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1 regulated by the transcription factor HIF-1 (hypoxia-inducible factor 1).
2 regulates Complex II expression and opposes hypoxia-inducible factor-1.
3 sion is mediated by the transcription factor hypoxia-inducible factor-1.
4 lly mediated at the transcriptional level by hypoxia-inducible factor-1.
5 riptional activator, which was identified as hypoxia-inducible factor-1.
7 phage glucose metabolism pathway via the Vpr-hypoxia inducible factor 1 alpha (HIF-1 alpha) axis to i
9 protein levels in macrophages and T cells of hypoxia inducible factor 1 alpha (HIF-1alpha), the regul
10 entified in this screen, only one candidate, hypoxia inducible factor 1 alpha (Hif1alpha), did not ha
11 from hydroxylating the transcription factor hypoxia inducible factor 1 alpha (HIF1alpha), targeting
13 found that E2 and PPT induced the binding of hypoxia inducible factor 1 alpha subunit (HIF1A) in the
14 ine production of VEGF with the induction of hypoxia inducible factor-1 alpha (HIF-1 alpha) and survi
15 control, and immunohistochemical staining of hypoxia inducible factor-1 alpha (HIF-1 alpha), vascular
17 nd it was accompanied by decreased levels of hypoxia inducible factor-1 alpha (HIF-1alpha) and Bcl-2.
21 trol, inhibition of PHD2 increased levels of hypoxia inducible factor-1 alpha protein and several dow
24 ationship for the VHL tumor suppressor gene, hypoxia inducible factor-1 alpha, and vascular endotheli
26 erminal phosphorylation, and the presence of hypoxia-inducible factor 1 alpha (HIF-1 alpha), the oxyg
27 oenvironments where the stabilization of the hypoxia-inducible factor 1 alpha (Hif-1alpha) subunit is
28 posttranscriptional control of expression of hypoxia-inducible factor 1 alpha (HIF-1alpha), a critica
29 not only that LOXL2 was regulated by hypoxia/hypoxia-inducible factor 1 alpha (HIF-1alpha), but also
33 ty to the cell death phenotype observed when hypoxia-inducible factor 1 alpha (Hif1a) expression was
36 sents a common pathway for the regulation of hypoxia-inducible factor 1 alpha (HIF1alpha)-dependent V
37 nd STAT6 phosphorylation, and down-regulated hypoxia-inducible factor 1 alpha and its downstream targ
38 activity associated with induction of tumor hypoxia-inducible factor 1 alpha expression and marked i
39 utyrate (SB) may indirectly (through reduced hypoxia-inducible factor 1 alpha stabilization) decrease
40 lower expression of lactate dehydrogenase 5, hypoxia-inducible factor 1 alpha subunit, and vascular e
41 opalisading cells show nuclear expression of hypoxia-inducible factor 1 alpha, consistent with their
42 terodimeric transcription factor, comprising hypoxia-inducible factor-1 alpha (HIF-1 alpha) and ARNT.
43 ealed that mTOR controls the accumulation of hypoxia-inducible factor-1 alpha (HIF-1 alpha) and the c
44 asts were hypersensitive to the induction of hypoxia-inducible factor-1 alpha (HIF-1 alpha) under hyp
45 EP1 receptor up-regulates the expression of hypoxia-inducible factor-1 alpha (HIF-1 alpha), which ca
49 conditions, HEXIM1 inhibits estrogen-induced hypoxia-inducible factor-1 alpha (HIF-1alpha) protein ex
50 that robustly and persistently expresses the hypoxia-inducible factor-1 alpha (HIF-1alpha) therapeuti
51 ng that cetuximab reduces cellular levels of hypoxia-inducible factor-1 alpha (HIF-1alpha), a transcr
52 hypoxic/ischemic retinal ganglion cells in a hypoxia-inducible factor-1 alpha (HIF-1alpha)-dependent
53 pimonidazole, macrophage marker RAM-11, and hypoxia-inducible factor-1 alpha subunit [HIF-1alpha]).
55 ene targeting to examine the contribution of hypoxia-inducible factor 1, alpha subunit (HIF-1alpha) t
57 , vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1-alpha (HIF-1alpha) and erythr
58 that the expression of NLRP3 is mediated by hypoxia-inducible factor 1-alpha (HIF-1alpha) during the
59 s to test whether constitutive expression of hypoxia-inducible factor 1-alpha (HIF-1alpha) influences
60 a mutated (ATM)-dependent phosphorylation of hypoxia-inducible factor 1-alpha (HIF-1alpha) on serine(
62 in physiological oxygen conditions through a hypoxia-inducible factor 1-alpha (HIF-1alpha)-dependent
64 miR-210 transcription was activated in an hypoxia-inducible factor 1-alpha (Hif1a)-dependent manne
65 nsiently increasing the transcription factor hypoxia-inducible factor 1-alpha (HIF1alpha) is required
66 mutant mice did not display accumulation of hypoxia-inducible factor 1-alpha (HIF1alpha), and deleti
67 ation and decreased nuclear translocation of hypoxia-inducible factor 1-alpha and vascular endothelia
68 ivin in endothelial cells and down-regulated hypoxia-inducible factor 1-alpha and VEGF expression in
69 TLR-primed cells was dependent, in part, on hypoxia-inducible factor 1-alpha and was essential for i
70 e kinase release spectrophotometrically, and hypoxia-inducible factor 1-alpha by Western blotting.
72 tors nuclear factor of activated T cells and hypoxia-inducible factor 1-alpha in PAH-PASMCs, previous
76 y, Leu increases the intracellular levels of hypoxia-inducible factor 1-alpha, a repressor of endocri
77 eration, up-regulation of AKT signaling, and hypoxia-inducible factor 1-alpha-related angiogenesis.
81 ered to express tumor-necrosis-factor-alpha, hypoxia-inducible-factor-1-alpha antibodies, interleukin
82 d stress-induced activation of cardiomyocyte hypoxia inducible factor 1 and the release of vascular e
84 rect transcriptional target of oxygen-labile hypoxia-inducible factor 1 and 2 that accentuates the fo
86 owth factor (VEGF) and blocked activation of hypoxia-inducible factor-1 and nuclear factor-kappaB in
87 E were dependent on the transcription factor hypoxia-inducible factor-1 and on formation of a single-
93 ated their ability to respond to hypoxia via hypoxia-inducible factors 1 and 2, tumor relapse was una
94 up-regulating such transcription factors as hypoxia-inducible factors 1 and 2, which in turn activat
95 ression, in part through the presence of the hypoxia-inducible factor-1-binding site, leading to an a
96 he novel GPx-3 promoter identified Sp-1- and hypoxia-inducible factor-1-binding sites, as well as the
99 reased expression of ErbB3 and inhibition of hypoxia-inducible factor-1-dependent responses to hypoxi
101 ith higher VEGF (3.65 vs. 5.98; P = 0.01) or hypoxia-inducible factor 1 expression (3.63 vs. 5.48; P
104 ntly, we demonstrated that factor-inhibiting hypoxia-inducible factor 1 (FIH-1) diminished glycogen s
105 n undergo hydroxylation by factor-inhibiting hypoxia-inducible factor 1 (FIH-1); however, the biologi
108 iCl(2) exposure leads to marked induction of hypoxia inducible factor 1 (HIF-1) in human osteosarcoma
111 lpha (AMPKalpha) degradation, (ii) increased hypoxia inducible factor-1 (HIF-1) alpha expression, and
112 ators have been identified for its promoter: hypoxia inducible factor-1 (HIF-1) and signal transducer
113 nical data provides evidence for the role of hypoxia inducible factor-1 (HIF-1) as a crucial mediator
119 with tumor resistance to therapy and express hypoxia inducible factor-1 (HIF-1), a transcription fact
121 stimulates tumor angiogenesis by activating hypoxia inducible factor-1 (HIF-1)-induced proangiogenic
128 alpha-ketoglutarate antagonist that induces hypoxia-inducible factor 1 (HIF-1) activity, results in
132 ROS production, we showed that ROS regulated hypoxia-inducible factor 1 (HIF-1) and vascular endothel
136 response to hypoxia in many cell types, and hypoxia-inducible factor 1 (HIF-1) has been implicated i
139 equent studies identified a binding site for hypoxia-inducible factor 1 (HIF-1) in the CD18 gene.
