-
Notifications
You must be signed in to change notification settings - Fork 7
New issue
Have a question about this project? Sign up for a free GitHub account to open an issue and contact its maintainers and the community.
By clicking “Sign up for GitHub”, you agree to our terms of service and privacy statement. We’ll occasionally send you account related emails.
Already on GitHub? Sign in to your account
Seperate each part with code block #123
Comments
Or a bold seperator in between: 👋 Hello! I'm your friendly social media assistant. Below are the previews of this post: matrix-eu-announce📝 New blog post Released! https://galaxyproject.org/news/2024-10-01-galaxy-in-reseach-degn/ Galaxy in Research: New insights into antibody activation using AlphaFold in GalaxyHow do antigens trigger B-cell receptors (BCRs), and can a single mechanism explain the activation of all BCR types? This study explores a unifying model that integrates various mechanisms of BCR triggering, providing fresh perspectives on antibody activation. The study by Søren E. Degn and Pavel Tolar addresses the complex question of how antigens trigger the activation of B-cell receptors (BCRs). BCRs play a key role in adaptive immunity by enabling B cells to respond to various antigens, from small molecules to large parasites. Despite advances in structural biology, no single molecular mechanism has been established to explain how antigens activate BCRs across different receptor types and immune contexts. This research reviews historical models of BCR activation, evaluating their relevance in light of current biochemical and structural insights. Key Findings· The study revisits and critiques several models for BCR triggering, including cross-linking, kinetic segregation, and oligomerization models. · It emphasizes that BCR activation balances kinases (phosphorylation) and phosphatases (dephosphorylation). · A proposed unifying model integrates cross-linking and kinetic segregation aspects, suggesting that BCR activation is driven by antigen footprint and the ability to exclude phosphatases. · The findings highlight that antigen size, affinity, and membrane dynamics all influence the strength and duration of the BCR signal. Galaxy’s RoleGalaxy facilitated the structural analysis crucial to this research. Specifically, the AlphaFold structure prediction tool within Galaxy was used to predict the structure of the CD22 ectodomain and transmembrane segment and generate the ovalbumin 17-mer OB1 peptide. These structures contributed to the study’s exploration of antigen-triggered BCR activation, enhancing the mechanistic insights drawn from the data. Significance of the StudyThis study is a major step toward a comprehensive model of BCR activation. Proposing a unifying framework that can accommodate different antigens, receptor variants, and physiological conditions opens up new avenues for understanding immune responses. These insights are fundamental for immunology and have potential implications for vaccine design and autoimmune disease research. AcknowledgmentThank you to Søren Degn and Pavel Tolar for employing Galaxy in their analysis. Their work adds to the growing knowledge of immune system function and its molecular underpinnings. --- Degn, S.E., Tolar, P. Towards a unifying model for B-cell receptor triggering. Nat Rev Immunol (2024). https://doi.org/10.1038/s41577-024-01073-x 🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸 mastodon-eu-freiburg📝 New blog post Released! Galaxy in Research: New insights into antibody activation using AlphaFold in Galaxy How do antigens trigger B-cell receptors (BCRs), and can a single mechanism explain the activation of all BCR types? This study explores a unifying model that integrates various mechanisms of BCR triggering, providing fresh perspectives on antibody activation. The study by Søren E. Degn and Pavel Tolar addresses the complex question of how antigens (1/6) 🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸 trigger the activation of B-cell receptors (BCRs). BCRs play a key role in adaptive immunity by enabling B cells to respond to various antigens, from small molecules to large parasites. Despite advances in structural biology, no single molecular mechanism has been established to explain how antigens activate BCRs across different receptor types and immune contexts. This research reviews historical models of BCR activation, evaluating their relevance in light of current biochemical and (2/6) 🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸 structural insights. Key Findings · The study revisits and critiques several models for BCR triggering, including cross-linking, kinetic segregation, and oligomerization models. · It emphasizes that BCR activation balances kinases (phosphorylation) and phosphatases (dephosphorylation). · A proposed unifying model integrates cross-linking and kinetic segregation aspects, suggesting that BCR activation is driven by antigen footprint and the ability to exclude phosphatases. · The (3/6) 🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸 findings highlight that antigen size, affinity, and membrane dynamics all influence the strength and duration of the BCR signal. Galaxy’s Role Galaxy facilitated the structural analysis crucial to this research. Specifically, the AlphaFold structure prediction tool within Galaxy was used to predict the structure of the CD22 ectodomain and transmembrane segment and generate the ovalbumin 17-mer OB1 peptide. These structures contributed to the study’s exploration of antigen-triggered BCR (4/6) 🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸 activation, enhancing the mechanistic insights drawn from the data. Significance of the Study This study is a major step toward a comprehensive model of BCR activation. Proposing a unifying framework that can accommodate different antigens, receptor variants, and physiological conditions opens up new avenues for understanding immune responses. These insights are fundamental for immunology and have potential implications for vaccine design and autoimmune disease research. (5/6) 🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸 Acknowledgment Thank you to Søren Degn and Pavel Tolar for employing Galaxy in their analysis. Their work adds to the growing knowledge of immune system function and its molecular underpinnings. Degn, S.E., Tolar, P. Towards a unifying model for B-cell receptor triggering. Nat Rev Immunol (2024). https://doi.org/10.1038/s41577-024-01073-x
🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸🔸 linkedin-galaxyproject📝 New blog post Released! Galaxy in Research: New insights into antibody activation using AlphaFold in Galaxy How do antigens trigger B-cell receptors (BCRs), and can a single mechanism explain the activation of all BCR types? This study explores a unifying model that integrates various mechanisms of BCR triggering, providing fresh perspectives on antibody activation. The study by Søren E. Degn and Pavel Tolar addresses the complex question of how antigens trigger the activation of B-cell receptors (BCRs). BCRs play a key role in adaptive immunity by enabling B cells to respond to various antigens, from small molecules to large parasites. Despite advances in structural biology, no single molecular mechanism has been established to explain how antigens activate BCRs across different receptor types and immune contexts. This research reviews historical models of BCR activation, evaluating their relevance in light of current biochemical and structural insights. Key Findings · The study revisits and critiques several models for BCR triggering, including cross-linking, kinetic segregation, and oligomerization models. · It emphasizes that BCR activation balances kinases (phosphorylation) and phosphatases (dephosphorylation). · A proposed unifying model integrates cross-linking and kinetic segregation aspects, suggesting that BCR activation is driven by antigen footprint and the ability to exclude phosphatases. · The findings highlight that antigen size, affinity, and membrane dynamics all influence the strength and duration of the BCR signal. Galaxy’s Role Galaxy facilitated the structural analysis crucial to this research. Specifically, the AlphaFold structure prediction tool within Galaxy was used to predict the structure of the CD22 ectodomain and transmembrane segment and generate the ovalbumin 17-mer OB1 peptide. These structures contributed to the study’s exploration of antigen-triggered BCR activation, enhancing the mechanistic insights drawn from the data. Significance of the Study This study is a major step toward a comprehensive model of BCR activation. Proposing a unifying framework that can accommodate different antigens, receptor variants, and physiological conditions opens up new avenues for understanding immune responses. These insights are fundamental for immunology and have potential implications for vaccine design and autoimmune disease research. Acknowledgment Thank you to Søren Degn and Pavel Tolar for employing Galaxy in their analysis. Their work adds to the growing knowledge of immune system function and its molecular underpinnings. Degn, S.E., Tolar, P. Towards a unifying model for B-cell receptor triggering. Nat Rev Immunol (2024). https://doi.org/10.1038/s41577-024-01073-x
|
For a better preview, we could separate each part of the text with code blocks.
for example in #122 it could be something like this:
👋 Hello! I'm your friendly social media assistant. Below are the previews of this post:
posts/feed_bot/galaxy_europe/2024-10-01-galaxy-in-reseach-degn-group1.md
matrix-eu-announce
mastodon-eu-freiburg
linkedin-galaxyproject
The text was updated successfully, but these errors were encountered: