak/STAT signaling may represent a promising therapeutic str
172 n ageing muscle, including Wnt, TGFbeta, JAK/STAT and senescence signalling.
173                   We recently found that JAK/STAT signaling in skeletal muscles is important for the
174                         The insight that JAK/STAT system activation is pervasive in T cell malignanci
175 sertions could be mapped to genes in the JAK/STAT and MAPK pathways, confirming the ability of this s
176 hat treating CADM1 null tumours with the JAK/STAT inhibitor ruxolitinib mimics CADM1 gene restoration
177 l, but were not previously linked to the JAK/STAT or MAPK pathways nor shown to functionally contribu
178  proteins are negative regulators of the JAK/STAT pathway activated by proinflammatory cytokines, inc
179 ate that Et/Lat negatively regulates the JAK/STAT pathway activity and can bind to Dome, thus reducin
180 t is down-regulated by inhibitors of the JAK/STAT pathway and enhanced by inhibitors of the Src kinas
181 uggests the feasibility of targeting the JAK/STAT pathway as a neuroprotective therapy for neurodegen
182  small-molecule inhibitors targeting the JAK/STAT pathway blocked proliferation elicited by IL-2 and
183 ese results indicate that inhibiting the JAK/STAT pathway can prevent neuroinflammation and neurodege
184 st documentation that suppression of the JAK/STAT pathway disrupts the circuitry of neuroinflammation
185 uggesting that PIV-3 interferes with the JAK/STAT pathway downstream of the IFN-lambdaR1/IL-10R2 rece
186  GPR45 regulates POMC expression via the JAK/STAT pathway in a cell-autonomous manner.
187              Given the importance of the JAK/STAT pathway in activating microglia and inducing cytoki
188  vitro, alpha-SYN exposure activated the JAK/STAT pathway in microglia and macrophages, and treatment
189 findings document that inhibition of the JAK/STAT pathway influences both innate and adaptive immune
190                                      The JAK/STAT pathway is a highly conserved regulatory module, ac
191              These data suggest that the Jak/STAT pathway plays a prominent role in PSC proliferation
192           Importantly, inhibition of the JAK/STAT pathway prevented the degeneration of dopaminergic
193  therapeutic potential of inhibiting the JAK/STAT pathway using the JAK1/2 inhibitor, AZD1480.
194 STAT3, suggesting the involvement of the JAK/STAT pathway.
195 ulating Claudin-2 expression through the JAK/STAT pathway.
196 okines, many of which signal through the JAK/STAT signaling pathway to exert their biological effects
197 bited monkeys revealed engagement of the JAK/STAT signaling pathway, suggesting alternative gammac cy
198 talk among enriched pathways, mainly the JAK/STAT signalling pathway and the EGF receptor signalling
199 tokine receptors that signal through the JAK/STAT signalling pathway are important for disease, infor
200  Mo-DC differentiation by regulating the JAK/STAT/MAPK and NFkappaB pathways.
201 a receptor-dependent cytokines and their JAK/STAT pathways play pivotal roles in T cell immunity.
202 s of IL-21R arose from signaling through JAK/STAT pathways and upregulation of caspase 3.
203  a greater role of MAPK/PI3K compared to JAK/STAT with the orphan nuclear receptor RXRalpha playing a
204 ansducer and activator of transcription (JAK/STAT) activation by IFN-gamma could not occur.
205 ansducer and activator of transcription (JAK/STAT) signaling activity.
206 sducers and activators of transcription (JAK/STAT) signaling via the IL-22 receptor, resulting in enh
207                   Whereas the vertebrate JAK/STAT signaling cascade is transduced via multiple recept
208 e metabolism in the infected animal, via JAK/STAT and insulin signaling in the muscles, and that ther
209 ing inhibits the growth of losers, while JAK/STAT signalling promotes competition-induced winner cell
210 n profiling indicates that the non-SMAD JAK1/STAT pathway is essential for the expression of a subset
211 induce ligand-independent activation of JAK2/STAT/phosphatydylinositol-3'-kinase (PI3-K) and mitogen-
212 ssical ISG expression independent of the JAT-STAT signaling pathway.
213 e MEK inhibitor trametinib, the Janus kinase-STAT inhibitor tofacitinib, and the STAT5 inhibitor pimo
214 pid attenuation of keratinocyte Janus kinase/STAT signaling; (2) removal of keratinocyte-induced cyto
215 naling axis and the composition of the c-Kit/STAT signalosome.
216                    C-188-9, a small molecule STAT-3 inhibitor, decreased pulmonary fibrosis in the in
217                           In the 24-month MS-STAT phase 2 trial, we showed that high-dose simvastatin
218            We did a secondary analysis of MS-STAT, a 24-month, double-blind, controlled trial of pati
219        We now describe the results of the MS-STAT cognitive substudy, in which we investigated the tr
220 ma), and that IL-6 regulation of MMPs is not STAT-3 dependent.
221 n quantitative immunoblotting experiments of STAT proteins, STAT1alpha, phosphorylated-STAT1alpha (pS
222 ving cells, THZ1 decreases the expression of STAT-regulated anti-apoptotic BH3 family members MCL1 an
223 onse characterised by selective induction of STAT target genes in the fat body through the cytokine U
224     In vitro studies show that inhibition of STAT-3 decreased IL-6- and TGF-beta-induced expression o
225                         STAT3 is a member of STAT (signal transducer and activator of transcription)
226 h the quantitative and qualitative nature of STAT-gene targeting.
227 ADs, TGF-beta also induces a second phase of STAT phosphorylation that requires SMADs, de novo protei
228  expression heightens the phosphorylation of STAT family members, causing aberrant expression of an i
229 d Janus kinases (Jak) and phosphorylation of STAT proteins in target cells.
230 IL-10 pathway by reducing phosphorylation of STAT proteins.
231  in SMAD2/SMAD3-dependent phosphorylation of STAT-3.
232 s absolutely required for phosphorylation of STATs in a SMAD-independent manner within minutes of TGF
233 tical for TA-CA1 LTD as inhibition of JAK or STAT blocked LTD induction and prevented NMDA-induced AM
234 of these T cell lines whether or not JAKs or STATs were mutated.
235 ion observed in STAT3 likely occurs in other STATs.
236 undant roles in the activation of particular STAT proteins and this tyrosine kinase is essential for
237 dless of the agents used, induces persistent STAT-1 and NF-kappaB activity in carcinoma-associated fi
238 anges in chromatin accessibility and phospho-STAT responsiveness to IFN.
239                               Phosphorylated STAT-3 was elevated in lung biopsies from patients with
240 hropoietin (EPO) receptor and phosphorylated STAT-5 relative to matched Q-HB, with increased phosphor
241  cytokines, in which tyrosine-phosphorylated STATs (pSTATs) function as transcription factors.
242 omprised of IRF9 and tyrosine-phosphorylated STATs 1 and 2, transmits the signal from the type I inte
243        However, the recent discovery of rare STAT mutations in hematopoietic malignancies suggests th
244 finity of IFN to the cell surface receptors, STAT phosphorylation, or gene induction.
245     Furthermore, the innate immune regulator STAT-5 and the kinase GSK3beta mediate the activation of
246 otocin diabetic, apoE-deficient mice), renal STAT activation status correlated with the severity of n
247  Resistance to IR-induced apoptosis requires STAT and Wg and is mediated by transcriptional repressio
248 alized with transcription factors RORgammat, STAT-3, and p300 at the Il23r, Il17a/f, and Csf2 cytokin
249 idence that in human cells, SFTSV sequesters STAT proteins in replication complexes, thereby inhibiti
250          Although IL-21 can activate several STAT family transcription factors, previous studies focu
251    In vitro, internalized peptide suppressed STAT activation and target gene expression induced by in
252  protects against nephropathy by suppressing STAT-mediated cell responses to diabetic conditions.
253              These findings demonstrate that STAT-3 contributes to the development of lung fibrosis a
254 evelopment of lung fibrosis and suggest that STAT-3 may be a therapeutic target in pulmonary fibrosis
255  in hematopoietic malignancies suggests that STAT mutants may be oncogenic.
