Human GDF-11/BMP-11 Antibody Summary
Asn299-Ser407
Accession # O95390
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Scientific Data
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GDF‑11/BMP‑11 in Human Colon Cancer Tissue. GDF-11/BMP-11 was detected in immersion fixed paraffin-embedded sections of human colon cancer tissue using Mouse Anti-Human GDF-11/BMP-11 Monoclonal Antibody (Catalog # MAB19581) at 15 µg/mL overnight at 4 °C. Tissue was stained using the Anti-Mouse HRP-DAB Cell & Tissue Staining Kit (brown; Catalog # CTS002) and counterstained with hematoxylin (blue). Lower panel shows a lack of labeling when primary antibodies are omitted and tissue is stained only with secondary antibody followed by incubation with detection reagents. Specific staining was localized to epithelia of the colon. View our protocol for Chromogenic IHC Staining of Paraffin-embedded Tissue Sections.
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Detection of Mouse Human GDF-11/BMP-11 Antibody by Western Blot GDF11 activates Smad2/3-dependent TGF-beta pathway.(a) Gene expression levels of the BMMs stimulated without or with 100 ng ml−1 rGDF11 for 24 h (three biological replicates per group). 467 genes (red) were upregulated and 679 genes (black) were downregulated. 100 ng ml−1 M-CSF was present in all settings. (b) Heatmap of the osteoclastogenesis associated genes. (c) Quantitative RT-PCR confirmed the increased expression of osteoclast key marker genes. Results are shown as mean±s.d.; n=3. ***P<0.001 by t test. (d) KEGG pathway analysis indicated the altered function of TGF-beta pathway. (e) Heatmap of the TGF-beta pathway associated genes. (f) Western blot analysis indicated that rGDF11 stimulated the phosphorylation of Smad2/3 in BMMs in 30 min. (g) Western blot analysis demonstrated that rGDF11 amplified the RANKL-induced expression of c-Fos. BMMs were starved overnight and then treated for 4 h. (h) Representative images of immunohistochemical staining. rGDF11 injections increased the phosphorylation of Smad2/3 and c-Fos, as well as the expression of Nfatc1 in vivo. Femurs were collected ∼2 h after the last injection of rGDF11. Scale bar, 50 μm. (i) Western blot analysis indicated that rGDF11 stimulated the RANKL-induced expression of Nfatc1. BMMs were treated for 2 days. (j) ChIP assay revealed that rGDF11 induced the co-occupancy of Smad2/3 and c-Fos to the binding region of Nfatc1. Results are shown as mean±s.d.; n=3. *P<0.05 and **P<0.01 by t test. (k) Western blot analysis of Nfatc1. Depletion of c-Fos eliminated the rGDF11 induced expression of Nfatc1. (l) ChIP assay. Depletion of c-Fos abolished rGDF11 triggered binding of Smad2/3 to Nfatc1. Results are shown as mean±s.d.; n=3. **P<0.01 by t test. Image collected and cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.
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Detection of Mouse Human GDF-11/BMP-11 Antibody by Western Blot GDF11 activates Smad2/3-dependent TGF-beta pathway.(a) Gene expression levels of the BMMs stimulated without or with 100 ng ml−1 rGDF11 for 24 h (three biological replicates per group). 467 genes (red) were upregulated and 679 genes (black) were downregulated. 100 ng ml−1 M-CSF was present in all settings. (b) Heatmap of the osteoclastogenesis associated genes. (c) Quantitative RT-PCR confirmed the increased expression of osteoclast key marker genes. Results are shown as mean±s.d.; n=3. ***P<0.001 by t test. (d) KEGG pathway analysis indicated the altered function of TGF-beta pathway. (e) Heatmap of the TGF-beta pathway associated genes. (f) Western blot analysis indicated that rGDF11 stimulated the phosphorylation of Smad2/3 in BMMs in 30 min. (g) Western blot analysis demonstrated that rGDF11 amplified the RANKL-induced expression of c-Fos. BMMs were starved overnight and then treated for 4 h. (h) Representative images of immunohistochemical staining. rGDF11 injections increased the phosphorylation of Smad2/3 and c-Fos, as well as the expression of Nfatc1 in vivo. Femurs were collected ∼2 h after the last injection of rGDF11. Scale bar, 50 μm. (i) Western blot analysis indicated that rGDF11 stimulated the RANKL-induced expression of Nfatc1. BMMs were treated for 2 days. (j) ChIP assay revealed that rGDF11 induced the co-occupancy of Smad2/3 and c-Fos to the binding region of Nfatc1. Results are shown as mean±s.d.; n=3. *P<0.05 and **P<0.01 by t test. (k) Western blot analysis of Nfatc1. Depletion of c-Fos eliminated the rGDF11 induced expression of Nfatc1. (l) ChIP assay. Depletion of c-Fos abolished rGDF11 triggered binding of Smad2/3 to Nfatc1. Results are shown as mean±s.d.; n=3. **P<0.01 by t test. Image collected and cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.
