Key Features
Enhance your research with our curated data sets and powerful platform features. Pluto Bio makes it simple to find and use the data you need.
Learn MorePKCb-null (Prkcb-/-) mice are severely immunodeficient. Here we show that mice whose B cells lack PKCb fail to develop germinal centers and plasma cells, which in concert undermine affinity maturation and antibody production in response to immunization. Moreover, Prkcb-/- B cells fail to differentiate into plasma cells in response to viral infection. At a cellular level, we show that activated Prkcb-/- B cells exhibit defective antigen polarization and mTORC1 signaling. While the loss of antigen polarization impairs antigen presentation and restricts the potential of Prkcb-/- B cells to develop into GC B cells, altered mTORC1 signaling affects gene expression, metabolic reprogramming and mitochondrial remodeling which together overwhelmingly oppose commitment to plasma cell differentiation. Mechanistically, we show that PKCb-mediated metabolic reprogramming is required for sustained heme biosynthesis that is essential for effector fate decision in B cells. Taken together, our study reveals mechanistic insights into the function of PKCb as a key regulator of B-cell polarity and metabolic reprogramming that instructs B-cell fate. SOURCE: Carlson Tsui (carlson.tsui@crick.ac.uk) - The Francis Crick Institute
View on GEOView in PlutoEnhance your research with our curated data sets and powerful platform features. Pluto Bio makes it simple to find and use the data you need.
Learn MoreUse Pluto's intuitive interface to analyze and visualize data for this experiment. Pluto's platform is equipped with an API & SDKs, making it easy to integrate into your internal bioinformatics processes.
Read about post-pipeline analysisView quality control data and experiment metadata for this experiment.
Request imports from GEO or TCGA directly within Pluto Bio.
Chat with our Scientific Insights team