141 rus encoding a constitutively active form of hypoxia-inducible factor 1 (HIF-1) induced VEGFR1 mRNA a
159 recent work delineating mechanisms by which hypoxia-inducible factor 1 (HIF-1) mediates adaptive met
166 Being key regulator of oxygen homeostasis hypoxia-inducible factor 1 (HIF-1) plays significant rol
167 y demonstrated that the transcription factor hypoxia-inducible factor 1 (HIF-1) promotes the onset of
168 der conditions of reduced O(2) availability, hypoxia-inducible factor 1 (HIF-1) reciprocally regulate
171 r concentrations of thioredoxin 1 (Trx1) and hypoxia-inducible factor 1 (HIF-1) than cells from unsup
172 EN increases the transcriptional activity of hypoxia-inducible factor 1 (HIF-1) through the inactivat
173 , a topoisomerase I (Top 1) poison, inhibits hypoxia-inducible factor 1 (HIF-1) transcriptional activ
175 ated, our results point to the activation of hypoxia-inducible factor 1 (HIF-1) upon HIV-1 infection
177 uestion and reveal that orexin activates the hypoxia-inducible factor 1 (HIF-1), a heterodimeric tran
180 ia-induced amoeboid detachment was driven by hypoxia-inducible factor 1 (HIF-1), followed the downreg
181 ons requires transcription through activated hypoxia-inducible factor 1 (HIF-1), increased mRNA stabi
182 g the relationship between the activation of hypoxia-inducible factor 1 (HIF-1), the primary transcri
184 rs increased production of erythropoietin by hypoxia-inducible factor 1 (HIF-1), which is a transcrip
185 A low dose of either H2S or HCN can activate hypoxia-inducible factor 1 (HIF-1), which is required fo
186 hypoxic pulmonary hypertension (HPH) include hypoxia-inducible factor 1 (HIF-1)-dependent transactiva
187 cin and daunorubicin as potent inhibitors of hypoxia-inducible factor 1 (HIF-1)-mediated gene transcr
199 pathway can increase VEGF expression via the hypoxia-inducible factor 1 (HIF-1); however, our results
200 ion regulates glycolysis in cancer cells via hypoxia-inducible factor 1 (HIF-1alpha) and its transcri
201 own-regulated sFlt1 production by inhibiting hypoxia-inducible factor 1 (HIF-1alpha) protein expressi
202 troversy in the literature as to the role of hypoxia-inducible factor-1 (HIF-1) and HIF-1 target gene
204 Here, we report that balanced activity of hypoxia-inducible factor-1 (HIF-1) and HIF-2 is critical
205 of the KRAS mutations and for expression of hypoxia-inducible factor-1 (HIF-1) and minichromosome ma
207 In this report, we address the dynamics of hypoxia-inducible factor-1 (HIF-1) binding to the vascul
210 of this study was to establish the effect of hypoxia-inducible factor-1 (HIF-1) directly on tumor gro
211 importance of the transcriptional regulator hypoxia-inducible factor-1 (HIF-1) for adaptive hypoxia
213 ion is regulated by the transcription factor hypoxia-inducible factor-1 (HIF-1) in endothelial cells,
214 to accumulation of the transcription factor hypoxia-inducible factor-1 (HIF-1) in skeletal muscle ce
215 (NF-kappaB), activator protein-1 (AP-1), and hypoxia-inducible factor-1 (HIF-1) in the hypoxic regula
216 Here we report that 1 h of HT activates hypoxia-inducible factor-1 (HIF-1) in tumors and its dow
228 a potent stimulator of VEGF expression, and hypoxia-inducible factor-1 (HIF-1) is considered to be c
239 ated during hypoxia due to direct binding by hypoxia-inducible factor-1 (HIF-1) to HIF-1 response ele
240 LOX in colorectal cancer synergizes with hypoxia-inducible factor-1 (HIF-1) to promote tumor prog
241 ion of gene expression occurs mainly via the hypoxia-inducible factor-1 (HIF-1) transcription factor
242 ntial feature of tumor angiogenesis, and the hypoxia-inducible factor-1 (HIF-1) transcription factor
243 Digoxin and other cardiac glycosides inhibit hypoxia-inducible factor-1 (HIF-1) transcriptional activ