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Detection of Mouse Human GDF-11/BMP-11 Antibody by Western Blot GDF11 activates Smad2/3-dependent TGF-beta pathway.(a) Gene expression levels of the BMMs stimulated without or with 100 ng ml−1 rGDF11 for 24 h (three biological replicates per group). 467 genes (red) were upregulated and 679 genes (black) were downregulated. 100 ng ml−1 M-CSF was present in all settings. (b) Heatmap of the osteoclastogenesis associated genes. (c) Quantitative RT-PCR confirmed the increased expression of osteoclast key marker genes. Results are shown as mean±s.d.; n=3. ***P<0.001 by t test. (d) KEGG pathway analysis indicated the altered function of TGF-beta pathway. (e) Heatmap of the TGF-beta pathway associated genes. (f) Western blot analysis indicated that rGDF11 stimulated the phosphorylation of Smad2/3 in BMMs in 30 min. (g) Western blot analysis demonstrated that rGDF11 amplified the RANKL-induced expression of c-Fos. BMMs were starved overnight and then treated for 4 h. (h) Representative images of immunohistochemical staining. rGDF11 injections increased the phosphorylation of Smad2/3 and c-Fos, as well as the expression of Nfatc1 in vivo. Femurs were collected ∼2 h after the last injection of rGDF11. Scale bar, 50 μm. (i) Western blot analysis indicated that rGDF11 stimulated the RANKL-induced expression of Nfatc1. BMMs were treated for 2 days. (j) ChIP assay revealed that rGDF11 induced the co-occupancy of Smad2/3 and c-Fos to the binding region of Nfatc1. Results are shown as mean±s.d.; n=3. *P<0.05 and **P<0.01 by t test. (k) Western blot analysis of Nfatc1. Depletion of c-Fos eliminated the rGDF11 induced expression of Nfatc1. (l) ChIP assay. Depletion of c-Fos abolished rGDF11 triggered binding of Smad2/3 to Nfatc1. Results are shown as mean±s.d.; n=3. **P<0.01 by t test. Image collected and cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.
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Detection of Mouse Human GDF-11/BMP-11 Antibody by Western Blot GDF11 activates Smad2/3-dependent TGF-beta pathway.(a) Gene expression levels of the BMMs stimulated without or with 100 ng ml−1 rGDF11 for 24 h (three biological replicates per group). 467 genes (red) were upregulated and 679 genes (black) were downregulated. 100 ng ml−1 M-CSF was present in all settings. (b) Heatmap of the osteoclastogenesis associated genes. (c) Quantitative RT-PCR confirmed the increased expression of osteoclast key marker genes. Results are shown as mean±s.d.; n=3. ***P<0.001 by t test. (d) KEGG pathway analysis indicated the altered function of TGF-beta pathway. (e) Heatmap of the TGF-beta pathway associated genes. (f) Western blot analysis indicated that rGDF11 stimulated the phosphorylation of Smad2/3 in BMMs in 30 min. (g) Western blot analysis demonstrated that rGDF11 amplified the RANKL-induced expression of c-Fos. BMMs were starved overnight and then treated for 4 h. (h) Representative images of immunohistochemical staining. rGDF11 injections increased the phosphorylation of Smad2/3 and c-Fos, as well as the expression of Nfatc1 in vivo. Femurs were collected ∼2 h after the last injection of rGDF11. Scale bar, 50 μm. (i) Western blot analysis indicated that rGDF11 stimulated the RANKL-induced expression of Nfatc1. BMMs were treated for 2 days. (j) ChIP assay revealed that rGDF11 induced the co-occupancy of Smad2/3 and c-Fos to the binding region of Nfatc1. Results are shown as mean±s.d.; n=3. *P<0.05 and **P<0.01 by t test. (k) Western blot analysis of Nfatc1. Depletion of c-Fos eliminated the rGDF11 induced expression of Nfatc1. (l) ChIP assay. Depletion of c-Fos abolished rGDF11 triggered binding of Smad2/3 to Nfatc1. Results are shown as mean±s.d.; n=3. **P<0.01 by t test. Image collected and cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.
