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1 expression of atrophic factors like Mstn and activin.
2 low upregulation of FoxA2 in the presence of Activin.
3  premature differentiation after exposure to Activin.
4 negatively regulated by myostatin (MSTN) and activins.
5 e previously demonstrated involvement of the activin 2a receptor in drug taking, the role of its liga
6 tigations showed that manipulating levels of activin A (INHBA) could rescue or compromise the RUNX2-m
7 incipient mesoderm-like cells (iMeLCs) using activin A and a WNT pathway agonist.
8 ght weeks after AAV injection, inhibition of activin A and activin B signaling produced moderate ( ap
9 on protocol uses different concentrations of activin A and bone morphogenetic protein 4 (BMP4) to pol
10       Here we have studied the activation of activin A and determined crystal structures of the unpro
11 ne morphogenetic protein-4 and inhibitors of activin A and fibroblast growth factor-2 signaling (BAP
12                                              Activin A and GluN2B-containing NMDARs have both previou
13 d liver) identified interactions between the activin A and IL6 signaling pathways.
14 otoxemia and endotoxin-induced expression of activin A and inducible T-cell costimulator ligand.
15                            Here, we identify Activin A and its antagonist follistatin as key regulato
16                                      We show activin A and other high affinity ligands directly inhib
17  molecules, involving IL-12p70 for IL-21 and activin A and TGFbeta for CXCL13.
18 was found to be mediated by the secretion of activin A and the low levels of IL-10 produced by M16.
19 file through PI3K-mediated downregulation of activin A and upregulation of MAFB, a critical transcrip
20                                     MSTN and activin A are capable of signaling through a complex of
21 screen of a human protein library identified activin A as a potent regulator of TFH cell differentiat
22                      Altogether, we identify activin A as a second negative regulator of muscle mass,
23 mor cells stimulated their growth through an activin A autocrine signaling pathway, a hypothesis conf
24 s, such as injury and wound healing, and how activin A could elicit disease phenotypes such as cancer
25 cts of activin A in skeletal muscle, whereas activin A curbed the IL6-induced acute-phase response in
26 in basic fibroblast growth factor (bFGF) and activin A develop as epiblast-like cells (EpiLCs) and ga
27                                    Moreover, activin A does not affect cocaine seeking on AD1 but reg
28 inflammatory profile by virtue of their high activin A expression unless additional anti-inflammatory
29                               We demonstrate activin A functions as a competitive inhibitor that bloc
30                                              Activin A functions in BMP signaling in two ways: it eit
31 culating levels of the tumorkines IL6 and/or activin A in animals in the absence of tumors as a tacti
32 , IL6 exacerbated the detrimental effects of activin A in skeletal muscle, whereas activin A curbed t
33 posure significantly increased the levels of activin A in the NAc of animals that had self-administer
34 oncentrations of the closely related protein activin A increased in parallel with hepcidin in serum f
35                             Mouse fat tissue activin A increased with aging.
36        Then we found that stromally-secreted activin A induced ligand-dependent CRC epithelial cell m
37 uppressed growth of HBV in cell culture, and activin A inhibited Zika virus replication alone and in
38 (ACVR2B/Fc) to test the effects of myostatin/activin A inhibition in the R6/2 mouse model of HD.
39 th factor-beta (TGF-beta) superfamily member activin A is increased in the DH on abstinence day (AD)
40                                 Secretion of activin A is known to be higher in tissues with a high M
41                            Here we show that activin A is the long-sought second negative muscle regu
42                           In addition, serum activin A levels are significantly increased in metastat
43                                              Activin A levels in the NAc were assessed via ELISA and
44  has the ability to respond to both Bmp7 and Activin A ligands.
45  weeks, whereas mice with elevated levels of activin A lost 11% of their body weight.
