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1 nse genes is controlled by the heterodimeric Hypoxia-Inducible Factor.
4 production of reactive oxygen species (ROS), hypoxia inducible factor 1 alpha (HIF-1alpha), and its t
5 mphedema, there is a significant increase of hypoxia inducible factor 1 alpha (HIF-1alpha), but a red
6 ovascular, resulting in the up-regulation of hypoxia inducible factor 1 alpha (HIF1A), which promotes
7 from hydroxylating the transcription factor hypoxia inducible factor 1 alpha (HIF1alpha), targeting
9 found that E2 and PPT induced the binding of hypoxia inducible factor 1 alpha subunit (HIF1A) in the
10 he stricture phenotype of ISMC showed stable hypoxia inducible factor 1 subunit alpha expression that
12 dies with the hydroxylase, factor inhibiting hypoxia-inducible factor 1 (FIH-1), we observed increase
13 ugh activation of transcription factors like hypoxia-inducible factor 1 (HIF-1) and c-Myc, yet the im
16 recent work delineating mechanisms by which hypoxia-inducible factor 1 (HIF-1) mediates adaptive met
17 Here, we delineate a pathway controlled by hypoxia-inducible factor 1 (HIF-1) that epigenetically a
18 ia-induced amoeboid detachment was driven by hypoxia-inducible factor 1 (HIF-1), followed the downreg
19 adhesion molecule 1, IL-10, heme oxygenase 1 hypoxia-inducible factor 1 (HIF-1), monocyte chemotactic
21 ngiogenic factors were partially mediated by hypoxia-inducible factor 1 alpha (HIF-1alpha) and recomb
25 utyrate (SB) may indirectly (through reduced hypoxia-inducible factor 1 alpha stabilization) decrease
26 activated phenotype (increased expression of hypoxia-inducible factor 1 alpha, glucose transporter 1,
29 g axis towards glycolysis with activation of hypoxia-inducible factor 1 subunit alpha (HIF-1alpha) an
31 , vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1-alpha (HIF-1alpha) and erythr
32 that the expression of NLRP3 is mediated by hypoxia-inducible factor 1-alpha (HIF-1alpha) during the
36 1, and the downstream transcription factors hypoxia-inducible factor 1-alpha and c-Myc, which togeth
37 was associated with increased expression of hypoxia-inducible factor 1-alpha and glucose transporter
38 TLR-primed cells was dependent, in part, on hypoxia-inducible factor 1-alpha and was essential for i
41 cIH induced systemic insulin resistance in a hypoxia-inducible factor 1-independent manner and impair
42 ontaining family, pyrin domain-containing-3; hypoxia-inducible factor 1/2alpha; and NF-kappaB were al
45 poxia-inducible angiogenic pathway involving hypoxia inducible factor-1 alpha (HIF-1alpha), vascular
48 LOX in colorectal cancer synergizes with hypoxia-inducible factor-1 (HIF-1) to promote tumor prog
49 the effects of pharmacological inhibition of hypoxia-inducible factor-1 (HIF-1), a critical regulator
51 label exchange between pyruvate and lactate, hypoxia-inducible factor-1 (HIF1alpha), and the monocarb
52 hown to reduce oxidative stress and increase hypoxia-inducible factor-1 alpha (HIF-1alpha) activation
53 eport that tamoxifen decreases the levels of hypoxia-inducible factor-1 alpha (HIF-1alpha) and the sy
54 ngiogenic effect, CSCs were transfected with hypoxia-inducible factor-1 alpha (HIF-1alpha) by using e
56 ially via direct and indirect effects of the hypoxia-inducible factor-1 alpha (HIF-1alpha) transcript
57 se inhibitors (PHI) promote stabilization of hypoxia-inducible factor-1 alpha and affect signaling ca
58 allogeneic recipients resulted in increased hypoxia-inducible factor-1 alpha expression and reduced
59 e B), SRC, and overexpression of HIF1-alpha (hypoxia-inducible factor-1 alpha), survivin, and VWF (Vo
60 oxide dismutase (SOD2), increases HIF1alpha (hypoxia-inducible factor-1), reduces endothelial cadheri
62 IF-1alpha and HIF-2alpha proteins.IMPORTANCE Hypoxia inducible factor 1alpha (HIF-1alpha) and HIF-2al
64 a hypoxia-induced pathway that utilizes the Hypoxia Inducible Factor 1alpha (HIF-1alpha) transcripti
68 Given that Leishmania parasites activate hypoxia-inducible factor 1alpha (HIF-1alpha) and this tr
69 trix (ECM) remodeling and angiogenesis, with hypoxia-inducible factor 1alpha (HIF-1alpha) being a maj
70 orted that the cellular transcription factor hypoxia-inducible factor 1alpha (HIF-1alpha) binds a hyp
73 d growth, blood vessel density, and VEGF and hypoxia-inducible factor 1alpha (HIF-1alpha) expression
76 Hif1a gene encoding the transcription factor hypoxia-inducible factor 1alpha (HIF-1alpha) is mediated
80 m a wide variety of partners, including p53, hypoxia-inducible factor 1alpha (HIF-1alpha), NF-kappaB,
81 ed by ERalpha, but it became predominantly a hypoxia-inducible factor 1alpha (HIF-1alpha)-dependent g
86 cells respond to hypoxia by upregulating the hypoxia-inducible factor 1alpha (HIF1A) transcription fa
87 ulatory signal that controls the activity of Hypoxia-Inducible Factor 1alpha (Hif1a), a mediator of t
89 romoting aryl hydrocarbon receptor (AhR) and hypoxia-inducible factor 1alpha (HIF1alpha) expression,
90 es at birth, and the von Hippel-Lindau (VHL)-hypoxia-inducible factor 1alpha (Hif1alpha) pathway regu
92 oC activation modulated the stabilization of hypoxia-inducible factor 1alpha (HIF1alpha) to upregulat
94 oxia-inducible factor 2alpha (HIF2alpha) and hypoxia-inducible factor 1alpha (HIF1alpha), were enrich
95 hat SHH-treated CGNPs feature high levels of hypoxia-inducible factor 1alpha (HIF1alpha), which is kn
96 e dehydrogenase (PDH) in an NO-dependent and hypoxia-inducible factor 1alpha (Hif1alpha)-independent
97 set of physiologically important mRNAs (e.g. hypoxia-inducible factor 1alpha [HIF-1alpha], fibroblast
99 Production of HERNA1 is initiated by direct hypoxia-inducible factor 1alpha binding to a hypoxia-res
102 vacuoles within knockout cardiomyocytes; (3) Hypoxia-inducible factor 1alpha protein instability was
103 at reduced Nkx2-5 expression and a prolonged hypoxia-inducible factor 1alpha response together precip
106 one morphogenetic protein 4) and HIF-1alpha (hypoxia-inducible factor 1alpha), blocking the BMP4/ALK
107 genous RNA sequesters miRNA let-7 to release Hypoxia-inducible factor 1alpha, leading to an increase
110 gen peroxide production and inactivated HIF (hypoxia-inducible factor)-1alpha, which was pathological
111 (PAECs), expression of transcription factor hypoxia inducible factor-1alpha (HIF-1alpha) is increase
112 nstrate that MUC1-regulated stabilization of hypoxia inducible factor-1alpha (HIF-1alpha) mediates su
114 DF-induced metabolic reprogramming required hypoxia inducible factor-1alpha (HIF-1alpha), downstream
115 ed 3D-printed hydrogel scaffolds seeded with hypoxia inducible factor-1alpha (HIF-1alpha)-mutated mus
118 lular metabolism, including up-regulation of hypoxia inducible factor-1alpha's downstream processes a
119 show detectable levels of the marker protein hypoxia-inducible factor-1alpha (HIF-1alpha) after 3 h o
120 tress-induced p53 physically interacted with hypoxia-inducible factor-1alpha (HIF-1alpha) and attenua
123 rotein-1-like (HSPA1L) expression stabilized hypoxia-inducible factor-1alpha (HIF-1alpha) protein and
124 diated PHLPP1 transcriptional inhibition and hypoxia-inducible factor-1alpha (HIF-1alpha) protein tra
128 nd VAT with downregulation of OPN, activated hypoxia-inducible factor-1alpha (HIF-1alpha), proliferat
129 diseases and identify their association with hypoxia-inducible factor-1alpha (HIF-1alpha), vascular e
130 NBC cells secrete high levels of GM-CSF in a hypoxia-inducible factor-1alpha (HIF1alpha)- and a NF-ka
131 n of the profibrotic markers fibronectin and hypoxia-inducible factor-1alpha and reversed TGF-beta1-i
132 f IDH2 caused ROS-dependent stabilization of hypoxia-inducible factor-1alpha in normoxia, which was r
133 evelopment of PH, mice lacking expression of hypoxia-inducible factor-1alpha in the Ly6C(lo) monocyte
134 e regulated by hypoxia-inducible factor, and hypoxia-inducible factor-1alpha induction was attenuated
135 In addition, there was reduced expression of hypoxia-inducible factor-1alpha relevant in the pathogen
136 a2 regulates alpha-ketoglutarate generation, hypoxia-inducible factor-1alpha stability, and neutrophi
137 pha-ketoglutarate, which negatively regulate hypoxia-inducible factor-1alpha stability, were attenuat
138 s accompanied by nonheme iron deposition and hypoxia-inducible factor-1alpha upregulation in the rena
140 phosphorylated PKM2, succinate, HIF-1alpha (hypoxia-inducible factor-1alpha), lactate, and the IL-1b
141 f hypoxia through suppression of HIF-1alpha (hypoxia-inducible factor-1alpha)-mediated neutrophil ada
142 A negatively regulates the metabolic sensor, hypoxia-inducible factor-1alpha, and key inflammatory pr
143 sues (eg, succinate, adenosine triphosphate, hypoxia-inducible factor-1alpha, nuclear factor erythroi
146 east cancer and its expression is induced by hypoxia-inducible factor 2 (HIF2), but not HIF1, in resp
147 yl hydroxylase gene (PHD) 1 and 2 and in the hypoxia-inducible factor 2 alpha (HIF2A) were also found
148 model, we show that the transcription factor hypoxia-inducible factor 2 alpha (Hif2alpha), which is i
155 portant transcription factor-binding motifs, hypoxia-inducible factor 2alpha (HIF2alpha) and hypoxia-
160 expression was downregulated, which involved hypoxia inducible factor-2alpha-dependent transcriptiona
161 y the hypoxia-inducible transcription factor hypoxia-inducible factor-2alpha (HIF-2alpha) as the top
163 entially bound to the promoter and activated hypoxia-inducible factor-2alpha (HIF2alpha) in Sca-1(+)
166 exhibit decreased expression of HIF-2alpha (hypoxia-inducible factor-2alpha)-regulated genes, and to
167 regulated the expression of the Egl-9 family hypoxia inducible factor 3(EGLN3) gene and targeted a si
168 component of a ubiquitin ligase complex) and hypoxia-inducible factors (a family of transcription fac
169 iferation and blood vessel formation through hypoxia inducible factor alpha (HIFalpha)-activated Wnt
170 in mammals that posttranslationally modifies hypoxia-inducible factor alpha (HIF-alpha) and targets i
172 dent prolyl hydroxylase (PHD) reaction, with hypoxia-inducible factor alpha (HIFalpha) being its most
174 xposed to physiological hypoxia, under which hypoxia-inducible factor alpha (HIFalpha) is stabilized
175 ein (pVHL), resulting in the accumulation of hypoxia-inducible factor alpha-subunits (HIF-alpha) and
176 s an O(2) sensor that controls levels of the Hypoxia Inducible Factor-alpha (HIF-alpha), which regula
178 he activity of the transcription factor HIF (hypoxia-inducible factor) and its regulatory hydroxylase
179 on NF-kappaB (nuclear factor-kappa B), HIF (hypoxia-inducible factor), and angiogenic response were
180 y angiogenic growth factors are regulated by hypoxia-inducible factor, and hypoxia-inducible factor-1
182 ascular endothelial growth factor (VEGF) and hypoxia-inducible factor by using a histone deacetylase
183 1 (EPAS1), a regulatory alpha subunit of the hypoxia-inducible factor complex, during angiotensin II-
186 ional program, mediated predominantly by the hypoxia inducible factor family of transcription factors
190 onocytes showed enrichment for metabolic and hypoxia inducible factor (HIF) pathways in sarcoidosis.
