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1 her miR-33b is induced during or involved in adipogenesis.
2 nesis, while antagonizing PPARgamma-mediated adipogenesis.
3 Siah2 in non-precursor fibroblasts promotes adipogenesis.
4 d autonomous differentiation and accelerated adipogenesis.
5 l marrow adiposity, due largely to increased adipogenesis.
6 dothelial cells, and hematopoietic cells for adipogenesis.
7 that have previously been reported to induce adipogenesis.
8 It is also the master regulator of adipogenesis.
9 nhibiting bone formation and inducing marrow adipogenesis.
10 ncRNA) NEAT1 signaling network necessary for adipogenesis.
11 oordinated but not in its composition during adipogenesis.
12 th lower expression of genes responsible for adipogenesis.
13 activation of Gq signalling abrogates brown adipogenesis.
14 fferentiation, whereas silencing TNMD blocks adipogenesis.
15 ated with adipocyte hypertrophy and impaired adipogenesis.
16 MM cells shift osteoblast progenitors toward adipogenesis.
17 ids by glycerol fermentation that can induce adipogenesis.
18 zation in coordination with lysosomes during adipogenesis.
19 ucocorticoid signaling to IGF-1 signaling in adipogenesis.
20 ater proliferation, consistent with elevated adipogenesis.
21 d, conversely, its overexpression attenuated adipogenesis.
22 of PPARgamma and Cebpa and driving increased adipogenesis.
23 importance of Dexras1 in IGF-1 signaling in adipogenesis.
24 ymal progenitors cells during white or brown adipogenesis.
25 n and ss-arrestin-mediated proliferation and adipogenesis.
26 ted receptor gamma (Pparg), to induce dermal adipogenesis.
27 noncoding RNA signaling networks involved in adipogenesis.
28 lunted senescent cell-mediated inhibition of adipogenesis.
29 odulate the shedding of DLK1, a regulator of adipogenesis.
30 in relieves the TNFalpha inhibition on brown adipogenesis.
31 indicate the importance of DPP8 and DPP9 on adipogenesis.
32 ed LD size but did not affect TAG storage or adipogenesis.
33 nt beta-adrenergic receptors to induce beige adipogenesis.
34 lular cholesterol reduction in the SC-to-BAT adipogenesis.
35 from FTO knockout (FTO-KO) mice show reduced adipogenesis.
36 mma and C/EBPalpha, the master regulators of adipogenesis.
37 physiological roles for ATXN1 and UBE2E2 in adipogenesis.
38 e II, which limits Cebpa gene expression and adipogenesis.
39 action, energy metabolism, lipid biology and adipogenesis.
40 and adiposity, and enhanced lipogenesis and adipogenesis.
41 ple pathways, including lipid metabolism and adipogenesis.
42 to re-activate adipogenic genes to reverting adipogenesis.
43 erance, vascular inflammation, and augmented adipogenesis.
44 the role of PKCdeltaI splice variant during adipogenesis.
45 er understanding of the role of PKCdeltaI in adipogenesis.
46 co-regulator to control lipid metabolism and adipogenesis.
47 ne whether and how EST plays a role in human adipogenesis.
48 ositively regulates PPARgamma2 stability and adipogenesis.
49 signaling pathways and consequently enhances adipogenesis.
50 receptor (PPARgamma), a master regulator of adipogenesis.
51 PCAF act upstream of PPARgamma to facilitate adipogenesis.
52 ne in the transcriptional system controlling adipogenesis.
53 d in MEF-WT after 5 days of treatment during adipogenesis.
54 s unclear whether the epidermis can regulate adipogenesis.
55 novel and specific roles of GR and CCAR1 in adipogenesis.
56 ing the expression of PKCdeltaI during 3T3L1 adipogenesis.
57 I, have different expression patterns during adipogenesis.
58 Z-dependent osteoblastogenesis and inhibited adipogenesis.
59 ention are boosted by VEGF thereby impairing adipogenesis.
60 e and metabolism, and adipose metabolism and adipogenesis.
61 amma, a TF that serves as a key regulator of adipogenesis.
62 wed impaired osteoblastogenesis and enhanced adipogenesis.
63 ase inhibitor, that inhibited MMP14 to block adipogenesis.
64 gulation of Ppargamma2 expression as well as adipogenesis.
65 P/p300 binding on enhancers activated during adipogenesis.
66 by BMP4 thereby allowing normal induction of adipogenesis.
67 understanding epigenomic regulation of brown adipogenesis.
68 (IMF) are involved in adipose metabolism and adipogenesis.
69 n of GR accelerates, but is dispensable for, adipogenesis.
70 spectrum that includes promoting bone marrow adipogenesis.
71 n action, while in preadipocytes it impaired adipogenesis.
72 ound GR accelerates, but is dispensable for, adipogenesis.
73 human adipocytes cultured in vitro inhibited adipogenesis.
74 r by increasing the number of adipocytes via adipogenesis.
75 pressed canonical Wnt signaling and enhanced adipogenesis.
76 genuine PPARgamma activators and inducers of adipogenesis.
77 duced osteogenesis and inhibits BMP2-induced adipogenesis.
78 brown preadipocytes showed severely delayed adipogenesis 1 week after induction of differentiation.
79 predicted to be active by the ToxPi promoted adipogenesis, 1 inhibited adipogenesis, and 2 of the 7 p
80 tiation, Ob-MSCs exhibit evidence of greater adipogenesis (+30% Oil Red O stain [ORO], +50% peroxisom
82 ished generation of beige adipocytes ('beige adipogenesis'), a thermogenic and energy-dissipating fun
84 n unanticipated increase in genes related to adipogenesis, adipokine signaling, and lipoprotein signa
87 preadipocytes but is strongly induced during adipogenesis and actively participates in adipocyte hype
95 These findings indicate a role for DYRK1B in adipogenesis and glucose homeostasis and associate its a
96 Rgamma has been long studied for its role in adipogenesis and glucose metabolism, but the discovery o
98 scriptional regulation in the early phase of adipogenesis and highlight the need of studying adipogen
99 nitiator of a signaling cascade that induces adipogenesis and highlight the role of epidermal Wnt sig
101 protein S-nitrosylation, exhibited decreased adipogenesis and increased osteoblastogenesis compared w
102 secreted protein FSTL1, a protein linked to adipogenesis and inflammation among other functions.
103 ects of salidroside may due to repression of adipogenesis and inflammation in eWAT and stimulation of
104 lly elicited the BMP2 adverse outcomes (i.e. adipogenesis and inflammation) in the mandibular defect
108 st for PPARgamma and RXRalpha activation and adipogenesis and it is likely that many obesogenic chemi
109 hers would demonstrate greater potential for adipogenesis and less potential for myogenesis, driven b
111 e accumulation of triglycerides by promoting adipogenesis and lipogenesis and by shutting down catabo
112 e WNT signaling pathway to the regulation of adipogenesis and low-grade inflammation in obesity.
114 ively regulates the lineage determination of adipogenesis and osteoblastogenesis by demethylating Wnt
117 tion media, these cultured hMSCs can undergo adipogenesis and osteogenesis without requiring cell tra
119 that PPARgamma regulates the balance between adipogenesis and osteogenesis, the roles of additional r
124 TGFbeta pathway in switching off hiPSC-brown adipogenesis and revealed novel factors to unlock their
125 ored the mechanism by which Dexras1 mediates adipogenesis and show a link to the insulin-like growth
127 introduces BA-DEG-BA as an enhancer of ADSC adipogenesis and suggests an integral interaction betwee
128 ncoding RNA signaling network that regulates adipogenesis and that is a potential new target in the p
129 on factor whose expression is induced during adipogenesis and that is required for the acquisition an
130 L4 and CBP identify super-enhancers (SEs) of adipogenesis and that MLL3/MLL4 are required for SE form
131 gamma (PPARgamma) is the master regulator of adipogenesis and the pharmacological target of the thiaz
132 dence for the first time that GPR30 promotes adipogenesis and therefore the development of obesity in
133 that cranberries are capable of suppressing adipogenesis and therefore they seem to be natural bioac
136 the ToxPi promoted adipogenesis, 1 inhibited adipogenesis, and 2 of the 7 predicted negatives were al
138 in expression was decreased by inhibition of adipogenesis, and adipocytes from Camp(-/-) mice lost th
139 lactosidase (Gla), are up-regulated in early adipogenesis, and are transcriptionally controlled by CC
140 We have shown that TIMP3 is downregulated in adipogenesis, and by inflammatory signals in adipocytes.
141 muscle repair and did not induce atrophy or adipogenesis, and was associated with improved muscle fu
147 1 (500 pM) to pre-adipocyte cultures reduced adipogenesis, as assessed by oil red O staining (n=2).
148 rther verified that Tudor-SN is required for adipogenesis, as deletion of Tudor-SN (MEF-KO) impairs d
149 rt that miR-33b is an important regulator of adipogenesis, as inhibition of miR-33b enhanced lipid dr
150 423 (zfp423), a key transcription factor in adipogenesis, as well as lower DNA methylation of its pr
151 roliferation and increased expression of the adipogenesis-associated factors PPARgamma, CEBPalpha, an
152 l alterations, a differentiation bias toward adipogenesis at the detriment of myogenesis and an inhib
153 Activation of PPARgamma by TZDs promotes adipogenesis at the expense of osteoblast formation, con
154 mechanisms of CLA include regulation of (a) adipogenesis, (b) lipid metabolism, (c) inflammation, (d
155 ving cilia from FAPs inhibited intramuscular adipogenesis, both after injury and in a mouse model of
156 function in vivo is to inhibit intramuscular adipogenesis, both through a cell-autonomous and a cell-
157 ay that are transcriptionally induced during adipogenesis but to a lower extent than lipid metabolism
158 ved laminin inhibits their proliferation and adipogenesis, but is indispensable for their myogenesis.
159 ds (PUFAs) is believed to regulate perinatal adipogenesis, but the cellular mechanisms and long-term
160 ogene (c-Abl) is a putative key regulator of adipogenesis, but the underlying mechanism remained obsc
161 nervation of iBAT reduced cold-induced brown adipogenesis by >85%, whereas infusion of norepinephrine
162 sue exert antagonistic effects on PPARG, but adipogenesis by a mixture containing emerging compounds
163 ed local effects of LepR on osteogenesis and adipogenesis by bone marrow stromal cells and systemic e
165 contrast, activation of ER in ASCs inhibited adipogenesis by decreasing the recruitment of the adipog
171 ndings support NEDD4 as a novel regulator of adipogenesis by modulating the stability of PPARgamma.
173 steoblasts and may also increase bone marrow adipogenesis by up-regulation of Pparg2 in the Cx43-defi
175 n of Tfeb or Tfe3 expression during in vitro adipogenesis causes dramatic downregulation of Ppargamma
176 ical functions, including stress resistance, adipogenesis, cell senescence and energy production.
180 define an S6K1-dependent mechanism in early adipogenesis, contributing to the promotion of obesity.
184 dentified ToxCast assays that should predict adipogenesis, developed an adipogenesis ToxPi, and asked
185 ved in CS fat storage, we used two models of adipogenesis differentiation: (i) SGBS pre-adipocytes wi
186 s adipogenesis by regulating events early in adipogenesis, during the process of mitotic clonal expan
187 Differentially expressed genes included key adipogenesis factors which can be used as blubber-specif
190 ent of adipose tissue and are formed through adipogenesis from precursor mesenchymal stem cells.
191 ger by volume and contained higher levels of adipogenesis gene transcripts, indicating enhanced adipo
194 Beige adipocytes can form through de novo adipogenesis; however, how "beiging" characteristics are
195 Polyamines were demonstrated necessary for adipogenesis; however, the underlying mechanism by which
196 rison of MLL4-defined SEs in brown and white adipogenesis identifies brown-specific SE-associated gen
200 tiation, evidenced by increased induction of adipogenesis in cholesterol-depleted SC from both LCAT-K
201 dogenous KLF4 and Krox20 are dispensable for adipogenesis in culture and for brown adipose tissue dev
202 endogenous KLF4 and Krox20 are required for adipogenesis in culture and in vivo Using conditional kn
203 s have been shown to be capable of promoting adipogenesis in culture when they are overexpressed.
208 apoptosis in liposarcoma cells and promoted adipogenesis in human adipose-derived stem cells (ASC).
209 ions identify a novel tissue niche for brown adipogenesis in iBAT and further define depot-specific m
214 mmation-driven inhibitory mechanism of beige adipogenesis in obesity that required direct adhesive in
217 the DPP8/9 selective inhibitor 1G244 blocks adipogenesis in preadipocyte 3T3-L1 and 3T3-F422A, while
218 ic and circadian regulation known to promote adipogenesis in preadipocytes, in HSC transdifferentiati
219 P diverted osteogenic differentiation toward adipogenesis in primary mouse bone marrow cultures.
220 nscription factor (TF) activity orchestrates adipogenesis in response to chemical cues, yet how cell-
221 Thus, reduction of Sirt1 activity restores adipogenesis in Sirt7(-/-) adipocytes in vitro and in vi
225 nd transcriptional activities and attenuates adipogenesis in various genetic and cell-based models.
227 mponent of the paraspeckle complex, promotes adipogenesis in vitro and is important for mature adipoc
229 , miR-378 and Pde1b inversely regulate brown adipogenesis in vitro in the absence of phosphodiesteras
231 These results clarify the role of GR in adipogenesis in vivo and demonstrate that DEX-mediated a
232 remained unclear whether GR is required for adipogenesis in vivo By deleting GR in precursors of bro
234 e expression of several factors that control adipogenesis, including Wnt pathway genes, beta-catenin,
235 hese findings suggest Ptn's novel role as an adipogenesis inducer with a therapeutic potential in sof
236 ulating PPARgamma and C/EBPalpha not only in adipogenesis induction medium, but also in chemically de
237 ering the regulation of pathways influencing adipogenesis, insulin sensitivity, and lipid metabolism.
243 that de novo synthesis of polyamines during adipogenesis is required for down-regulation of CHOP to
244 aveling the regulatory mechanisms underlying adipogenesis is therefore highly relevant from a biomedi
247 ulation of subcutaneous adipose tissue (SAT) adipogenesis/lipogenesis in obese adolescents with alter
248 GR-deficient preadipocytes showed levels of adipogenesis marker expression and lipid accumulation si
249 alysis showed upregulated expression of some adipogenesis markers in visceral adipose tissue (VAT) of
250 -1 to stimulate Wnt signaling and to repress adipogenesis may highlight new treatment approaches for
252 age-related switch between osteogenesis and adipogenesis of BMSCs and may represent a potential ther
256 , transcriptome and chromatin opening during adipogenesis of immortalized preadipocytes derived from
257 cysteine dioxygenase type 1 (Cdo1) promoted adipogenesis of primary mouse bone marrow stromal cells
261 novel function of Ffar4 in modulating brown adipogenesis partly through a mechanism involving cAMP a
262 ession of major transcription factors of the adipogenesis pathway, such as PPARgamma, C/EBPalpha and
266 ese, Tfeb and Tfe3, control the regulator of adipogenesis, peroxisome proliferator-activated receptor
268 increases the expression of genes related to adipogenesis preventing adipocytes from becoming hypertr
269 treatment of diabetic mice with P5 increased adipogenesis, reduced adipose tissue inflammation as wel
274 ated cells toward osteogenesis and away from adipogenesis requires intact canonical Wnt signaling.
277 Removal of beta-catenin causes MMPs to favor adipogenesis, resulting in osteopenia coupled with incre
278 postoperative inflammation and inappropriate adipogenesis, resulting in well-documented life-threaten
280 tethering, but did not affect osteogenesis, adipogenesis, surface-protein unfolding or underlying su
281 4, DKK2) and pathways (melatonin signalling, adipogenesis) that are likely to be implicated in the ke
282 our study reveals that Gcn5/PCAF facilitate adipogenesis through regulation of PPARgamma expression
283 ay an essential role in orchestrating dermal adipogenesis through secreting Sonic Hedgehog (SHH).
284 Erk1/2) activity, which otherwise suppresses adipogenesis through the phosphorylation of PPARgamma.
288 at should predict adipogenesis, developed an adipogenesis ToxPi, and asked how well the ToxPi predict
289 e evidence that LS mutant expression impairs adipogenesis, triggers energy expenditure, and enhances
291 expression of nuclear receptors involved in adipogenesis underlie the differences between OP9 and 3T
293 ological roles of WNT4 and WNT5A involved in adipogenesis, we aimed to investigate whether SNPs in WN
296 lity of ASCs at early but not late stages of adipogenesis, which can be reversed by antagonism of RA
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