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critical regulator of kidney fibrosis and tubular function
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study indicates that GDF11/8 in the kidney decreases with age and that GDF11 can increase tubular cell dedifferentiation and proliferation as well as improve tubular regeneration after acute kidney injury (AKI) in old mice.
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Our results showed that GDF11 inhibited osteoblastic differentiation of bone marrow mesenchymal stem cells in vitro and had no effect on osteoclast differentiation or bone resorption
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In conclusion, our findings show that GDF11 expression declines with age and the protective effects of ultrasound-targeted microbubble destruction-mediated delivery of GDF11 on the aged ischemic heart provide support for the classification of GDF11 as an anti-aging factor
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we found that myostatin forms a complex with LTBP4 and that overexpression of LTBP4 led to a decrease in myostatin levels. LTBP4 also interacted with TGFbeta and GDF11, a protein highly related to myostatin. These data identify LTBP4 as a multi-TGFbeta family ligand binding protein with the capacity to modify muscle disease through overexpression
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Circulating levels of GDF11/8 declines with age in mice (and sheep, horses and rats).
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Data show that circulating myostatin levels decreased with age and estimates of growth differentiation factor 11 (GDF11) levels using myostatin null mice indicate that they were almost 500 times lower than those for myostatin.
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Two new studies demonstrate that GDF11 this "factor of youth" rejuvenates stem cells found in the skeletal muscle and brain of aged mice.
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Therefore, we postulate that GDF-11DeltaEx1 may act as a long non-coding RNA to regulate the transcription of canonical GDF-11 and/or other genes in skeletal muscle and other tissues
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Expression of GDF11, a cytokine which blocks terminal erythroid maturation, was increased in erthyroblasts of thalassemic mice.
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GDF11 inhibited erythroid maturation in mice in vivo and ex vivo. Expression of GDF11 in erythroid precursors decreased progressively with maturation, suggesting an inhibitory role for GDF11 in late-stage erythroid differentiation.
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Gdf11 stimulates expression of a Hoxd11/lacZ transgene in the mouse embryo tailbud.
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GASP-1 and GASP-2 are important modulators of GDF-11 and MSTN activity in vivo.
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Gdf11 signaling is a major coordinator of the trunk-to-tail transition during mouse development
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Using modified aptamer-based proteomics, study identified the TGF-beta superfamily member GDF11 as a circulating factor in young mice that declines with age.
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Reducing GDF11 levels might promote restoration of retinal development in the microophthalmic Vsx2 mutant mouse.
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These results suggest that over-expression of BMP11 propeptide stimulates bone formation by increasing osteoblast cell functions.
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PCSK5 and GDF11 expression during hindgut morphogenesis could be key factors for normal anorectal development, which can be disturbed by the administration of an overdose of all-trans retinoic acid, leading to anorectal malformations.
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the transition between stem cells and committed progenitors is neither sharp nor irreversible and GDF11, ACTbetaB and FST are crucial components of a circuit that controls both total cell number and the ratio of neuronal versus glial cells in this system
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Significant effects of GDF11 propeptide transgene on vertebral formation.