anti activin monoclonal antibody  (R&D Systems)

Journal: Biology

Article Title: BMP-2-Driven Osteogenesis: A Comparative Analysis of Porcine BMSCs and ASCs and the Role of TGF-β and FGF Signaling.

doi: 10.3390/biology14060610

Figure Lengend Snippet: Figure 6. Receptor expressions of ALK2, ALK4, ALK6, ALK5, ALK7, BMPR-II in pASC. Grouped representation of the respective receptor expression in the course of osteogenic differentiation (OM +/−BMP-2). From day 19, there is a significant induction of ALK 2, ALK 6, and ALK 5 with the addition of BMP-2. BMPR-II expression in the OM group decreased in OM and tended to stay increased under BMP-2 supplementation from day 19, but was not considered significant (* p ≤0.05, ** p ≤0.01; n = 6, BMP-2 450 ng/mL).

Article Snippet: The respective conjugated antibodies were used for the expressions of ALK3 (Cat. No.: AF436), ALK 5 (Cat. No.: FAB5871), ALK6 (Cat. No.: FAB5051A), TGF-β2-RII (Cat. No.: FAB532P), ALK7 (Cat. No.: FAB77491A), ALK2 (Cat. No.: AF637), ALK4 (Cat. No.: MAB2221), and BMPR-II (Cat. No.: AF811) (by R&D Systems, Minneapolis, MN, USA), and the pASCs and pBMSCs were compared for their expressions of the specific surface antigens CD45 (Cat. No.: MCA1568GA, BioRad, Hercules, CA, USA), HLA-DR (human leukocyte antigen–antigen D-related surface molecule) (Cat. No.: MCA2314F, Bio-Rad, Hercules, CA, USA), CD29 (Cat. No.: 561,496, BD Pharmingen, Franklin Lakes, NJ, USA), CD79alpha (Bio-Rad, Cat. No.: MCA2538GA), CD14 (Cat. No.: MCA1568GA, Bio-Rad, Hercules, CA, USA), CD31 (Cat. No.: AF3387, R&D Systems, Minneapolis, MN, USA), CD105 (Cat. No.: NB110-58718APC, Novus Biologicals, Minneapolis, MN, USA), CD26 (, Cat. No.: NB600-552APC, Novus Biologicals, Minneapolis, MN, USA), CD73 (, Cat. No.: AF4488, R&D Systems, Minneapolis, MN, USA), CD90 (Cat. No.: 559,869, BD Pharmingen, Franklin Lakes, NJ, USA), CD34 (Cat. No.: 81289, abcam, Cambridge, UK), and CD44 (Cat. No.: 5531, BD Pharmingen, Franklin Lakes, NJ, USA).

Techniques: Expressing

Journal: Anticancer research

Article Title: Potential roles of activin in head and neck squamous cell carcinoma progression in epithelial-mesenchymal transition, metastasis, and mortality

doi: 10.21873/anticanres.16733

Figure Lengend Snippet: The canonical activin A pathway. Activin A is composed of inhibin βA subunits (βA) and binds to activin receptor type II and IIB (ACVR2/2B). Inhibin, composed of a βA and α subunit, competitively binds and sequesters ACVR2/2B, ultimately inhibiting the activin axis. Contrariwise, activin binding ultimately forms a Smad transcriptions complex (comprised of Smad 2, 3 and 4), the phosphorylation of activin receptor type IB (ACVR1B) subsequently stimulating and activating the Smad transcription complex, thereby eliciting downstream cellular behaviors such as proliferation inhibition, apoptosis, and epithelial mesenchymal transition. Of note, activin may have proliferative effects outside of this axis, as described in the introduction and discussion.

Article Snippet: ACVR1B (MAB222) , Monoclonal , R & D Systems , 1:200.

Techniques: Binding Assay, Phospho-proteomics, Inhibition

Journal: Anticancer research

Article Title: Potential roles of activin in head and neck squamous cell carcinoma progression in epithelial-mesenchymal transition, metastasis, and mortality

doi: 10.21873/anticanres.16733

Figure Lengend Snippet: Immunohistochemistry expression of inhibin subunits (INHA, INHBA, INHBB) and activin receptors (ACVR1B, ACVR2, ACVR2B) in five normal, 15 oral premalignant (OPL) and 12 HNSCC tumor tissue samples. Chi-square tests were employed for analysis with p <0.05 being significant; diffuse and focal positivity were scored as positive. Premalignant and malignant lesions demonstrated a statistically significant increase in the prevalence of ligand inhibin βA (INHBA) (χ 2 (2, N = 32) = 18.98, p < .0001) (Row 6) as well as ACVR1B (χ 2 (2, N = 32) = 11.52, p < .0032) (Row 11). There was also a decreased prevalence of ACVR2B among pre-malignant and malignant lesions in comparison to normal mucosa (χ 2 (2, N = 32) = 0.0018, p < .0018) (Row 13).