46       These functions could help explain how activin A modulates physiological signaling during extra
47 role of the NSC, we generated 'agonist-only' Activin A muteins that activate ACVR1B but cannot form t
48                                              Activin A orchestrated the expression of multiple genes
49                                     Blocking activin A partially restored lipid accumulation and expr
50   Analysis of body composition revealed that activin A primarily triggered loss of lean mass, whereas
51      JAK inhibitor suppressed senescent cell activin A production and blunted senescent cell-mediated
52                                     In fact, activin A receptor blockade during the M-CSF-driven diff
53                                              Activin A receptor type 1 (ACVR1) is a BMP type 1 recept
54 horylation of SMAD2 via the type 1 receptors activin A receptor type 1B (ALK4), TGFBR1, and activin A
55 eral disease-related microRNAs targeting the activin A receptor type 1C (ACVR1C), a component of the
56 tivin A receptor type 1B (ALK4), TGFBR1, and activin A receptor type 1C (ALK7).
57 eceptor-mediated phosphorylation of SMAD1 by activin A receptor type 1L, bone morphogenetic protein r
58 their interactions with the type II receptor activin A receptor type 2B (ActRIIB).
59 dorsomorphin homolog 1 (DMH1) or CRISPR/Cas9 activin A receptor type I (ACVR1) knockout in OPCs.
60 ocarcinomas contain somatic mutations in the activin A receptor type IB (ACVR1B) gene, indicating tha
61 the bone morphogenic protein receptor kinase activin A receptor, type I (ACVR1), and the subsequent r
62                          Next, we found that activin A regulates phosphorylation of NMDA receptor (NM
63 that CAF-generated mechanical forces lead to activin A release and associated downstream effects.
64 P(+) astrocytes that were immunopositive for activin A remained unaltered.
65 signaling pathway, a hypothesis confirmed by activin A secretion in cultured GCT cells, which prolife
66 hypothesis, we first determined that stromal activin A secretion increased with increasing substrate
67 P8B broadly support human SPG culture, while activin A selectively supports more advanced human SPG.
68        Our high-resolution structures of pro-activin A share features seen in the pro-TGF-beta1 and p
69                      Inhibition of myostatin/activin A signaling activated transcriptional profiles t
70 va (FOP) provides a unique window into ACVR1/Activin A signaling because in that disease Activin can
71  to investigate the effect of targeting MSTN/activin A signaling in mice that were sent to the Intern
72                  Systemic inhibition of MSTN/activin A signaling using a soluble form of the activin
73 genetic approaches, that a local gradient of Activin A signaling within the auditory sensory epitheli
74  relying on the induction and utilization of activin A signaling.
75                                              Activin A specific inhibition, on top of GDF8 inhibition
76 partial signaling blockade upon myostatin or activin A stimulation, and this leads to only a small in
77  with DeltamiR-UL148D are more responsive to activin A stimulation, as demonstrated by their increase
78                        Furthermore, BMP6 and activin A suppressed growth of HBV in cell culture, and
79 n rate was positively correlated with a high activin A to inhibin A ratio.
80 ombination of T3SS-mediated GMT delivery and Activin A treatment showed an additive effect, resulting
81                      TFH cell programming by activin A was antagonized by the cytokine IL-2.
82                                              Activin A's ability to drive TFH cell differentiation in
83                                              Activin A, a TGF-beta family member, is a strong pro-met
84 83 binds and potently neutralizes myostatin, activin A, activin B and growth differentiation factor 1
85 ally-aged INK-ATTAC mice reduced circulating activin A, blunted fat loss, and enhanced adipogenic tra
86 of hPSCs into definitive endoderm (DE) using activin A, followed by the generation of free-floating 3
87 ptor in drug taking, the role of its ligand, activin A, in cocaine relapse is unknown.
88 ese data suggest that increased secretion of activin A, particularly from microglia, in the NAc repre
89 proved JAK1/2 inhibitor, reduced circulating activin A, preserved fat mass, reduced lipotoxicity, and
90 tivin antagonists were then shown to inhibit activin A-mediated cell proliferation in ex vivo ovary c
91 is also independently validated by profiling activin A-secreted protein.