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Detection of Mouse Human GDF-11/BMP-11 Antibody by Western Blot GDF11 activates Smad2/3-dependent TGF-beta pathway.(a) Gene expression levels of the BMMs stimulated without or with 100 ng ml−1 rGDF11 for 24 h (three biological replicates per group). 467 genes (red) were upregulated and 679 genes (black) were downregulated. 100 ng ml−1 M-CSF was present in all settings. (b) Heatmap of the osteoclastogenesis associated genes. (c) Quantitative RT-PCR confirmed the increased expression of osteoclast key marker genes. Results are shown as mean±s.d.; n=3. ***P<0.001 by t test. (d) KEGG pathway analysis indicated the altered function of TGF-beta pathway. (e) Heatmap of the TGF-beta pathway associated genes. (f) Western blot analysis indicated that rGDF11 stimulated the phosphorylation of Smad2/3 in BMMs in 30 min. (g) Western blot analysis demonstrated that rGDF11 amplified the RANKL-induced expression of c-Fos. BMMs were starved overnight and then treated for 4 h. (h) Representative images of immunohistochemical staining. rGDF11 injections increased the phosphorylation of Smad2/3 and c-Fos, as well as the expression of Nfatc1 in vivo. Femurs were collected ∼2 h after the last injection of rGDF11. Scale bar, 50 μm. (i) Western blot analysis indicated that rGDF11 stimulated the RANKL-induced expression of Nfatc1. BMMs were treated for 2 days. (j) ChIP assay revealed that rGDF11 induced the co-occupancy of Smad2/3 and c-Fos to the binding region of Nfatc1. Results are shown as mean±s.d.; n=3. *P<0.05 and **P<0.01 by t test. (k) Western blot analysis of Nfatc1. Depletion of c-Fos eliminated the rGDF11 induced expression of Nfatc1. (l) ChIP assay. Depletion of c-Fos abolished rGDF11 triggered binding of Smad2/3 to Nfatc1. Results are shown as mean±s.d.; n=3. **P<0.01 by t test. Image collected and cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.
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Detection of Mouse Human GDF-11/BMP-11 Antibody by PCR GDF11 activates Smad2/3-dependent TGF-beta pathway.(a) Gene expression levels of the BMMs stimulated without or with 100 ng ml−1 rGDF11 for 24 h (three biological replicates per group). 467 genes (red) were upregulated and 679 genes (black) were downregulated. 100 ng ml−1 M-CSF was present in all settings. (b) Heatmap of the osteoclastogenesis associated genes. (c) Quantitative RT-PCR confirmed the increased expression of osteoclast key marker genes. Results are shown as mean±s.d.; n=3. ***P<0.001 by t test. (d) KEGG pathway analysis indicated the altered function of TGF-beta pathway. (e) Heatmap of the TGF-beta pathway associated genes. (f) Western blot analysis indicated that rGDF11 stimulated the phosphorylation of Smad2/3 in BMMs in 30 min. (g) Western blot analysis demonstrated that rGDF11 amplified the RANKL-induced expression of c-Fos. BMMs were starved overnight and then treated for 4 h. (h) Representative images of immunohistochemical staining. rGDF11 injections increased the phosphorylation of Smad2/3 and c-Fos, as well as the expression of Nfatc1 in vivo. Femurs were collected ∼2 h after the last injection of rGDF11. Scale bar, 50 μm. (i) Western blot analysis indicated that rGDF11 stimulated the RANKL-induced expression of Nfatc1. BMMs were treated for 2 days. (j) ChIP assay revealed that rGDF11 induced the co-occupancy of Smad2/3 and c-Fos to the binding region of Nfatc1. Results are shown as mean±s.d.; n=3. *P<0.05 and **P<0.01 by t test. (k) Western blot analysis of Nfatc1. Depletion of c-Fos eliminated the rGDF11 induced expression of Nfatc1. (l) ChIP assay. Depletion of c-Fos abolished rGDF11 triggered binding of Smad2/3 to Nfatc1. Results are shown as mean±s.d.; n=3. **P<0.01 by t test. Image collected and cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.
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Detection of Mouse Human GDF-11/BMP-11 Antibody by Immunohistochemistry GDF11 activates Smad2/3-dependent TGF-beta pathway.(a) Gene expression levels of the BMMs stimulated without or with 100 ng ml−1 rGDF11 for 24 h (three biological replicates per group). 467 genes (red) were upregulated and 679 genes (black) were downregulated. 100 ng ml−1 M-CSF was present in all settings. (b) Heatmap of the osteoclastogenesis associated genes. (c) Quantitative RT-PCR confirmed the increased expression of osteoclast key marker genes. Results are shown as mean±s.d.; n=3. ***P<0.001 by t test. (d) KEGG pathway analysis indicated the altered function of TGF-beta pathway. (e) Heatmap of the TGF-beta pathway associated genes. (f) Western blot analysis indicated that rGDF11 stimulated the phosphorylation of Smad2/3 in BMMs in 30 min. (g) Western blot analysis demonstrated that rGDF11 amplified the RANKL-induced expression of c-Fos. BMMs were starved overnight and then treated for 4 h. (h) Representative images of immunohistochemical staining. rGDF11 injections increased the phosphorylation of Smad2/3 and c-Fos, as well as the expression of Nfatc1 in vivo. Femurs were collected ∼2 h after the last injection of rGDF11. Scale bar, 50 μm. (i) Western blot analysis indicated that rGDF11 stimulated the RANKL-induced expression of Nfatc1. BMMs were treated for 2 days. (j) ChIP assay revealed that rGDF11 induced the co-occupancy of Smad2/3 and c-Fos to the binding region of Nfatc1. Results are shown as mean±s.d.; n=3. *P<0.05 and **P<0.01 by t test. (k) Western blot analysis of Nfatc1. Depletion of c-Fos eliminated the rGDF11 induced expression of Nfatc1. (l) ChIP assay. Depletion of c-Fos abolished rGDF11 triggered binding of Smad2/3 to Nfatc1. Results are shown as mean±s.d.; n=3. **P<0.01 by t test. Image collected and cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.
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Detection of Mouse Human GDF-11/BMP-11 Antibody by Western Blot GDF11 activates Smad2/3-dependent TGF-beta pathway.(a) Gene expression levels of the BMMs stimulated without or with 100 ng ml−1 rGDF11 for 24 h (three biological replicates per group). 467 genes (red) were upregulated and 679 genes (black) were downregulated. 100 ng ml−1 M-CSF was present in all settings. (b) Heatmap of the osteoclastogenesis associated genes. (c) Quantitative RT-PCR confirmed the increased expression of osteoclast key marker genes. Results are shown as mean±s.d.; n=3. ***P<0.001 by t test. (d) KEGG pathway analysis indicated the altered function of TGF-beta pathway. (e) Heatmap of the TGF-beta pathway associated genes. (f) Western blot analysis indicated that rGDF11 stimulated the phosphorylation of Smad2/3 in BMMs in 30 min. (g) Western blot analysis demonstrated that rGDF11 amplified the RANKL-induced expression of c-Fos. BMMs were starved overnight and then treated for 4 h. (h) Representative images of immunohistochemical staining. rGDF11 injections increased the phosphorylation of Smad2/3 and c-Fos, as well as the expression of Nfatc1 in vivo. Femurs were collected ∼2 h after the last injection of rGDF11. Scale bar, 50 μm. (i) Western blot analysis indicated that rGDF11 stimulated the RANKL-induced expression of Nfatc1. BMMs were treated for 2 days. (j) ChIP assay revealed that rGDF11 induced the co-occupancy of Smad2/3 and c-Fos to the binding region of Nfatc1. Results are shown as mean±s.d.; n=3. *P<0.05 and **P<0.01 by t test. (k) Western blot analysis of Nfatc1. Depletion of c-Fos eliminated the rGDF11 induced expression of Nfatc1. (l) ChIP assay. Depletion of c-Fos abolished rGDF11 triggered binding of Smad2/3 to Nfatc1. Results are shown as mean±s.d.; n=3. **P<0.01 by t test. Image collected and cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.