256                                          The STAT-signalling pathway is highly vulnerable to THZ1 eve
257  myocardial response, and neprilysin and the STAT family as key regulators of intrinsic remote condit
258 ineages, and strengthen the link between the STAT family of transcription factors and autoimmunity.
259  the mRNAs of SOCS family genes encoding the STAT signalling inhibitory proteins SOCS1, SOCS3 and CIS
260                    Among 140 patients in the STAT database, 46 had skin involvement.
261 amily and transcription factors (TFs) of the STAT ('signal transducer and activator of transcription'
262 nd due to the structural conservation of the STAT family of proteins, the inter-domain allosteric com
263 c DNA activates STAT3, another member of the STAT family, via an autocrine mechanism involving interf
264 related to inflammation or activation of the STAT signal transduction pathway.
265 t the therapeutic potential of targeting the STAT/TET1 axis by selective inhibitors in AML treatment.
266  downstream effectors, more particularly the STATs.
267 een widely implicated in cancer, therapeutic STAT inhibitors are still largely absent from the clinic
268 -6 family of cytokines, which signal through STAT-3, may also contribute to lung fibrosis.
269 STAT5 triggers its genome-wide relocation to STAT consensus sites with two distinct transcriptional c
270 l transducer and activator of transcription (STAT) 1 and STAT3, which is significantly enhanced by an
271 l transducer and activator of transcription (STAT) 1 pathway in human type 1 diabetes and in mouse mo
272 l transducer and activator of transcription (STAT) 3 signaling pathway, and osteogenic differentiatio
273 l transducer and activator of transcription (STAT) 5 activation by IM allowed the specific enhancemen
274 l transducer and activator of transcription (STAT) 5 signaling by TSLP.
275 l transducer and activator of transcription (STAT) binding elements (SBEs) within the proximal promot
276 l transducer and activator of transcription (STAT) family of transcription factors orchestrate hemato
277 l transducer and activator of transcription (STAT) mutations have been discovered in many T-cell mali
278 l transducer and activator of transcription (STAT) pathway.
279 l transducer and activator of transcription (STAT) protein to promote cell division only in OB-ISCs.
280 l transducer and activator of transcription (STAT) proteins, leads to inappropriate gene expression p
281 l transducer and activator of transcription (STAT) signaling contributes to diabetic nephropathy by i
282 l transducer and activator of transcription (STAT) signaling pathway is involved in numerous cellular
283 l transducer and activator of transcription (STAT) signaling pathways is a hallmark of a variety of B
284 l transducer and activator of transcription (STAT) signaling pathways led us to hypothesize that ETP-
285 l transducer and activator of transcription (STAT) target genes.
286 l transducer and activator of transcription (STAT)-1 knockout mouse showed that IFN-gamma signaling i
287 l transducer and activator of transcription (STAT)-3 signaling to decrease angiogenesis in human and
288 l transducer and activator of transcription (STAT)-6 phosphorylation level in murine heart fibroblast
289 l transducer and activator of transcription (STAT)5 activation in left ventricular myocardium is asso
290 Transducers and Activators of Transcription (STATs) are principal transcription factors downstream of
291 transducers and activators of transcription (STATs), essential functions of their upstream Janus kina
292 l transducer and activator of transcription [STAT] homolog) activity and would normally form the hing
293                   However, in tumorigenesis, STAT proteins become constitutively active and promote t
294 retcher, registering the patient as unknown, STAT stroke protocol, and administering alteplase in CT
295 vented Th1 and Th17 cell differentiation via STAT/NFkappaB signaling pathways.
296 ng cytokine regulation of MMP expression via STAT-1, and increases our understanding of the links bet
297             However, the mechanisms by which STAT activation modulates lineage-affiliated transcripti
298 udy was to determine the mechanisms by which STAT-3 activation might result in intestinal fibrosis.
299  the current manuscript, the extent to which STAT-3 inhibition decreases lung fibrosis is investigate
300 lation lead to constitutive activation of WT STATs.

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