GDF-11/BMP-11 Antibody (743833)

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.

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 (//pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.

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 (//pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.

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 (//pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.

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 (//pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.

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 (//pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.

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 (//pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.

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 (//pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.

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 (//pubmed.ncbi.nlm.nih.gov/27653144), licensed under a CC-BY license. Not internally tested by R&D Systems.

• Reactivity: Hu
• Applications: IHC
• Clone: 743833
• Clonality: Monoclonal
• Host: Mouse
• Conjugate: Unconjugated
• Concentration: LYOPH

GDF-11/BMP-11 Antibody (743833) Summary

• Immunogen: E. coli-derived recombinant human GDF-11/BMP-11
  Asn299-Ser407
  Accession # O95390
• Specificity: Detects human GDF-11/BMP-11 in direct ELISAs. In direct ELISAs, no cross-reactivity with recombinant human BMP-6 or recombinant mouse GDF-8 is observed.
• Source: N/A
• Isotype: IgG1
• Clonality: Monoclonal
• Host: Mouse
• Gene: GDF11
• Purity Statement: Protein A or G purified from hybridoma culture supernatant

Applications/Dilutions

• Dilutions:
  • Immunohistochemistry 8-25 ug/mL

Packaging, Storage & Formulations

• Storage: Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  • 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.
• Buffer: Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied either lyophilized or as a 0.2 µm filtered solution in PBS.
• Preservative: No Preservative
• Concentration: LYOPH
• Reconstitution Instructions: Sterile PBS to a final concentration of 0.5 mg/mL.

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for GDF-11/BMP-11 Antibody (743833)

• BMP11
• BMP-11
• BMP-11BMP11Bone morphogenetic protein 11
• GDF11
• GDF-11
• growth differentiation factor 11
• growth/differentiation factor 11

Background

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).

1. Gamer, L.W. et al. (1999) Dev. Biol. 208: 222. 
2. Nakashima, M. et al. (1999) Mech. Dev. 80:185.  
3. Gad, J.M. and P.P.L. Tam (1999) Curr. Biol. 9:R783.  
4. McPherron, A.C. et al. (1999) Nat. Genet. 22:260.
5. Esquela, A.F. and S.J. Lee (2003) Dev. Biol. 257:356.
6. Gamer, L.W. et al. (2001) Dev. Biol. 229:407.
7. Oh, S.P. et al. (2002) Genes & Dev. 16:274.

Limitations

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

Publications for GDF-11/BMP-11 Antibody (MAB19581)(19)