92 glia in the NAc that were immunopositive for activin A.
93 ted signaling proteins, myostatin (MSTN) and activin A.
94 sive to the noncanonical inflammatory ligand Activin A.
95 reted levels of the inhibin betaA homodimer, activin A.
96 ed in the presence of high concentrations of activin A.
97 with that of another TGF-beta family member, activin A.
98 s of ACVR1C receptor and its ligands (Nodal, Activin A/B, and GDF3) were expressed in six retinoblast
99 tiated following treatment with the chimeric Activin A/BMP2 ligand AB235.
100                                              Activin, a member of the transforming growth factor-beta
101 paB activity is required to upregulate INHBA/Activin, a morphogen in the TGFbeta superfamily.
102 we report that therapeutic administration of activin-A ameliorates disease severity and alleviates CN
103                       These findings uncover activin-A as a critical controller of Th17 cell pathogen
104              Here, we show that the cytokine activin-A instructs the generation of CD4(+) T cells tha
105 translational relevance, we demonstrate that activin-A is induced in the CNS of individuals with MS a
106                        Notably, we show that activin-A negatively regulates the metabolic sensor, hyp
107    Moreover, mechanistic studies reveal that activin-A signaling induces the activation of the transc
108                                     In fact, activin-A signaling through activin-like kinase-4 recept
109 atory T (Treg) cells induced by the cytokine activin-A suppress TH2-mediated allergic responses and l
110            In fact, IRF4 silencing abrogates activin-A-driven IL10 and ICOS up-regulation and impairs
111             Overall, our findings uncover an activin-A-induced IRF4-aryl hydrocarbon receptor (AhR)-d
112                        Still, the effects of activin-A-induced regulatory T (Act-A-iTreg) cells on th
113  and CD73 ectonucleotidases is essential for activin-A-induced suppression of the pathogenic signatur
114                                     Finally, activin-A-induced TFH programming was dependent on signa
115 d impairs the suppressive functions of human activin-A-induced Tr1-like (act-A-iTr1) cells.
116 heir expression in Th17 cells in response to activin-A.
117 -binding EGF-like growth factor (HB-EGF) and activin AB in LTBI samples.
118 However, antibody-mediated neutralization of activin activity during murine malaria infection did not
119 y is perturbed in malaria infection but that activins, although raised in malaria infection, may not
120 d in muscle atrophy, such as angiotensin-II, activin and Acvr2b, in SIRT6 depleted cells.
121                  TGFbeta superfamily ligands Activin and BMP, which coordinate with WNT signaling to
122              Previous studies show that both activin and Bmp4 act as crucial mesenchymal odontogenic
123           Signaling driven by TGFbeta ligand Activin and constitutively active receptors Alk4 and Alk
124                                    Targeting activin and its related signaling pathways holds promise
125                    Remarkably, codelivery of activin and myostatin inhibitors induced a synergistic r
126                               In conclusion, activin and TGF-beta are strongly connected signaling pa
127  most prominent TGF-beta superfamily members activin and TGF-beta in advanced colorectal cancer.
128 e-based assay that combined serum and tissue activin and TGF-beta ligand levels predicts outcome in C
129                           mRNA expression of activin and TGF-beta pathway members were queried in sil
130 tor expression is common in solid tumors for activin and TGF-beta pathway members.
131                                    Assessing activin and TGF-beta signaling as a unit yields importan
132 ng growth factor-beta superfamily, including activins and growth differentiation factors (GDFs), is a
133  and cancer cachexia, combined inhibition of activins and myostatin increased mass or prevented muscl
134                                    TGF-beta, activins, and growth differentiation factors exert inhib
135 t to determine whether intervention with the Activin antagonist Follistatin can ameliorate the diabet
136                              These potential activin antagonists were then shown to inhibit activin A
137                            Myostatin and the activins are capable of binding to both ActRIIA and ActR
138                                              Activins are growth factors with multiple roles in the d
139                                              Activins are members of the TGF-beta superfamily and dri
140 GF-beta family ligands myostatin, GDF11, and activins are negative regulators of skeletal muscle mass
141  Like all TGF-beta family of growth factors, activins are synthesized as large precursors from which
142      However, structural information for how activins assemble a ternary receptor complex is lacking.
143 d potently neutralizes myostatin, activin A, activin B and growth differentiation factor 11 (GDF11).
144 d muscle reduced the serum concentrations of Activin B and improved glycemic control in the db/db mou
145 egulated concomitant with down-regulation of activin B during tumorigenesis, suggestive of functional
146               In the absence of uterine FST, activin B expression and signaling are up-regulated, and
147  expression of BMP2 in human hepatocytes and activin B in mouse liver.
148 r AAV injection, inhibition of activin A and activin B signaling produced moderate ( approximately 20
149       Overexpression of Inhbb or addition of activin B stimulates rat islet cell and beta-cell prolif
150 of Plasmodium berghei-infected mice; hepatic activin B was also upregulated at peak parasitemia durin
151 nd and inhibited the TGF-beta family ligands Activin B, BMP-6, and BMP-7, but not the frog Cerberus l
152 dentify candidate miRNAs that might regulate activin B, the principal ligand for ALK7, identifying th
153                                 In contrast, activin B, which can signal through the BMP/SMAD pathway
154 w that pro-apoptotic signals mediated by the Activin B-ALK7 axis suppress ectopic proliferation and m
155 r Nodal, whereas Cryptic interacts only with Activin B.
156                                              Activin-beta has a key role in this regulation, which is
157                          Here we report that Activin-beta, a TGF-beta family ligand, is expressed by
158  identified in the interface between the two activin betaA subunits and was used for a virtual high-t
159                     Remarkably, mice lacking activin-betaA ( Inhba(-/-)) and mice with neural crest-s
160 competitive manner at the critical myostatin/activin binding site, hence preventing signal transducti
161                                        Thus, activin/BMP gradients specify distinct mesodermal subpop
162 /Activin A signaling because in that disease Activin can either signal through FOP-mutant ACVR1 or fo
163 roviding a molecular explanation for how the activin class accommodates low-affinity type I interacti
164                We report the structure of an activin class member, GDF11, in complex with the type II
165    FOXH1 is a primitive-streak specifier and ACTIVIN co-effector that plays an important role in deve
166          Furthermore, in mice, inhibition of activin conveys survival benefits in pancreatitis.
167      Consequently, YAP-null hESCs exposed to Activin differentiate precisely into beating cardiomyocy
168 re, we demonstrate that Myoglianin (Myo), an Activin family member, and a close homolog of mammalian
169 st-type pluripotency that is maintained with ACTIVIN/FGF2 signaling.
170  (ALK) receptors 4/5/7 recognizing TGF-beta, activin, growth and differentiation factor, and nodal li
171                  The pro-inflammatory factor Activin has been implicated as a positive correlate of s
172 3 phosphorylation via activin receptors, but activins have not been studied in the context of PKD.
173  and prevents the gene from being induced by Activin in proliferating hESCs.
174 an unappreciated important role for BMPs and activins in cellular antiviral immunity, which acts inde
175 a induced cellular migration is dependent on activin, indicating pathway cross-regulation and functio
176 ize beta-catenin, which then synergizes with Activin-induced SMADs to activate a subset of ME genes t
177 Interestingly, exposure of YAP(-/-) hESCs to Activin induces cardiac mesoderm markers (BAF60c and HAN
178 beta (TGFbeta) superfamily includes TGFbeta, activins, inhibins, and bone morphogenetic proteins (BMP
179                                              Activin is a critical modulator of inflammatory response
180                              Taken together, activin is a novel candidate as a clinical marker to ide
181              Here, we demonstrate that serum activin is elevated and strongly correlates with disease
182 cal cohort of pancreatitis patients and high activin levels in patients at admission are predictive o
183                           In addition, serum activin levels were measured from a retrospective clinic
184                             We show that the activin ligand Myoglianin from glia regulates the tempor
185 ceive non-redundant signaling from the three Activin ligands, activating the transcription factor dSm
186 n, which acts as a soluble trap to sequester activin ligands, effectively inhibited cyst formation in
187    Mice with PKD had increased expression of activin ligands, even at early stages of disease.
188 s of phosphorylated Smad2/3 upon exposure to activin ligands.
189 n part on the ability of broad inhibition of activin-like kinase (ALK) receptors 4/5/7 recognizing TG
190 sis and the binding of BMP-9 to the receptor activin-like kinase 1 (ALK-1) promotes endothelial cell
191                        Here we show that the activin-like kinase 1 (ALK1) mediates LDL uptake into en
192 s simulations and free energy calculation of Activin-Like Kinase 2 (ALK2), we found that GS domain ph
193 hogenetic protein (BMP) receptor 1A (BMPR1A)/activin-like kinase 3 (ALK3), but not carbonic anhydrase
194 this study, we discovered that signaling via activin-like kinase 3 (ALK3/BMPR1A), a BMP type 1 recept
195 cible factor 1alpha), blocking the BMP4/ALK (activin-like kinase) 2/ALK1/ALK5 and Notch signaling pat
196         In fact, activin-A signaling through activin-like kinase-4 receptor represses pathogenic tran
197                 However, the role of TGFbeta/Activin-like ligands in disc growth control remains ill-
198 d culture medium in which IGF1 together with Activin maintain self-renewal in the absence of fibrobla
199  would benefit from aggressive treatment and activin may be a therapeutic target in severe acute panc
200                                              Activin-mediated ALK4 signaling in MGE cells induced int
201 gs are consistent with other observations of Activin-mediated mechanisms exerting deleterious effects
202 phroblastoma overexpressed gene, and BMP and activin membrane-bound inhibitor (BAMBI).
203      Here, we determine the role of both the Activin/Nodal and BMP pathways as they function in Capit
204 1/5/8, transcription factors specific to the Activin/Nodal and BMP pathways, respectively.
205 rfamily comprises two distinct branches: the Activin/Nodal and BMP pathways.
206 ignaling, we unexpectedly identified the BMP/Activin/Nodal inhibitor Coco as an enhancer of TGFbeta1
207                      We demonstrate that the Activin/Nodal pathway of the TGF-beta superfamily, but n
208 hat the dorsal-ventral axis is patterned via Activin/Nodal signaling.
209 d by interactions between morphogens such as activin/nodal, BMPs and Wnt/beta-catenin that define ant
210 independent of loss of cell-cell contact and Activin/Nodal-dependent pluripotency and a peptide is de
211  gene transcript alterations and a switch to Activin/Nodal-dependent pluripotency.
212 and that the differential effects of loss of activin or Bmp4 signaling on maxillary and mandibular mo
213 unction of ALK4, a key receptor for the MSTN/activin pathway in skeletal muscle.
214 g IGSF1 as an important regulator of TGFbeta/Activin pathways in the pituitary.
215 eveloping therapies that interfere with MSTN/activin pathways.
216 iviral response to IFN, but BMP6 and related activin proteins also potently blocked HCV replication i
217  generated mice with conditional deletion of activin receptor (ACVR) type 2A, ACVR2B, or both, in ost
218               ACVR2B/Fc, an inhibitor of the Activin Receptor 2B signaling, has been shown to preserv
219                        Here we show that the activin receptor ALK4 is a key regulator of the specific
220 Here we report that specific deletion of the activin receptor ALK7 in BAT resulted in fasting-induced
221                      Neuroblasts missing the activin receptor Baboon have a delayed intrinsic program
222                             We find that the Activin receptor Baboon is required in R8 to receive non
223                   Our data led us to propose activin receptor IIB as a novel DYNLT1 ligand and sugges
224        In addition, treatment with a soluble activin receptor IIB fusion (sActRIIB-Fc) protein, which
225 escribe the basis for biological activity of activin receptor ligand traps, novel fusion proteins suc
226 r binding affinities for the type I receptor activin receptor like kinase 1 (ALK1), ALK2 and ALK3.
227 steoblasts, to determine the contribution of activin receptor signaling in regulating bone mass.
228  Taken together, these results indicate that activin receptor signaling, predominantly through ACVR2A
229 rentiation factor 11 (GDF11) through soluble activin receptor type II (ActRII) ligand traps or neutra
230  and its murine ortholog RAP-011) acts as an activin receptor type IIA ligand trap, increasing hemogl
231 g diseases, with a decrease of myostatin and activin receptor, and an increase of the myostatin antag
232                      When activated by BMP9, activin receptor-like kinase (ALK) 1 induces HOXD3 expre
233  inhibition was dependent on type I receptor activin receptor-like kinase (ALK)3-dependent phosphoryl
234 ns were used to determine the involvement of activin receptor-like kinase 1 (ALK1) and ALK5 downstrea
235 t of BMPRII receptor is mediated through the activin receptor-like kinase 1 (ALK1) but not the ALK3 r
236 dent on the endoglin signaling pathway using activin receptor-like kinase 1 (ALK1) Fc blocking peptid
237                                              Activin receptor-like kinase 1 (ALK1) is an endothelial
238 -of-function mutations in the genes encoding activin receptor-like kinase 1 (ALK1), endoglin, Smad4,
239 pro-domain-complexed BMP9 to type I receptor activin receptor-like kinase 1 (ALK1), type II receptors
240                                              Activin receptor-like kinase 1 (ALK1)-mediated endotheli
241  quiescence through its endothelial receptor activin receptor-like kinase 1 (ALK1).
242 e arterial-specific TGFbeta type I receptor, activin receptor-like kinase 1 (ALK1; ACVRL1), causes he
243           Small interfering RNA knockdown of activin receptor-like kinase 1 inhibited the BMP9-induce
244 e the physiologic role of BMP9, BMP10, ALK1 (activin receptor-like kinase 1), and SMAD7 in vivo.
245 mouse model with conditional inactivation of activin receptor-like kinase 5 (ALK5) in the mouse uteru
246                                              Activin receptor-like kinase 5 (Alk5) inhibitor (Alk5i),
247  growth factor beta receptor I (TGF-betaRI) (activin receptor-like kinase 5 [ALK-5]) and TGF-beta rec
248 at, conversely, the type I TGF-beta receptor activin receptor-like kinase 5 is dispensable for trypsi
249 n a small increase in TGF-beta signaling via activin receptor-like kinase 5 to maintain early integri
250 ed the TGF-beta type 1 receptor (also termed activin receptor-like kinase 5) in renal epithelial cell
251 ve inhibitor of the type 1 TGF-beta receptor activin receptor-like kinase 5, orally active) to inhibi
252 ur variants in the gene ACVR1C (encoding the activin receptor-like kinase 7 receptor expressed on adi
253 TGFbeta1 levels, endothelial TGFbetaRI/ALK1 (activin receptor-like kinase), and TGFbetaRI/ALK5 expres
254 LK1-Fc, a BMP9 ligand trap consisting of the activin receptor-like kinase-1 extracellular domain, exa
255 landscape surrounding DIPG has revealed that activin receptor-like kinase-2 (ALK2) constitutes a pote
256 n granulosa cells via type I receptors (i.e. activin receptor-like kinase-4/5 (ALK4/5)) and SMAD2/3 t
257 et cell and beta-cell proliferation, and the activin receptors RIIA and RIIB are required for the ful
258 family and drive SMAD2/3 phosphorylation via activin receptors, but activins have not been studied in
259 eases in TA mass, indicating that endogenous activins repress muscle growth.
260 tivin, TGF-beta treatment leads to increased activin secretion in colon cancer cells and TGF-beta ind
261 gands, which include the TGFbetas, BMPs, and activins, signal by forming a ternary complex with type
262 ogenetic protein 4 (BMP4) plus inhibitors of ACTIVIN signaling (A83-01) and FGF2 (PD173074), followed
263 dition to ActRIIB in mediating myostatin and activin signaling and highlight the need for blocking bo
264                          These data point to activin signaling as a key pathway in PKD and a promisin
265 dings support a model in which repression of activin signaling by FST enables uterine receptivity by
266                Primary osteoblasts expressed activin signaling components, including ACVR2A, ACVR2B,
267 nd suggest that interventions that attenuate Activin signaling could help further understanding of T2
268                               To investigate activin signaling in osteoblasts in vivo, we analyzed th
269                                        NODAL/Activin signaling induces dramatic chromatin landscape c
270                                        NODAL/Activin signaling orchestrates key processes during embr
271                                          The activin signaling pathway is an attractive candidate to
272 arly stages of pancreatic tumorigenesis; the activin signaling pathway therefore might be a therapeut
273 esenchyme, these data indicate that Bmp4 and activin signaling pathways converge on activation of the
274                                    Extrinsic activin signaling regulates the production of alpha'beta
275        However, the mechanism by which nodal/activin signaling regulates XY PGC fate is unknown.
276 show that simultaneous modulation of WNT and ACTIVIN signaling yields CD34(+) hematopoietic cells wit
277 riptional responses requires continued NODAL/Activin signaling.
278  targets the cellular receptor ACVR1B of the activin signalling axis.
279    Moreover, ASPN perturbed the Wnt, BMP and Activin signalling pathways, suggesting that ASPN thereb
280  pathways that can inhibit both TGF-beta and activin signals while enhancing bone morphogenetic prote
281  contrast, IGSF1 strongly down-regulates the activin-Smad pathway, leading to reduced expression of F
282                                              Activin/SMAD signaling in human embryonic stem cells (hE
283           In the presence of Wnt ligand, the Activin/SMAD transcription network switches to cooperate
284 mbryonic stem cells (hESCs) to show that the Activin-SMAD2/3 signaling pathway cooperates with the co
285                                        Thus, Activin/Smad3 signaling is induced following withdrawal
286 alysis identified inhibin beta-B (Inhbb), an activin subunit and member of the transforming growth fa
287 GF-beta growth suppression is independent of activin, TGF-beta treatment leads to increased activin s
288 by preventing WNT3 expression in response to Activin, thereby blocking a direct route to embryonic ca
289 CRISPR/CAS9 knockout of YAP in hESCs enables Activin to induce Wnt3 expression and stabilize beta-cat
290 scorbic acid, prolyl hydroxylase inhibitors, activin traps, hepcidin, and bone morphogenetic protein
291 I bone morphogenetic protein receptor ACVR1 (Activin type 1 receptor).
292 cription factor activities through alternate Activin type 2 receptors.
293                New function of the myostatin/activin type I receptor (ALK4) as a mediator of muscle a
294 on of negative muscle regulators through the activin type II receptors with bimagrumab treatment safe
295 ly human monoclonal antibody that blocks the activin type II receptors, preventing the activity of my
296               We have used i.p. injection of activin type IIB receptor (ActRIIB)-mFc (an inhibitor of
297 ivin A signaling using a soluble form of the activin type IIB receptor (ACVR2B), which can bind each
298 ic administration of the soluble form of the activin type IIB receptor (ACVR2B/Fc).
299        Furthermore, we provide evidence that Activin-type signaling regulates a radial gradient of te
300 he expansion of EYFP+ cells, while Wnt3a and Activin were marginally effective.

 
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