コーパス検索結果 (１語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 ansgenic mice, which have a genetic block in adipogenesis.
2 n T cell homing factors, erythropoiesis, and adipogenesis.
3 -3 fatty acid receptor FFAR4/GPR120 promotes adipogenesis.
4 regarding the role of steroid metabolism in adipogenesis.
5 d C/EBPdelta, PAGR1 plays a critical role in adipogenesis.
6 acid metabolism, xenobiotic metabolism, and adipogenesis.
7 n stimulates physiological processes such as adipogenesis.
8 NA levels were decreased dramatically during adipogenesis.
9 es and is potentially involved in regulating adipogenesis.
10 amily members may play a role also in normal adipogenesis.
11 ces liposarcoma cell viability and increases adipogenesis.
12 transcriptional and epigenomic regulators of adipogenesis.
13 ssion is regulated by DNA methylation during adipogenesis.
14 A 34c, a microRNA functionally implicated in adipogenesis.
15 tify novel factors and mechanisms regulating adipogenesis.
16 ne ear mesenchymal stem cells (EMSCs) during adipogenesis.
17 Moreover, Bcl2l13 prevented apoptosis during adipogenesis.
18 aracrine loop to activate SMAD2 and suppress adipogenesis.
19 PPARgamma), a key physiological regulator of adipogenesis.
20 ation of PPARgamma and CEBPalpha to initiate adipogenesis.
21 ids by glycerol fermentation that can induce adipogenesis.
22 ymal progenitors cells during white or brown adipogenesis.
23 nt beta-adrenergic receptors to induce beige adipogenesis.
24 physiological roles for ATXN1 and UBE2E2 in adipogenesis.
25 Z-dependent osteoblastogenesis and inhibited adipogenesis.
26 ention are boosted by VEGF thereby impairing adipogenesis.
27 e and metabolism, and adipose metabolism and adipogenesis.
28 amma, a TF that serves as a key regulator of adipogenesis.
29 wed impaired osteoblastogenesis and enhanced adipogenesis.
30 ase inhibitor, that inhibited MMP14 to block adipogenesis.
31 gulation of Ppargamma2 expression as well as adipogenesis.
32 P/p300 binding on enhancers activated during adipogenesis.
33 by BMP4 thereby allowing normal induction of adipogenesis.
34 y deficiency in adipose tissue have impaired adipogenesis.
35 understanding epigenomic regulation of brown adipogenesis.
36 (IMF) are involved in adipose metabolism and adipogenesis.
37 establish tissue- specific expression during adipogenesis.
38 n of GR accelerates, but is dispensable for, adipogenesis.
39 spectrum that includes promoting bone marrow adipogenesis.
40 n action, while in preadipocytes it impaired adipogenesis.
41 ound GR accelerates, but is dispensable for, adipogenesis.
42 n decreases collagen alignment and increases adipogenesis.
43 human adipocytes cultured in vitro inhibited adipogenesis.
44 r by increasing the number of adipocytes via adipogenesis.
45 pressed canonical Wnt signaling and enhanced adipogenesis.
46 EBPbeta and C/EBPdelta in the early phase of adipogenesis.
47 genuine PPARgamma activators and inducers of adipogenesis.
48 duced osteogenesis and inhibits BMP2-induced adipogenesis.
49 her miR-33b is induced during or involved in adipogenesis.
50 nesis, while antagonizing PPARgamma-mediated adipogenesis.
51 Siah2 in non-precursor fibroblasts promotes adipogenesis.
52 d autonomous differentiation and accelerated adipogenesis.
53 l marrow adiposity, due largely to increased adipogenesis.
54 dothelial cells, and hematopoietic cells for adipogenesis.
55 that have previously been reported to induce adipogenesis.
56 It is also the master regulator of adipogenesis.
57 nhibiting bone formation and inducing marrow adipogenesis.
58 and H2B-Ser36 phosphorylation that controls adipogenesis.
59 ncRNA) NEAT1 signaling network necessary for adipogenesis.
60 oordinated but not in its composition during adipogenesis.
61 th lower expression of genes responsible for adipogenesis.
62 activation of Gq signalling abrogates brown adipogenesis.
63 fferentiation, whereas silencing TNMD blocks adipogenesis.
64 ated with adipocyte hypertrophy and impaired adipogenesis.