Article Snippet: ACVR1B (MAB222) , Monoclonal , R & D Systems , 1:200.

Techniques: Immunohistochemistry, Expressing, Comparison

Journal: Anticancer research

Article Title: Potential roles of activin in head and neck squamous cell carcinoma progression in epithelial-mesenchymal transition, metastasis, and mortality

doi: 10.21873/anticanres.16733

Figure Lengend Snippet: Immunohistochemistry

Article Snippet: ACVR1B (MAB222) , Monoclonal , R & D Systems , 1:200.

Techniques:

Journal: Anticancer research

Article Title: Potential roles of activin in head and neck squamous cell carcinoma progression in epithelial-mesenchymal transition, metastasis, and mortality

doi: 10.21873/anticanres.16733

Figure Lengend Snippet: The canonical activin A pathway. Activin A is composed of inhibin βA subunits (βA) and binds to activin receptor type II and IIB (ACVR2/2B). Inhibin, composed of a βA and α subunit, competitively binds and sequesters ACVR2/2B, ultimately inhibiting the activin axis. Contrariwise, activin binding ultimately forms a Smad transcriptions complex (comprised of Smad 2, 3 and 4), the phosphorylation of activin receptor type IB (ACVR1B) subsequently stimulating and activating the Smad transcription complex, thereby eliciting downstream cellular behaviors such as proliferation inhibition, apoptosis, and epithelial mesenchymal transition. Of note, activin may have proliferative effects outside of this axis, as described in the introduction and discussion.

Article Snippet: Antibody Clone Source Dilution ACVR1B (MAB222) Monoclonal R & D Systems 1:200 ACVR2 (AF340) Polyclonal R & D Systems 1:100 ACVR2B (AF339) Polyclonal R & D Systems 1:80 INHA (MCA951S) Monoclonal Biorad 1:800 INHBA (Serotec/Biorad) Monoclonal Biorad 1:100 INHBB (Serotec/Biorad) Monoclonal Biorad 1:100 Open in a separate window Immunohistochemistry MTT assay Cell proliferation was determined by MTT incorporation.

Techniques: Binding Assay, Phospho-proteomics, Inhibition

Journal: Anticancer research

Article Title: Potential roles of activin in head and neck squamous cell carcinoma progression in epithelial-mesenchymal transition, metastasis, and mortality

doi: 10.21873/anticanres.16733

Figure Lengend Snippet: Immunohistochemistry expression of inhibin subunits (INHA, INHBA, INHBB) and activin receptors (ACVR1B, ACVR2, ACVR2B) in five normal, 15 oral premalignant (OPL) and 12 HNSCC tumor tissue samples. Chi-square tests were employed for analysis with p <0.05 being significant; diffuse and focal positivity were scored as positive. Premalignant and malignant lesions demonstrated a statistically significant increase in the prevalence of ligand inhibin βA (INHBA) (χ 2 (2, N = 32) = 18.98, p < .0001) (Row 6) as well as ACVR1B (χ 2 (2, N = 32) = 11.52, p < .0032) (Row 11). There was also a decreased prevalence of ACVR2B among pre-malignant and malignant lesions in comparison to normal mucosa (χ 2 (2, N = 32) = 0.0018, p < .0018) (Row 13).

Article Snippet: Antibody Clone Source Dilution ACVR1B (MAB222) Monoclonal R & D Systems 1:200 ACVR2 (AF340) Polyclonal R & D Systems 1:100 ACVR2B (AF339) Polyclonal R & D Systems 1:80 INHA (MCA951S) Monoclonal Biorad 1:800 INHBA (Serotec/Biorad) Monoclonal Biorad 1:100 INHBB (Serotec/Biorad) Monoclonal Biorad 1:100 Open in a separate window Immunohistochemistry MTT assay Cell proliferation was determined by MTT incorporation.

Techniques: Immunohistochemistry, Expressing, Comparison

Journal: Anticancer research

Article Title: Potential roles of activin in head and neck squamous cell carcinoma progression in epithelial-mesenchymal transition, metastasis, and mortality

doi: 10.21873/anticanres.16733

Figure Lengend Snippet: Immunohistochemistry

Article Snippet: Antibody Clone Source Dilution ACVR1B (MAB222) Monoclonal R & D Systems 1:200 ACVR2 (AF340) Polyclonal R & D Systems 1:100 ACVR2B (AF339) Polyclonal R & D Systems 1:80 INHA (MCA951S) Monoclonal Biorad 1:800 INHBA (Serotec/Biorad) Monoclonal Biorad 1:100 INHBB (Serotec/Biorad) Monoclonal Biorad 1:100 Open in a separate window Immunohistochemistry MTT assay Cell proliferation was determined by MTT incorporation.

Techniques: