作者: Luojing Chen , David Oleksyn , Mary Pulvino , Ignacio Sanz , Daniel Ryan
DOI: 10.1016/J.IMLET.2016.02.015
关键词:
摘要: Protein kinase C associated (PKK) regulates NF-κB activation and is required for the survival of certain lymphoma cells. Mice lacking PKK die soon after birth, previous studies suggest that role in B cell development might be context dependent. We have generated a mouse strain harboring conditional null alleles Cre-recombinase transgene under control endogenous CD19 promoter. In present study, we show knockout cells results reduction long-lived recirculating mature population lymph nodes bone marrow as well decrease peritoneal B1 cells, while deficiency has no apparent effect on early or follicular marginal zone spleen. addition, demonstrate PKK-deficient display defective proliferation responses to stimulation receptor (BCR), which may underlie mutant mice. Consistently, BCR-mediated activation, known activated but not resting attenuated Thus, our reveal critical maintenance