Contents
Vol 11, Issue 533
Research Articles
- The ion channel TRPM7 is required for B cell lymphopoiesis
B cell development is critically impaired by loss of the channel-kinase TRPM7.
- The channel-kinase TRPM7 regulates antigen gathering and internalization in B cells
B cell antigen uptake and presentation require the dual ion channel–kinase TRPM7.
- Lgl reduces endosomal vesicle acidification and Notch signaling by promoting the interaction between Vap33 and the V-ATPase complex
Lgl reduces Notch activation by cooperating with Vap33 to inhibit the vacuolar ATPase, thereby reducing endosome acidification.
- K63-linked polyubiquitin chains bind to DNA to facilitate DNA damage repair
Mutations in the DNA-interacting patch of ubiquitin sensitize cells to DNA-damaging agents.
Editors' Choice
- Highlight: Distinct functions of the ion channel–kinase TRPM7
Two studies in this week’s issue of Science Signaling identify distinct activities of the ion channel–kinase TRPM7 that control discrete functions in B cells.
About The Cover

Online Cover This week features two studies about how the cation channel–kinase TRPM7 controls B cell development and function. The issue includes a Research Article that identifies a kinase-independent requirement for TRPM7 in the development of mature peripheral B cells. The issue also includes a Research Article that demonstrates that both the ion channel and kinase activity of TRPM7 are involved in B cell receptor antigen gathering and internalization. The image shows fluorescent staining of a mouse spleen tissue section for B, T, and myeloid cells. [Image: Krishnamoorthy et al./Science Signaling]