65 FRbeta also enhances white, brown, and beige adipogenesis.
66 ytoskeleton dynamics have been implicated in adipogenesis.
67 of small GTPases were down-regulated during adipogenesis.
68 implicated in oxidative phosphorylation and adipogenesis.
69 th cartilage and bone lineages, but inhibits adipogenesis.
70 enescence emerged, impairing later stages of adipogenesis.
71 esis, and signatures from immobile MPCs with adipogenesis.
72 induction of PPARgamma and C/EBPalpha during adipogenesis.
73 nd C/EBPdelta and leads to severe defects in adipogenesis.
74 tment but not the maintenance phase of beige adipogenesis.
75 t plays important roles in tumorigenesis and adipogenesis.
76 Cebpa promoter-proximal binding site during adipogenesis.
77 shared by both white adipogenesis and brown adipogenesis.
78 e enriched for oxidative phosphorylation and adipogenesis.
79 patient adipose derived stromal cell (PASC) adipogenesis.
80 e tissue progenitor cells to undergo de novo adipogenesis.
81 inhibits osteoblastogenesis, while promoting adipogenesis.
82 brown preadipocytes showed severely delayed adipogenesis 1 week after induction of differentiation.
83 predicted to be active by the ToxPi promoted adipogenesis, 1 inhibited adipogenesis, and 2 of the 7 p
84 tiation, Ob-MSCs exhibit evidence of greater adipogenesis (+30% Oil Red O stain [ORO], +50% peroxisom
86 ished generation of beige adipocytes ('beige adipogenesis'), a thermogenic and energy-dissipating fun
88 provide an update on the role of lncRNAs in adipogenesis and adipose tissue function to promote iden
89 natal mosaic deletion of PDGFRalpha enhances adipogenesis and adult deletion enhances beta3-adrenergi
91 e that GPAT3 plays a modest positive role in adipogenesis and argue against the potential of GPAT inh
92 s a positive regulator of insulin action and adipogenesis and as a potential therapeutic target for c
95 pendent loss of dermal fat and a decrease in adipogenesis and cathelidicin production in response to
100 mous TGFbeta signaling in ASCs to facilitate adipogenesis and healthy remodeling in Abdsc and these p
102 scriptional regulation in the early phase of adipogenesis and highlight the need of studying adipogen
104 adipose tissue (AT) expansion by suppressing adipogenesis and increasing gluteal adipocyte susceptibi
105 secreted protein FSTL1, a protein linked to adipogenesis and inflammation among other functions.
106 lly elicited the BMP2 adverse outcomes (i.e. adipogenesis and inflammation) in the mandibular defect
107 we found that NKX1-2 both promotes ST2 cell adipogenesis and inhibits their osteoblastogenic differe
108 is occurs through a mechanism independent of adipogenesis and involves FGF receptor-3 (FGFR3), prosta
113 ively regulates the lineage determination of adipogenesis and osteoblastogenesis by demethylating Wnt
115 tion media, these cultured hMSCs can undergo adipogenesis and osteogenesis without requiring cell tra
117 sults support a role for NKX1-2 in promoting adipogenesis and possibly in regulating the balance betw
119 ancy and lactation could promote brown/beige adipogenesis and protect against HFD-induced adiposity i
120 ighlight the role of SWI/SNF bromodomains in adipogenesis and provide a framework for the development
122 exhibited dynamic expression patterns during adipogenesis and robust expression in mature human adipo
123 ored the mechanism by which Dexras1 mediates adipogenesis and show a link to the insulin-like growth
125 introduces BA-DEG-BA as an enhancer of ADSC adipogenesis and suggests an integral interaction betwee
126 ncoding RNA signaling network that regulates adipogenesis and that is a potential new target in the p
127 L4 and CBP identify super-enhancers (SEs) of adipogenesis and that MLL3/MLL4 are required for SE form
129 lin also acts on inflammation, appetite, and adipogenesis and therefore has been considered a promisi
130 dence for the first time that GPR30 promotes adipogenesis and therefore the development of obesity in
132 the ToxPi promoted adipogenesis, 1 inhibited adipogenesis, and 2 of the 7 predicted negatives were al
134 ional network that is dissociated from brown adipogenesis, and act to modulate systemic energy metabo
135 lls do not significantly contribute to adult adipogenesis, and deleting Pdgfra in adult adipose linea
136 a gene expression signature consistent with adipogenesis, and the phospholipid-binding protein annex
137 nic stem cells showed a dramatic decrease in adipogenesis, and the resulting adipocytes exhibited low
138 muscle repair and did not induce atrophy or adipogenesis, and was associated with improved muscle fu
139 alterations in small GTPase proteome during adipogenesis, and we reveal a previously unrecognized ro
144 rt that miR-33b is an important regulator of adipogenesis, as inhibition of miR-33b enhanced lipid dr
145 Thy1 locus have increased methylation during adipogenesis, as well as increased methylation in adipos
146 423 (zfp423), a key transcription factor in adipogenesis, as well as lower DNA methylation of its pr
147 vascular (SV) cells revealed increased beige adipogenesis associated with increased thermogenic gene
149 l alterations, a differentiation bias toward adipogenesis at the detriment of myogenesis and an inhib
150 ne suppressed TGFbeta signaling and enhanced adipogenesis, at least in part by increasing TGFBR3 prot
152 mechanisms of CLA include regulation of (a) adipogenesis, (b) lipid metabolism, (c) inflammation, (d
153 e highlight the role of mTOR in lipogenesis, adipogenesis, beta-oxidation of lipids, and ketosis of c
154 ving cilia from FAPs inhibited intramuscular adipogenesis, both after injury and in a mouse model of
155 ved laminin inhibits their proliferation and adipogenesis, but is indispensable for their myogenesis.
156 ds (PUFAs) is believed to regulate perinatal adipogenesis, but the cellular mechanisms and long-term
157 sue exert antagonistic effects on PPARG, but adipogenesis by a mixture containing emerging compounds
158 ed local effects of LepR on osteogenesis and adipogenesis by bone marrow stromal cells and systemic e
159 lly, H3.3K4M prevents enhancer activation in adipogenesis by destabilizing MLL3/4 proteins but not ot
160 ecently, seipin has been reported to promote adipogenesis by directly inhibiting GPAT3, leading to th
162 the mitochondrial receptor Bcl2l13 promotes adipogenesis by increasing oxidative phosphorylation, su
163 onal findings suggested that NKX1-2 promotes adipogenesis by inhibiting expression of the antiadipoge
166 t saturated fatty acids, trigger mitosis and adipogenesis by rapidly activating cAMP production insid
168 m cell differentiation at the early stage of adipogenesis cause a change in the nuclear morphology an
169 n of Tfeb or Tfe3 expression during in vitro adipogenesis causes dramatic downregulation of Ppargamma
170 ical functions, including stress resistance, adipogenesis, cell senescence and energy production.
174 define an S6K1-dependent mechanism in early adipogenesis, contributing to the promotion of obesity.
177 involved in triglyceride (TG) synthesis and adipogenesis decreased, and this was associated with gre
181 Differentially expressed genes included key adipogenesis factors which can be used as blubber-specif
183 ent of adipose tissue and are formed through adipogenesis from precursor mesenchymal stem cells.
184 ) mice, we found reduced expression of brown adipogenesis genes, whereas myogenesis genes were not af
185 vestigate role for macrophages in modulating adipogenesis, HA production, and contractility in orbita
186 in understanding of epigenomic regulation of adipogenesis have revealed critical roles of histone met
187 Studies on the transcriptional regulation of adipogenesis highlight the importance of investigating a
190 Beige adipocytes can form through de novo adipogenesis; however, how "beiging" characteristics are
191 O pathogenesis, which includes inflammation, adipogenesis, hyaluronic acid (HA) secretion, and fibros
192 n, suppressing other relevant key drivers of adipogenesis (i.e., PPARgamma, PGC-1alpha), presumably b
193 rison of MLL4-defined SEs in brown and white adipogenesis identifies brown-specific SE-associated gen
198 NA methylation alters Thy1 expression during adipogenesis in both mouse 3T3-L1 preadipocytes and mous
200 dogenous KLF4 and Krox20 are dispensable for adipogenesis in culture and for brown adipose tissue dev
201 endogenous KLF4 and Krox20 are required for adipogenesis in culture and in vivo Using conditional kn
202 s have been shown to be capable of promoting adipogenesis in culture when they are overexpressed.
207 apoptosis in liposarcoma cells and promoted adipogenesis in human adipose-derived stem cells (ASC).
