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dc.contributor.authorYang L.
dc.contributor.authorJing Y.
dc.contributor.authorWang W.
dc.contributor.authorYing W.
dc.contributor.authorLin L.
dc.contributor.authorChang J.
dc.contributor.authorLuo L.
dc.contributor.authorKang D.
dc.contributor.authorJiang P.
dc.contributor.authorLiu J.
dc.contributor.authorChen Q.
dc.contributor.authorMiller H.
dc.contributor.authorHerrada A.A.
dc.contributor.authorKubo M.
dc.contributor.authorSun J.
dc.contributor.authorLiu C.
dc.date.accessioned2020-09-02T22:30:35Z
dc.date.available2020-09-02T22:30:35Z
dc.date.issued2020
dc.identifier10.1016/j.bbrc.2020.05.152
dc.identifier.citation529, 2, 296-302
dc.identifier.issn0006291X
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6641
dc.descriptionDedicator of cytokinesis 2 (DOCK2) is essential for the B cell differentiation, BCR signaling and humoral immune response. However, the role of DOCK2 in the memory response of B cell is unknown. By using two DOCK2 deficient patients, we found that the memory B cells were decreased and the early activation of DOCK2 deficient memory B cells was abolished to the degree of naïve B cells due to the decreased expression of CD19 and CD21 mechanistically. Interestingly the expression of LEF-1, a negative regulator of CD21, was increased in DOCK2 deficient B cells. This was linked to the increased expression of HIF-1α and cell metabolism, which in turn affected the ER structure. Finally, the reduction of memory B cells in DOCK2 patients was due to the increased apoptosis, which might be related with the increased metabolism. © 2020
dc.language.isoen
dc.publisherElsevier B.V.
dc.subjectB cell
dc.subjectDOCK2
dc.subjectLEF-1
dc.subjectB lymphocyte receptor
dc.subjectCD19 antigen
dc.subjectcomplement component C3d receptor
dc.subjectdedicator of cytokinesis 2
dc.subjecthypoxia inducible factor 1alpha
dc.subjectlymphoid enhancer factor 1
dc.subjectRac protein
dc.subjectunclassified drug
dc.subjectanimal cell
dc.subjectArticle
dc.subjectB lymphocyte activation
dc.subjectB lymphocyte differentiation
dc.subjectcell metabolism
dc.subjectclinical article
dc.subjectcontrolled study
dc.subjectfemale
dc.subjecthuman
dc.subjecthuman cell
dc.subjectmale
dc.subjectmemory cell
dc.subjectmouse
dc.subjectnonhuman
dc.subjectpriority journal
dc.titleDOCK2 couples with LEF-1 to regulate B cell metabolism and memory response
dc.typeArticle


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