Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA382543 | ENA |
REPOSITORIES: ENA
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Project description:The effects of doxorubicin and blocking activin receptor 2B ligands in mice [muscle]
| PRJNA311341 | ENA
Project description:The effects of doxorubicin and blocking activin receptor 2B ligands in mice
| PRJNA382541 | ENA
Project description:Doxorubicin is a widely used and effective anthracycline chemotherapy drug. However, it causes cardiotoxicity and also a few negative effects on skeletal muscle as well. As a result, cancer treatment might actually worsen cancer-induced cachexia and consequently the prognosis of the disease. Inhibiting myostatin/activin signaling is known to increase muscle size. This pathway blockade by soluble activin receptor IIB (sAcvR2B-Fc) has also prolonged survival in cancer, even of animals in which tumor growth is not inhibited. It is not known, however, whether blocking this pathway affects chemotherapy-induced muscle wasting. We found that doxorubicin induces muscle atrophy which is prevented by a blocker for activin receptor 2B ligands (sAcvR2B-Fc).
2016-09-25 | GSE77745 | GEO
Project description:Doxorubicin is a widely used and effective anthracycline chemotherapy drug. However, it causes cardiotoxicity and also a few negative effects on skeletal muscle as well. As a result, cancer treatment might actually worsen cancer-induced cachexia and consequently the prognosis of the disease. Inhibiting myostatin/activin signaling is known to increase muscle size. This pathway blockade by soluble activin receptor IIB (sAcvR2B-Fc) has also prolonged survival in cancer, even of animals in which tumor growth is not inhibited. It is not known, however, whether blocking this pathway affects chemotherapy-induced muscle wasting. We found that doxorubicin induces muscle atrophy which is prevented by a blocker for activin receptor 2B ligands (sAcvR2B-Fc)
2017-12-04 | GSE97642 | GEO
Project description:This study was to compare the gene expression of our anti-GDF8 (i.e. anti-myostatin) and anti-activin A antibody combination to that of the activin receptor type IIB (ActRIIB.hFc) trap in SCID mice. The study was conducted in tibialis anterior muscle that is a common muscle type for the hypertrophy study. The combination treatment produces very similar muscle growth in tibialis muscle as the ActRIIB.hFc trap, however our combination blocks two specific ligands compared to the many ligands the receptor trap will inhibit. The difference in gene expression between these groups demonstrates that despite producing similar muscle growth, the trap affecting more genes in muscle without producing additional muscle hypertrophy.
2017-06-01 | E-MTAB-4943 | biostudies-arrayexpress
Project description:TGFβ/Activin subfamilies of ligands. In Drosophila the TGFβ/Activin branch includes three ligands, Myoglianin (Myo), Activin-β (Actβ) and Dawdle (Daw). All three ligands signal through the same type I receptor, Baboon, in conjunction with a type II receptor, Punt or Wit. Baboon has three distinct splice isoforms, termed Babo A, Babo B and Babo C, that differ only in exon 4, which encodes the ligand binding domain. This difference enables each ligand to potentially signal through a single splice isoform39. Formation of the ligand receptor complex stimulates phosphorylation of the receptor-Smad, dSmad2/Smox, which translocates to the nucleus as a complex with the co-Smad Medea where it serves as a transcriptional transducer. In order to gain insight into the genes regulated by Actβ we carried out a transcriptomic analysis comparing Actβ mutants to wild-type controls.
2024-06-28 | GSE270911 | GEO
Project description:Th17 cells are known to exert pathogenic and non-pathogenic functions. Although the cytokine transforming growth factor β1 (TGF-β1) is instrumental for Th17 cell differentiation, it is dispensable for generation of pathogenic Th17 cells. Here, we examined the T cell-intrinsic role of Activin-A, a TGF-β superfamily member closely related to TGF-β1, in pathogenic Th17 cell differentiation. Activin-A expression was increased in individuals with relapsing-remitting multiple sclerosis and in mice with experimental autoimmune encephalomyelitis. Stimulation with interleukin-6 and Activin-A induced a molecular program that mirrored that of pathogenic Th17 cells and was inhibited by blocking Activin-A signaling. Genetic disruption of Activin-A and its receptor ALK4 in T cells impaired pathogenic Th17 cell differentiation in vitro and in vivo. Mechanistically, extracellular-signal-regulated kinase (ERK) phosphorylation, which was essential for pathogenic Th17 cell differentiation, was suppressed by TGF-β1-ALK5 but not Activin-A-ALK4 signaling. Thus, Activin-A drives pathogenic Th17 cell differentiation, implicating the Activin-A-ALK4-ERK axis as a therapeutic target for Th17 cell-related diseases.
2021-01-11 | GSE151533 | GEO
Project description:Human embryonic stem cells can be maintained in a basic Serum Replacement (Invitrogen) based medium that has been conditioned on mouse embryonic fibroblasts (MEFs), yielding MEF-CM. Ligands secreted into the medium by the MEFs include Activin A, TGFß1, and Gremlin. This experiment served the purpose of identifying the short-term effects of MEF-CM and its substitute UM_GTA (unconditioned medium plus Activin A, TGFb1, and Gremlin) on gene expression in human embryonic stem cells. Keywords: Media / growth factor stimulation experiment
2008-03-12 | GSE9059 | GEO
Project description:The effects of MyD88 deficiency on disease phenotype in dysferlin-deficient A/J mice: Role of endogenous toll-like receptor (TLR) ligands
| PRJNA200304 | ENA