Reconstitution Calculator
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: GDF-11/BMP-11
Growth Differentiation Factor 11 (GDF-11), also known as BMP-11, is a member of the TGF-beta superfamily and is highly related to GDF-8. GDF-11 encodes a 407 amino acid (aa) prepropeptide which contains a signal sequence for secretion and an RXXR proteolytic processing site to yield a 109 aa residue carboxy-terminal mature protein (1). Mature GDF-11 contains the canonical 7-cysteine motif common to other TGF-beta superfamily members; however, like the TGF-beta s, Activins and GDF-8, GDF-11 also contains one extra pair of cysteine residues. At the amino acid sequence level, mature human, mouse, rat and chicken GDF-11 are 99‑100% identical. GDF-11 and GDF-8 share 90% amino acid sequence identity within the mature protein. As detected by in situ hybridization, GDF-11 is expressed in diverse regions of the mouse embryo: tailbud, somitic precursors, limbs, mandibular and branchial arches, dorsal neural tube, odontoblasts, nasal epithelium, and particular regions of the brain (1, 2). Likewise, a targeted deletion of GDF-11 in mice results in a spectrum of abnormalities including palatal malformation, vertebral defects, elongated trunks with a reduced or absent tail, missing or malformed kidneys, and an increased number of neurons in the olfactory epithelium (2-5). An intriguing finding in the knockout mice was that the trunk elongation was due to an increase in the number of thoracic vertebrae (4). This implicates GDF-11 as the first secreted factor to influence the specification of segmental identity in vertebrates (3). In fact, GDF-11 does regulate expression of segmental transcription factors, the Hox genes (6). GDF-11 signals through the Activin type II receptors and induces phosphorylation of Smad2 to mediate axial patterning (7). Despite the strong expression in the limb throughout development, no limb abnormalities were found in the knockout mice. However, in vitro micromass studies indicate that GDF-11 inhibits myogenic and chondrogenic cell differentiation and may impact formation and development of the limb skeleton (6).
- Gamer, L.W. et al. (1999) Dev. Biol. 208: 222.
- Nakashima, M. et al. (1999) Mech. Dev. 80:185.
- Gad, J.M. and P.P.L. Tam (1999) Curr. Biol. 9:R783.
- McPherron, A.C. et al. (1999) Nat. Genet. 22:260.
- Esquela, A.F. and S.J. Lee (2003) Dev. Biol. 257:356.
- Gamer, L.W. et al. (2001) Dev. Biol. 229:407.
- Oh, S.P. et al. (2002) Genes & Dev. 16:274.
Product Datasheets
Citations for Human GDF-11/BMP-11 Antibody
R&D Systems personnel manually curate a database that contains references using R&D Systems products. The data collected includes not only links to publications in PubMed, but also provides information about sample types, species, and experimental conditions.
19
Citations: Showing 1 - 10
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Quantification of GDF11 and Myostatin in Human Aging and Cardiovascular Disease
Authors: Marissa J Schafer
Cell Metab, 2016-06-14;23(6):1207-15.
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Acute endurance exercise modulates growth differentiation factor 11 in cerebrospinal fluid of healthy young adults
Authors: Martin Schön, Karin Marček Malenovská, Michal Nemec, Nikoleta Alchus Laiferová, Igor Straka, Zuzana Košutzká et al.
Front Endocrinol (Lausanne)
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GDF11 promotes wound healing in diabetic mice via stimulating HIF-1?-VEGF/SDF-1?-mediated endothelial progenitor cell mobilization and neovascularization
Authors: Y Zhang, YY Zhang, ZW Pan, QQ Li, LH Sun, X Li, MY Gong, XW Yang, YY Wang, HD Li, LN Xuan, YC Shao, MM Li, MY Zhang, Q Yu, Z Li, XF Zhang, DH Liu, YM Zhu, ZY Tan, YY Zhang, YQ Liu, Y Zhang, L Jiao, BF Yang
Acta pharmacologica Sinica, 2022-11-08;0(0):.
Species: Mouse
Sample Types: Tissue Homogenates
Applications: Western Blot -
Growth differentiation factor 11 accelerates liver senescence through the inhibition of autophagy
Authors: J Sun, Y Li, X Yang, W Dong, J Yang, Q Hu, C Zhang, H Fang, A Liu
Aging Cell, 2021-12-14;0(0):e13532.
Species: Mouse
Sample Types: Tissue Homogenates
Applications: Western Blot -
GDF11 inhibits cardiomyocyte pyroptosis and exerts cardioprotection in acute myocardial infarction mice by upregulation of transcription factor HOXA3
Authors: Z Li, H Xu, X Liu, Y Hong, H Lou, H Liu, X Bai, L Wang, X Li, SM Monayo, JN Mokembo, NK Jha, B Yang, Y Zhang
Cell Death Dis, 2020-10-25;11(10):917.