191 atically alters mitochondrial metabolism and hypoxia inducible factor (HIF) signaling due to iron dep
192 nes, treatment with chemicals that stabilize hypoxia inducible factor (HIF), including desferrioxamin
193 The role of prolyl hydroxylase (PHD)-3 as a hypoxia inducible factor (HIF)-1alpha cofactor is contro
195 r 24 hours, or by APC specific deficiency in hypoxia inducible factor (HIF)-2alpha, an oxygen labile
196 e to hydroxylate specific prolyl residues on hypoxia inducible factor (HIF)-alpha proteins, labeling
197 geted therapeutics, such as those abrogating hypoxia inducible factor (HIF)/vascular endothelial grow
198 The effects of pharmacologic inhibitors of hypoxia-inducible factor (HIF) 1alpha and HIF-2alpha wer
199 lysis, we identified increased expression of hypoxia-inducible factor (HIF) 1alpha target genes (expr
200 ted information on the importance of the VHL-hypoxia-inducible factor (HIF) axis to human phenotypes.
202 nfected corneas, and the outcome of blocking hypoxia-inducible factor (HIF) dimerization on the sever
206 prominent role for the transcription factor hypoxia-inducible factor (HIF) in the regulation of inna
208 vironment with variable hypoxia, but whether hypoxia-inducible factor (HIF) is involved is unknown.
211 e overlap between cis-acting elements of the hypoxia-inducible factor (HIF) pathway and cancer-suscep
212 ing and lipidomic profiling, we identify the hypoxia-inducible factor (HIF) pathway as a driver of th
213 and regulation is primarily performed by the hypoxia-inducible factor (HIF) pathway, and the key comp
215 , much research in this field has focused on hypoxia-inducible factor (HIF) signaling and reactive ox
219 s known to activate the transcription factor hypoxia-inducible factor (HIF) that increases lactate ef
220 d changes in gene expression are mediated by hypoxia-inducible factor (HIF) transcription factors tha
222 nizes a field traditionally dominated by the hypoxia-inducible factor (HIF) transcriptional program.
223 demethylating RACK1 protein, a component of hypoxia-inducible factor (HIF) ubiquitination machinery,
224 specific prolyl and asparaginyl residues in hypoxia-inducible factor (HIF), a key transcription fact
225 n regulates cellular function is through the hypoxia-inducible factor (HIF), a transcription factor c
226 system include the transcriptional regulator hypoxia-inducible factor (HIF), which controls a wide ra
227 inal homeostasis is the transcription factor hypoxia-inducible factor (HIF), which is stabilized unde
229 reprogramming and glucose uptake mediated by hypoxia-inducible factor (HIF)-1 alpha and glucose trans
230 mary endothelial cell-specific regulation of hypoxia-inducible factor (HIF)-1 and HIF-2 and their tar
232 factors GATA-binding protein 4 (GATA-4) and hypoxia-inducible factor (HIF)-1alpha and -2alpha in res
233 phages accumulate in hypoxic areas through a hypoxia-inducible factor (HIF)-1alpha dependent manner a
235 r atpenin A5 in normoxia robustly stabilizes hypoxia-inducible factor (HIF)-1alpha in primary monocyt
236 was confirmed with histological staining for hypoxia-inducible factor (HIF)-1alpha, a cellular transc
237 found that burn injury activated mTORC1 and hypoxia-inducible factor (HIF)-1alpha, which paralleled
239 oxia-responsive master transcription factors hypoxia-inducible factor (HIF)-1alpha/2alpha, and their
243 me of hypoxia-targeted therapeutics, such as hypoxia-inducible factor (HIF-1) inhibitors and hypoxia-
245 alysis identified specific binding sites for hypoxia-inducible factors (HIF) and TGF-beta1-activated
247 of pVHL is to regulate the stability of the hypoxia-inducible factors (HIF), which become constituti
248 1), AMP-activated protein kinase (AMPK), and hypoxia-inducible factors (HIF-1alpha and HIF-2alpha)-ca
250 eased under hypoxic conditions and following hypoxia-inducible factor (HIF1) induction, suggesting th
251 or mTOR, NAD(+)-dependent deacetylase SIRT1, hypoxia-inducible factor HIF1alpha, oxidative stress-ind
252 ow the critical importance of high levels of hypoxia-inducible factor, HIF2alpha/EPAS1, and the nucle
256 which targets hydroxylated alpha subunit of hypoxia inducible factors (HIFs) for ubiquitination and
258 ed mechanism of response to hypoxia involves hypoxia inducible factors (HIFs), which are stabilized b
260 1), AMP-activated protein kinase (AMPK), and hypoxia inducible factors (HIFs; especially HIF-2alpha);
262 tion in response to oxygen fluctuations, and hypoxia-inducible factors (HIFs) are central mediators o
265 in the VHL tumor suppressor stabilizing the hypoxia-inducible factors (HIFs) are the most prevalent
266 nsive changes in gene expression mediated by Hypoxia-Inducible Factors (HIFs) contribute significantl
267 a has been shown to up-regulate MALAT1, only hypoxia-inducible factors (HIFs) have been implicated in
268 esults in the constitutive activation of the hypoxia-inducible factors (HIFs) HIF-1 and HIF-2 and the
269 (PHD1 to PHD3) regulate the activity of the hypoxia-inducible factors (HIFs) HIF-1 and HIF-2, transc
271 that APAP challenge caused stabilization of hypoxia-inducible factors (HIFs) in the liver and hepati
273 oiesis and leukemogenesis are dependent upon hypoxia-inducible factors (HIFs), a family of essential
275 l fatty acid (FA) transport, is repressed by hypoxia-inducible factors (HIFs), reducing FA oxidation
276 ecules including proteins that interact with hypoxia-inducible factors (HIFs), transcription factors
283 oxia, a cellular adaptive response activates hypoxia-inducible factors (HIFs; HIF-1 and HIF-2) that r
284 , we report that hypoxia induces a rapid and hypoxia-inducible factor-independent induction of histon
285 ligand 26 production in cancer cells by the hypoxia-inducible factor inhibitor digoxin or blockade o
286 iological processes, including regulation of hypoxia-inducible factor-mediated adaptation to hypoxia,
290 A (protein phosphatase 2) regulates the HIF (hypoxia-inducible factor)/PHD-2 (prolyl hydroxylase 2)-c
292 or other 2OG oxygenases, e.g. screens of the hypoxia-inducible factor prolyl-hydroxylase inhibitors r
293 in-5-yl}benzonitrile-based inhibitors of the hypoxia-inducible factor prolylhydroxylase domain-1 (PHD
294 with a focus on its relations with VEGF and hypoxia inducible factor related angiogenesis pathways,
295 hases cysl-1 and cysl-2 and the regulator of hypoxia inducible factor rhy-1 in progeny, and that thes
297 caused by the hypoxic induction of the HIF (hypoxia-inducible factor) transcription factor or the 2-
298 Increased VE-PTP expression was dependent on hypoxia-inducible factor transcriptional activity in viv
300 tress management is under the control of the Hypoxia Inducible Factors, whose activity depends on the