244 rubicin (DXR) and daunorubicin (DNR) inhibit hypoxia-inducible factor-1 (HIF-1) transcriptional activ
245 the effects of pharmacological inhibition of hypoxia-inducible factor-1 (HIF-1), a critical regulator
247 These tumor cells are hypoxic and express hypoxia-inducible factor-1 (HIF-1), a prosurvival transc
248 rimary factor mediating this response is the hypoxia-inducible factor-1 (HIF-1), an oxygen-sensitive
249 -kappaB), STAT3, activator protein-1 (AP-1), hypoxia-inducible factor-1 (HIF-1), and tumor protein 53
250 suppresses hypoxia-sensitive genes, e.g. via hypoxia-inducible factor-1 (HIF-1), but mutations in Com
251 ecular key players in tumor hypoxia, such as hypoxia-inducible factor-1 (HIF-1), have been discovered
252 cellular response, the transcription factor hypoxia-inducible factor-1 (HIF-1), is correlated with p
253 bunit of the host cell transcription factor, hypoxia-inducible factor-1 (HIF-1), is up-regulated by i
254 n angiogenesis during hypoxia is mediated by hypoxia-inducible factor-1 (HIF-1), it was conceivable t
255 gene delivery and small molecules targeting hypoxia-inducible factor-1 (HIF-1), we evaluated the imp
256 tivation in transcription are dependent upon hypoxia-inducible factor-1 (HIF-1), whereas others are H
257 y and voltage dependency as full-length, was hypoxia-inducible factor-1 (HIF-1)-dependent and could b
258 Hypoxia-induced angiogenesis is mediated by hypoxia-inducible factor-1 (HIF-1)-dependent transcripti
265 nds the functional NF-kappaB binding site in hypoxia-inducible factor-1 (HIF-1alpha) promoter and res
267 tidinyl hydroxylase FIH-1 (factor inhibiting hypoxia-inducible factor 1 [HIF-1]), the lysyl hydroxyla
268 alt chloride (CoCl(2), a chemical inducer of hypoxia-inducible factor 1, HIF-1), suggesting a regulat
269 elanoma and clear cell sarcoma cells through hypoxia inducible factor 1 (HIF1)-mediated induction of
275 is increased by pharmacologic inhibition of hypoxia-inducible factor 1 (HIF1) or its target gene pyr
276 family of transcription factors, among which hypoxia-inducible factor 1 (HIF1) plays a major role.
277 In exercise, as well as cancer and ischemia, hypoxia-inducible factor 1 (HIF1) transcriptionally acti
278 the metabolic reprogramming associated with hypoxia-inducible factor 1 (HIF1), as constitutive activ
279 cancer cells was under strict control of the hypoxia-inducible factor 1 (HIF1), which drove redox- an
286 ption, lactate production, and expression of Hypoxia-inducible factor 1 (HIF1alpha) target genes, sug
287 by an oxygen-sensitive transcription factor, hypoxia-inducible factor-1 (HIF1alpha), which becomes ac
289 cIH induced systemic insulin resistance in a hypoxia-inducible factor 1-independent manner and impair
290 ent chemotherapy, antiangiogenic agents with hypoxia-inducible factor-1 inhibitors, tissue-selective
291 in mild hypoxia (0.25-1 kPa O(2)) through a hypoxia-inducible factor 1-mediated response, cannot sur
292 P=9.8x10(-10)) and HIF1AN (factor inhibiting hypoxia-inducible factor-1; P=5.7x10(-9)) polymorphisms
293 dermal growth factor receptor-MAP/ERK kinase-hypoxia-inducible factor 1 signaling but on RhoA pathway
295 t of a transcriptional complex involving the hypoxia-inducible factor-1 transcription factor, p300, R
296 d by mTORC1 regulate the expression of HIF1 (hypoxia-inducible factor 1) transcription factor complex
297 y foci, evidencing induction of an epidermal hypoxia-inducible factor-1 transcriptional program, and
299 f asTF is mediated via the activation of the hypoxia-inducible factor-1/vascular endothelial growth f
300 erodimeric, functional transcription factor, hypoxia-inducible factor-1, which activates a gene progr
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