Species: Mouse
Sample Types: Cell Culture Supernates
Applications: Western Blot -
Endogenous GDF11 regulates odontogenic differentiation of dental pulp stem cells
Authors: X Qi, Q Xiao, R Sheng, S Jiang, Q Yuan, W Liu
J. Cell. Mol. Med., 2020-08-26;0(0):.
Species: Human
Sample Types: Whole Tissue
Applications: IHC -
Prostate tumor-derived GDF11 accelerates androgen deprivation therapy-induced sarcopenia
Authors: C Pan, N Jaiswal Ag, Y Zulia, S Singh, K Sha, JL Mohler, KH Eng, J Chakkalaka, JJ Krolewski, KL Nastiuk
JCI Insight, 2020-03-26;0(0):.
Species: Mouse
Sample Types: In Vivo
Applications: In Vivo -
Mutations in GDF11 and the extracellular antagonist, Follistatin, as a likely cause of Mendelian forms of orofacial clefting in humans
Authors: Timothy C. Cox, Andrew C. Lidral, Jason C. McCoy, Huan Liu, Liza L. Cox, Ying Zhu et al.
Human Mutation
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Effects of Exercise Training on Growth and Differentiation Factor 11 Expression in Aged Mice
Authors: Minjung Lee, Satoshi Oikawa, Takashi Ushida, Katsuhiko Suzuki, Takayuki Akimoto
Frontiers in Physiology
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A GDF11/myostatin inhibitor, GDF11 propeptide-Fc, increases skeletal muscle mass and improves muscle strength in dystrophic mdx mice
Authors: Q Jin, C Qiao, J Li, B Xiao, J Li, X Xiao
Skelet Muscle, 2019-05-27;9(1):16.
Species: Human
Sample Types: Cell Lysates
Applications: Western Blot -
Growth Differentiation Factor 11 treatment leads to neuronal and vascular improvements in the hippocampus of aged mice
Authors: C Ozek, RC Krolewski, SM Buchanan, LL Rubin
Sci Rep, 2018-11-23;8(1):17293.
Species: Mouse
Sample Types: Serum
Applications: Western Blot -
Neonatal Systemic AAV-Mediated Gene Delivery of GDF11 Inhibits Skeletal Muscle Growth
Authors: Q Jin, C Qiao, J Li, J Li, X Xiao
Mol. Ther., 2018-02-02;26(4):1109-1117.
Species: Mouse
Sample Types: Cell Lysates, Whole Tissue
Applications: IHC, Western Blot -
Modulation of GDF11 expression and synaptic plasticity by age and training
Authors: E De Domenic, G D'Arcangel, I Faraoni, M Palmieri, V Tancredi, G Graziani, P Grimaldi, L Tentori
Oncotarget, 2017-08-03;8(35):57991-58002.
Species: Mouse
Sample Types: Tissue Homogenates
Applications: Western Blot -
Exogenous GDF11 induces cardiac and skeletal muscle dysfunction and wasting
Authors: Teresa A. Zimmers, Yanling Jiang, Meijing Wang, Tiffany W. Liang, Joseph E. Rupert, Ernie D. Au et al.
Basic Research in Cardiology
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Activin A more prominently regulates muscle mass in primates than does GDF8
Authors: E Latres, J Mastaitis, W Fury, L Miloscio, J Trejos, J Pangilinan, H Okamoto, K Cavino, E Na, A Papatheodo, T Willer, Y Bai, J Hae Kim, A Rafique, S Jaspers, T Stitt, AJ Murphy, GD Yancopoulo, J Gromada
Nat Commun, 2017-04-28;8(0):15153.
Species: Human, Mouse, Primate - Macaca fascicularis (Crab-eating Monkey or Cynomolgus Macaque), Rat
Sample Types: In Vivo, Serum
Applications: ELISA Development, Neutralization -
GDF11 Attenuates Development of Type 2 Diabetes via Improvement of Islet ? cell Function and Survival
Authors: H Li, Y Li, L Xiang, J Zhang, B Zhu, L Xiang, J Dong, M Liu, G Xiang
Diabetes, 2017-04-27;0(0):.
Species: Mouse
Sample Types: In Vivo
Applications: In Vivo -
Supraphysiological levels of GDF11 induce striated muscle atrophy
Authors: DW Hammers, M Merscham-B, JY Hsiao, S Engst, JJ Hartman, HL Sweeney
EMBO Mol Med, 2017-04-01;0(0):.
Species: Mouse
Sample Types: Serum
Applications: Western Blot -
The Immateriality of Circulating GDF11
Authors: Buel D. Rodgers
Circulation Research
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Tumor-Suppressor Inactivation of GDF11 Occurs by Precursor Sequestration in Triple-Negative Breast Cancer
Authors: Bajikar SS, Wang CC, Borten MA et al.
Dev. Cell.
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