{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["104(35)"],"submitter":["Marechal Y"],"pubmed_abstract":["The contribution of the B isoform of inositol 1,4,5-trisphosphate [Ins(1,4,5)P(3)] 3-kinase (or Itpkb) and inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P(4)], its reaction product, to B cell function and development remains unknown. Here, we show that mice deficient in Itpkb have defects in B cell survival leading to specific and intrinsic developmental alterations in the B cell lineage and antigen unresponsiveness in vivo. The decreased B cell survival is associated with a decreased phosphorylation of Erk1/2 and increased Bim gene expression. B cell survival, development, and antigen responsiveness are normalized in parallel to reduced expression of Bim in Itpkb(-/-) Bim(+/-) mice. Analysis of the signaling pathway downstream of Itpkb revealed that Ins(1,3,4,5)P(4) regulates subcellula"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pagination":["13978-83"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC1955816"],"repository":["biostudies-literature"],"pubmed_title":["Inositol 1,3,4,5-tetrakisphosphate controls proapoptotic Bim gene expression and survival in B cells."],"pmcid":["PMC1955816"],"pubmed_authors":["Pouillon V","Luo HR","Daniel J","Schurmans S","Marechal Y","Izui S","Jia Y","Perez-Morga D","Erneux C","Leo O","Pesesse X","Cullen PJ"],"additional_accession":[]},"is_claimable":false,"name":"Inositol 1,3,4,5-tetrakisphosphate controls proapoptotic Bim gene expression and survival in B cells.","description":"The contribution of the B isoform of inositol 1,4,5-trisphosphate [Ins(1,4,5)P(3)] 3-kinase (or Itpkb) and inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P(4)], its reaction product, to B cell function and development remains unknown. Here, we show that mice deficient in Itpkb have defects in B cell survival leading to specific and intrinsic developmental alterations in the B cell lineage and antigen unresponsiveness in vivo. The decreased B cell survival is associated with a decreased phosphorylation of Erk1/2 and increased Bim gene expression. B cell survival, development, and antigen responsiveness are normalized in parallel to reduced expression of Bim in Itpkb(-/-) Bim(+/-) mice. Analysis of the signaling pathway downstream of Itpkb revealed that Ins(1,3,4,5)P(4) regulates subcellula","dates":{"release":"2007-01-01T00:00:00Z","publication":"2007 Aug","modification":"2026-03-16T16:43:09.223Z","creation":"2019-03-27T02:21:26Z"},"accession":"S-EPMC1955816","cross_references":{"pubmed":["17709751"],"doi":["10.1073/pnas.0704312104"]}}