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acvr1b mab222  (R&D Systems)


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    R&D Systems acvr1b mab222
    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 <t>(ACVR1B)</t> 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.
    Acvr1b Mab222, supplied by R&D Systems, used in various techniques. Bioz Stars score: 91/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/acvr1b+mab222/Human+Activin+RIB%2FALK-4+Antibody/pmc11285815-6-0-5
    Average 91 stars, based on 7 article reviews
    acvr1b mab222 - by Bioz Stars, 2026-09
    91/100 stars

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    1) Product Images from "Potential roles of activin in head and neck squamous cell carcinoma progression in epithelial-mesenchymal transition, metastasis, and mortality"

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

    Journal: Anticancer research

    doi: 10.21873/anticanres.16733

    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.
    Figure Legend 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.

    Techniques Used: Binding Assay, Phospho-proteomics, Inhibition

    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).
    Figure Legend 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).

    Techniques Used: Immunohistochemistry, Expressing, Comparison

    Immunohistochemistry
    Figure Legend Snippet: Immunohistochemistry

    Techniques Used:



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    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 <t>(ACVR1B)</t> 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.
    Acvr1b Mab222, supplied by R&D Systems, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/acvr1b+mab222/Human+Activin+RIB%2FALK-4+Antibody/pmc11285815-6-0-5
    Average 91 stars, based on 1 article reviews
    acvr1b mab222 - by Bioz Stars, 2026-09
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    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 <t>(ACVR1B)</t> 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.
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    Image Search Results


    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.

    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

    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).

    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

    Immunohistochemistry

    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:

    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.

    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

    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).

    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

    Immunohistochemistry

    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: