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1 id cells in disease states where p21(ras) is hyperactivated.
2 lls in which the beta-catenin/Tcf pathway is hyperactivated.
3 ast some CSF-1R-associated proteins also are hyperactivated.
4 arental Kras(G12D) mice, where STAT3 was not hyperactivated.
5 duced while ER O-glycosylation initiation is hyperactivated.
6 ome various barriers, their motility must be hyperactivated, a motion that is characterized by vigoro
7 nhibition of the Rheb-mTOR pathway, which is hyperactivated after loss of TSC2, decreased MCP-1 produ
13 d progenitor cells (HSPCs), whereas they are hyperactivated and lost in the circulation when wild-typ
15 urther that CD4+ T cells of 4.1R-/- mice are hyperactivated and that they displayed hyperproliferatio
16 hock sensitivity of a strain in which RAS is hyperactivated and the heat shock sensitivity of a wscDe
17 /RSK MAPK signaling module is constitutively hyperactivated, and Bad is maintained in its inactive st
18 Lymphocytes from these transgenic mice were hyperactivated, and T cells produced large amounts of ty
19 Aurora kinases A, B, and C, were found to be hyperactivated, and the altered expression of CDK1 was f
20 Thus, neither costimulatory tumor cells nor hyperactivated antitumor lymphocytes were sufficient to
21 Nevertheless, doubly deficient B cells were hyperactivated, as evidenced by extremely elevated serum
23 ession and binding to p300 may contribute to hyperactivated beta-catenin transcriptional activity in
25 increased parasympathetic signaling leads to hyperactivated bronchoconstriction and abnormal respirat
26 e, extramedullary splenic erythropoiesis was hyperactivated, but this did not lead to accelerated rec
27 nnel critical for mechanosensation that when hyperactivated by a mec-4(d) mutation induces necrosis o
28 s, most genes from the male X chromosome are hyperactivated by a special dosage compensation system.
34 genes), in which the reporter construct was hyperactivated by low temperature, but not by abscisic a
35 ns between MPFC and DLPFC, a region that was hyperactivated by patients and relatives during WM perfo
40 vation of c-Raf containing mutated W342 in a hyperactivated c-Raf, but not in a wild type c-Raf and (
41 nases (TALERs): engineered fusions between a hyperactivated catalytic domain from the DNA invertase G
42 oly(ADP-ribose) polymerase-1 (PARP-1) can be hyperactivated, causing (ADP-ribosyl)ation of nuclear pr
43 cumulation of proinflammatory CD57(+)CD28(-) hyperactivated CD8(+) T cells that may promote atheroscl
45 partial inhibition of the spliceosome in MYC-hyperactivated cells leads to global intron retention, w
46 tor 2 (TRAF2), are upstream of JNK in PARP-1 hyperactivated cells, because PARP-1-induced JNK activat
47 protein (MAP) kinase (MAPK) is significantly hyperactivated compared with ERalpha+ breast cancer.
48 es in sarcomas where PI3K and mTOR are often hyperactivated could improve the suitable recruitment of
49 h increasing prevalence, is characterized by hyperactivated cytokines of helper T cell subset 2 and i
50 1) and Hop(T42) both hyperphosphorylated and hyperactivated D-Stat when overexpressed in Drosophila c
54 al that an important mTOR substrate is found hyperactivated downstream of Myc oncogenic activity to p
57 pressed in body wall muscle precursor cells, hyperactivated EGL-15 can also interfere with the proper
59 ulin-binding region from ACVIII results in a hyperactivated enzyme state and a loss of Ca2+ sensitivi
61 gh incidence of activating RAS mutations and hyperactivated ERK1/2 signaling observed in many human t
66 t process of capacitation, the transition to hyperactivated flagellar motility, develops with a simil
69 hey may be related to the stabilization of a hyperactivated form of the enzyme, like in the case of l
70 s not the sole activator of Race, although a hyperactivated form of zen (a zen-VP16 fusion protein) c
71 essed endosperm and seed coat regulators and hyperactivated genes encoding ribosomal, photosynthetic,
73 tism and inflammatory liver cancer caused by hyperactivated GH signaling (GH(tg) ) to mice with hepat
75 in a pure C57BL/6 background does not induce hyperactivated granulocyte macrophage colony-stimulating
76 ese findings correlated with the presence of hyperactivated helper T cells, which proliferated more v
79 s identify a pathway, present in WT mice and hyperactivated in 53BP1-deficient mice, by which microbi
81 PARP1 is highly expressed and constitutively hyperactivated in a majority of human CDDP-resistant can
84 ase 5 (Cdk5), a critical neuronal kinase, is hyperactivated in AD brains and is, in part, responsible
86 ion of normal T cells and are constitutively hyperactivated in both HTLV-1-transformed human T cell l
89 udies show that Rac1 GTPase is overexpressed/hyperactivated in breast cancer cells and is associated
91 he phosphoinositide 3-kinase/Akt pathway was hyperactivated in cells expressing physiologic levels of
92 ecretions and that this signaling pathway is hyperactivated in CF human, pig, ferret, and mouse SMGs.
95 Akt is a key component of this pathway and hyperactivated in different tumors including neuroblasto
96 n summary, these data suggest that mTORC2 is hyperactivated in gliomas and functions in promoting tum
100 EK and JAK/STAT signaling, which is commonly hyperactivated in human and mouse CMML, potently inhibit
104 -activated protein kinases (MAPKs) are often hyperactivated in human cancers, where they affect multi
107 androgen receptor (AR) is overexpressed and hyperactivated in human castration-resistant prostate ca
108 K1; official name RPS6KA1) was significantly hyperactivated in human melanoma lines and metastatic ti
111 Clinically, this PML degradation pathway is hyperactivated in lung cancer and correlates with poor p
114 the mammalian target of rapamycin (mTOR) is hyperactivated in many human tumors, including hamartoma
116 radation of subcellular constituents that is hyperactivated in many neurodegenerative conditions.
117 he mechanistic target of rapamycin (mTOR) is hyperactivated in many types of cancer, rendering it a c
118 ctor receptor (EGFR) and Torso pathways, are hyperactivated in maternal Rho1 mutants, consistent with
120 the target of cucurbitacin-I inhibition, was hyperactivated in NF1-deficient primary astrocytes and n
121 ng phosphatase 2 (SHP-2) that is mutated and hyperactivated in Noonan syndrome and a significant port
123 ested the hypothesis that AMPK would also be hyperactivated in O vs YA fast-twitch extensor digitorum
124 Because the AKT-mTOR pathway is frequently hyperactivated in ovarian cancer, we hypothesized that t
125 In this report we have shown that mTOR is hyperactivated in Pkd1-null mouse cells due to failure o
127 , phosphoinositide 3-kinase/Akt signaling is hyperactivated in Pten conditional knock-out (cKO) retin
129 f rapamycin complex 1 (mTORC1) signaling was hyperactivated in several tissues from Pip4k2c(-/-) mice
132 ssion, and that when the PI3K-Akt pathway is hyperactivated in Teff cells, these cells are resistant
133 ond to astrocyte-derived matrices and become hyperactivated in the Lamc3(-/-) retina or when tested i
134 AT3, AKT, and Wnt/beta-catenin pathways were hyperactivated in the skin and the lungs of diseased mic
135 t of rapamycin complex 1 (mTORC1) pathway is hyperactivated in tissues and tumors derived from LKB1-d
138 g A20-deficient NKT1 and NKT2 thymocytes are hyperactivated in vivo and secrete elevated levels of Th
139 he percentage of reactivated sperm that were hyperactivated increased to 80% when free Ca2+ was incre
140 e inactivated and enhancing it when they are hyperactivated, indicative of cells that normally play a
143 a direct consequence, both Akt and Rac1 are hyperactivated, leading to cytoskeletal rearrangements a
144 des from abnormally low levels to normal pre-hyperactivated levels and, in 20-40% of sperm, induced h
145 growth in the adult CNS at both moderate and hyperactivated levels of ERK1/2 when upregulation commen
146 locus in a snf5Delta mutant and resulted in hyperactivated levels of SUC2 mRNA under inducing condit
147 ic components within the oxPAPC mixture that hyperactivated macrophages, allowing these cells to rele
151 in hematopoiesis, it remains unclear whether hyperactivated mitophagy affects the maintenance and dif
152 of the gene encoding the AAA+-ATPase Atad3a hyperactivated mitophagy in mouse hematopoietic cells.
155 CatSper4 also abrogated ICatSper, sperm cell hyperactivated motility and male fertility but did not a
159 Ca(2+) entry pathways that support not only hyperactivated motility but possibly also normal pre-hyp
160 motility in the sperm population increasing hyperactivated motility by more than 10-fold as assessed
161 mportant for the sperm to be able to achieve hyperactivated motility in order to reach and fertilize
162 nnel that controls Ca2+ entry to mediate the hyperactivated motility needed late in the preparation o
163 ibited normal motility but could not achieve hyperactivated motility needed to traverse the female ge
164 ed Ca(2+)-selective channel required for the hyperactivated motility of spermatozoa and male fertilit
165 amplitude flagellar bends characteristic of hyperactivated motility than to produce activated motili
166 ll sperm indicates that a critical lesion in hyperactivated motility underlies the infertility phenot
169 , they acquire progressive motility, develop hyperactivated motility, and are readied for the acrosom
170 Thus, CatSper2 is responsible for driving hyperactivated motility, and, even with typical sperm fo
171 equired for successful fertilization such as hyperactivated motility, chemotaxis, and the acrosome re
172 ases in protein tyrosine phosphorylation and hyperactivated motility, which occur late in capacitatio
173 the null sperm cells is a failure to acquire hyperactivated motility, which seems to render spermatoz
189 nhibit ligand binding, and gain-of-function, hyperactivated mutant alphaPS2 proteins cause blistering
190 cence response triggered by Tax is caused by hyperactivated NF-kappaB and mediated by cyclin-dependen
191 s remodeling, including normalization of the hyperactivated p38, in the setting of pre-existing heart
196 isingly, Sphk2(-/-) CD4(+) T cells exhibit a hyperactivated phenotype with significantly enhanced pro
199 tion reverses trastuzumab resistance via the hyperactivated PIK/AKT/mTOR pathway due to PTEN loss, by
200 AP) kinase signaling pathway were abnormally hyperactivated prior to the onset of significant cardiac
202 n the absence of IL-27R myeloid cells become hyperactivated, produce pro-inflammatory cytokines and a
206 -jun gene deletion reduced c-Src expression, hyperactivated ROCK II signaling, and reduced cellular p
209 ay from a tethering point and consequently a hyperactivated sperm cell bound to an epithelial surface
213 3 dimerization inhibitor capable of blocking hyperactivated STAT3 and suppressing malignant transform
221 ent cations and shift dramatically upward to hyperactivated states with cell signaling in leukocytes.
223 One form of sepsis, or endotoxic shock, is a hyperactivated systemic response caused by excessive exp
225 is is an inflammatory skin disease caused by hyperactivated T cells regulated by positive and negativ
227 or the majority of these adverse events is a hyperactivated T-cell response with reactivity directed
228 of development, the innate immune system was hyperactivated to a contraproductive level that impaired
229 ned when its downstream effector kinases are hyperactivated to trigger the negative feedback inhibiti
230 ncreased aliphatic glucosinolate content and hyperactivated transcript accumulation of the jasmonic a
233 ell subsets: they inhibited T(reg) cells and hyperactivated tumor-infiltrating cytotoxic T lymphocyte
235 phorylation in ubp8Delta ubp10Delta cells is hyperactivated upon stress, which may compensate for the
239 spleens, of diseased 5B6 transgenic mice are hyperactivated when compared with age-matched healthy mi
240 3(25,26,53,54) mutant protein stabilized and hyperactivated wild-type p53, which then inappropriately
241 ther immune and inflammatory pathways become hyperactivated with age and promote degeneration or whet
243 extant macrophages and dendritic cells were hyperactivated, with CD11b and GR1 (Ly6G/C) highly expre
244 We have established a Drosophila model with hyperactivated Wnt signaling caused by partial loss of a
247 isingly, the Overinduced phenotype caused by hyperactivated Wnt signaling is not dependent on signali
248 cient embryos (embryonic day 8.0-8.5) showed hyperactivated Wnt signaling, as well as aberrant differ
249 tion of TAK1 is linked to its suppression of hyperactivated Wnt signaling, evident in both endogenous
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