209 mmation-driven inhibitory mechanism of beige adipogenesis in obesity that required direct adhesive in
212 a and PPARdelta subtypes and did not promote adipogenesis in primary human fibroblasts, discriminatin
213 Thus, reduction of Sirt1 activity restores adipogenesis in Sirt7(-/-) adipocytes in vitro and in vi
216 in the phenomenon of bone loss and increased adipogenesis in some patients during long-term carbamaze
219 nd transcriptional activities and attenuates adipogenesis in various genetic and cell-based models.
221 mponent of the paraspeckle complex, promotes adipogenesis in vitro and is important for mature adipoc
222 A-seq profiles of human preadipocytes during adipogenesis in vitro identifies at least two distinct c
223 These results clarify the role of GR in adipogenesis in vivo and demonstrate that DEX-mediated a
224 remained unclear whether GR is required for adipogenesis in vivo By deleting GR in precursors of bro
226 ARgamma) and C/EBPalpha and are required for adipogenesis in vivo However, the mechanism that control
228 namics contribute to the inhibition of beige adipogenesis in WAT, and also promotes age-related and d
229 n blocked the expression of key genes during adipogenesis, including the transcription factors PPARga
230 hese findings suggest Ptn's novel role as an adipogenesis inducer with a therapeutic potential in sof
231 ulating PPARgamma and C/EBPalpha not only in adipogenesis induction medium, but also in chemically de
232 Rab32 in 3T3-L1 and C3H10T1/2 cells prior to adipogenesis induction suppressed their differentiation.
235 the ability to recruit new fat cells through adipogenesis is a critical determinant of healthy adipos
244 3 insulin-sensitizing mechanisms, including adipogenesis, lipid metabolism, and insulin signaling.
246 to the adipose compartments, with effects on adipogenesis, lipolysis, and ectopic fat accumulation.
247 GR-deficient preadipocytes showed levels of adipogenesis marker expression and lipid accumulation si
248 alysis showed upregulated expression of some adipogenesis markers in visceral adipose tissue (VAT) of
250 derstanding of adipose stem cell biology and adipogenesis may lead to novel strategies to uncouple ob
258 , transcriptome and chromatin opening during adipogenesis of immortalized preadipocytes derived from
262 and changes in genomic architecture favoring adipogenesis over osteogenesis, resulting in decreased f
264 novel function of Ffar4 in modulating brown adipogenesis partly through a mechanism involving cAMP a
265 ese, Tfeb and Tfe3, control the regulator of adipogenesis, peroxisome proliferator-activated receptor
272 Removal of beta-catenin causes MMPs to favor adipogenesis, resulting in osteopenia coupled with incre
273 postoperative inflammation and inappropriate adipogenesis, resulting in well-documented life-threaten
276 ed nuclear shape did not efficiently undergo adipogenesis, suggesting the cellular and nuclear proces
277 4, DKK2) and pathways (melatonin signalling, adipogenesis) that are likely to be implicated in the ke
279 /protein kinase B signaling is important for adipogenesis, the role of regulated development of DNA d
281 peripheral adipose tissue, adenosine induces adipogenesis through peripheral adenosine A(1) receptor
282 MSCs and PASCs produced a robust increase in adipogenesis through the direct targeting of the circadi
283 Erk1/2) activity, which otherwise suppresses adipogenesis through the phosphorylation of PPARgamma.
286 nhanced preadipocyte proliferation, in vitro adipogenesis, transcription of Retn, and resistin secret
288 expression of nuclear receptors involved in adipogenesis underlie the differences between OP9 and 3T
289 nantly from progenitors (i.e., de novo beige adipogenesis) upon the first exposure to cold temperatur
291 on stimulated 3T3L1 cell differentiation and adipogenesis via increased protein S-glutathionylation o
293 ological roles of WNT4 and WNT5A involved in adipogenesis, we aimed to investigate whether SNPs in WN
294 he soy isoflavones genistein and daidzein on adipogenesis were examined in cell-based assays using th
297 lity of ASCs at early but not late stages of adipogenesis, which can be reversed by antagonism of RA
298 recapitulated the effects of pioglitazone on adipogenesis, which was p66Shc independent, and double k
300 transcriptional and epigenomic regulation of adipogenesis, with a focus on factors and mechanisms sha