Publications using MAB19581

• Martin Schön, Karin Marček Malenovská, Michal Nemec, Nikoleta Alchus Laiferová, Igor Straka, Zuzana Košutzká et al. Acute endurance exercise modulates growth differentiation factor 11 in cerebrospinal fluid of healthy young adults Front Endocrinol (Lausanne) 2023-03-22 [PMID: 37033257]
• 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 GDF11 promotes wound healing in diabetic mice via stimulating HIF-1?-VEGF/SDF-1?-mediated endothelial progenitor cell mobilization and neovascularization Acta pharmacologica Sinica, 2022-11-08;0(0):. 2022-11-08 [PMID: 36347996] (Western Blot, Mouse)
• J Sun, Y Li, X Yang, W Dong, J Yang, Q Hu, C Zhang, H Fang, A Liu Growth differentiation factor 11 accelerates liver senescence through the inhibition of autophagy Aging Cell, 2021-12-14;0(0):e13532. 2021-12-14 [PMID: 34905649] (Western Blot, Mouse)
• 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 GDF11 inhibits cardiomyocyte pyroptosis and exerts cardioprotection in acute myocardial infarction mice by upregulation of transcription factor HOXA3 Cell Death Dis, 2020-10-25;11(10):917. 2020-10-25 [PMID: 33100331] (Western Blot, Mouse)
• X Qi, Q Xiao, R Sheng, S Jiang, Q Yuan, W Liu Endogenous GDF11 regulates odontogenic differentiation of dental pulp stem cells J. Cell. Mol. Med., 2020-08-26;0(0):. 2020-08-26 [PMID: 32845070] (IHC, Human)
• C Pan, N Jaiswal Ag, Y Zulia, S Singh, K Sha, JL Mohler, KH Eng, J Chakkalaka, JJ Krolewski, KL Nastiuk Prostate tumor-derived GDF11 accelerates androgen deprivation therapy-induced sarcopenia JCI Insight, 2020-03-26;0(0):. 2020-03-26 [PMID: 32078585] (In Vivo, Mouse)
• Minjung Lee, Satoshi Oikawa, Takashi Ushida, Katsuhiko Suzuki, Takayuki Akimoto Effects of Exercise Training on Growth and Differentiation Factor 11 Expression in Aged Mice Frontiers in Physiology 2019-07-31 [PMID: 31417428]
• Timothy C. Cox, Andrew C. Lidral, Jason C. McCoy, Huan Liu, Liza L. Cox, Ying Zhu et al. Mutations in GDF11 and the extracellular antagonist, Follistatin, as a likely cause of Mendelian forms of orofacial clefting in humans Human Mutation 2019-10-01 [PMID: 31215115] (Immunohistochemistry, Human)
• Q Jin, C Qiao, J Li, B Xiao, J Li, X Xiao A GDF11/myostatin inhibitor, GDF11 propeptide-Fc, increases skeletal muscle mass and improves muscle strength in dystrophic mdx mice Skelet Muscle, 2019-05-27;9(1):16. 2019-05-27 [PMID: 31133057] (Western Blot, Human)
• C Ozek, RC Krolewski, SM Buchanan, LL Rubin Growth Differentiation Factor 11 treatment leads to neuronal and vascular improvements in the hippocampus of aged mice Sci Rep, 2018-11-23;8(1):17293. 2018-11-23 [PMID: 30470794] (Western Blot, Mouse)
• Q Jin, C Qiao, J Li, J Li, X Xiao Neonatal Systemic AAV-Mediated Gene Delivery of GDF11 Inhibits Skeletal Muscle Growth Mol. Ther., 2018-02-02;26(4):1109-1117. 2018-02-02 [PMID: 29503194] (IHC, Western Blot, Mouse)
• Bajikar SS, Wang CC, Borten MA et al. Tumor-Suppressor Inactivation of GDF11 Occurs by Precursor Sequestration in Triple-Negative Breast Cancer Dev. Cell. 11/20/2017 [PMID: 29161592]
• E De Domenic, G D'Arcangel, I Faraoni, M Palmieri, V Tancredi, G Graziani, P Grimaldi, L Tentori Modulation of GDF11 expression and synaptic plasticity by age and training Oncotarget, 2017-08-03;8(35):57991-58002. 2017-08-03 [PMID: 28938532] (Western Blot, Mouse)
• Teresa A. Zimmers, Yanling Jiang, Meijing Wang, Tiffany W. Liang, Joseph E. Rupert, Ernie D. Au et al. Exogenous GDF11 induces cardiac and skeletal muscle dysfunction and wasting Basic Research in Cardiology 2017-07-01 [PMID: 28647906]
• 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 Activin A more prominently regulates muscle mass in primates than does GDF8 Nat Commun, 2017-04-28;8(0):15153. 2017-04-28 [PMID: 28452368] (ELISA Development, Neutralization, Human, Mouse, Primate - Macaca fascicularis (Crab-eating Monkey or Cynomolgus Macaque), Rat)
• H Li, Y Li, L Xiang, J Zhang, B Zhu, L Xiang, J Dong, M Liu, G Xiang GDF11 Attenuates Development of Type 2 Diabetes via Improvement of Islet ? cell Function and Survival Diabetes, 2017-04-27;0(0):. 2017-04-27 [PMID: 28450417] (In Vivo, Mouse)
• DW Hammers, M Merscham-B, JY Hsiao, S Engst, JJ Hartman, HL Sweeney Supraphysiological levels of GDF11 induce striated muscle atrophy EMBO Mol Med, 2017-04-01;0(0):. 2017-04-01 [PMID: 28270449] (Western Blot, Mouse)
• Marissa J Schafer Quantification of GDF11 and Myostatin in Human Aging and Cardiovascular Disease Cell Metab, 2016-06-14;23(6):1207-15. 6/14/2016 [PMID: 27304512]
• Buel D. Rodgers The Immateriality of Circulating GDF11 Circulation Research 2016-05-14 [PMID: 27174947]

Bioinformatics

• Gene Symbol: GDF11
• Uniprot:
  • O95390()