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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
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
17 y or advanced stages of diabetes ameliorated STAT activity and resulted in reduced serum creatinine l
21 s from this patient exhibit reduced JAK1 and STAT phosphorylation following cytokine stimulations, re
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
28 ate transcriptional activity of NFkappaB and STATs, we hypothesized that these kinases support RS cel
30 es as privileged structures for antagonizing STAT SH2 domains, and demonstrates that apoptosis can be
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
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
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
48 tivation of transcription factors, including STATs, is known to promote tumor initiation and progress
50 JAK2 inhibitors also blocked C26 CM-induced STAT reporter activation, STAT3 phosphorylation, and atr
52 Mycobacterium marinum, mycobacterium-induced STAT activity triggered by unpaired-family cytokines red
55 vival and fate, specifically PDGFR, ERK, JAK STAT, MAPK, and TCR/NF-kappaB signaling; epigenetic regu
59 f genes involved in RNAi, Toll, Imd, and JAK-STAT pathways, but the majority of differentially expres
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
65 indicate an essential role for canonical JAK-STAT signaling in activity-dependent LTD at TA-CA1 synap
67 elation analysis links PinT to host cell JAK-STAT signalling, and we identify infection-specific alte
69 driver mutations leading to constitutive JAK-STAT activation, the cellular and molecular biology of m
72 )) and used pathway analysis to identify JAK-STAT/IL12/IL27 signalling and cytokine-cytokine pathways
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
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
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
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
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
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
103 ficant increase in the expression of the JAK-STAT target gene Pim1 and muscles from 2-day and 3-week
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
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 (
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
124 included components of the Toll, Imd and JAK/STAT pathways, consistent with interactions between the
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
130 of main immune pathways (Toll, Imd, and JAK/STAT), and immune effectors in P. xylostella in response
137 The HEL cell line, in which constitutive JAK/STAT pathway activation is caused by JAK2V617F, was used
139 the molecular basis of this constitutive JAK/STAT signaling in cHL has not been completely understood
143 with high MPL expression showed enhanced JAK/STAT signaling and proliferation in response to THPO in
146 erferon-gamma- and interleukin-4-induced JAK/STAT activity in HEK293 or HEK293-STAT6 cells, and on th
150 e contraction, focal adhesion, integrin, JAK/STAT, MAPK, growth factor, and p53 signaling pathways we
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
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
159 l studies underscore the central role of JAK/STAT signaling in myeloproliferative neoplasms (MPNs).
161 cytokine Upd3, leading to activation of JAK/STAT signaling, differentiation of cells that form the p
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
171 perimental CP, suggesting that targeting Jak/STAT signaling may represent a promising therapeutic str
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
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
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
201 a receptor-dependent cytokines and their JAK/STAT pathways play pivotal roles in T cell immunity.
203 a greater role of MAPK/PI3K compared to JAK/STAT with the orphan nuclear receptor RXRalpha playing a
206 sducers and activators of transcription (JAK/STAT) signaling via the IL-22 receptor, resulting in enh
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-
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
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
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
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
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
240 hropoietin (EPO) receptor and phosphorylated STAT-5 relative to matched Q-HB, with increased phosphor
242 omprised of IRF9 and tyrosine-phosphorylated STATs 1 and 2, transmits the signal from the type I inte
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
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.
254 evelopment of lung fibrosis and suggest that STAT-3 may be a therapeutic target in pulmonary fibrosis
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
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
265 t the therapeutic potential of targeting the STAT/TET1 axis by selective inhibitors in AML treatment.
267 een widely implicated in cancer, therapeutic STAT inhibitors are still largely absent from the clinic
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
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
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-
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
294 retcher, registering the patient as unknown, STAT stroke protocol, and administering alteplase in CT
296 ng cytokine regulation of MMP expression via STAT-1, and increases our understanding of the links bet
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
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