Showing papers by "Masahiko Hatano published in 2007"
TL;DR: It is suggested that Bcl6 in CD4(+) T cells plays a role in protection of memory precursor CD4 (+) T Cells from apoptosis and may involve in survivability of long-term memoryCD4(-) T cells.
Abstract: Bcl6 plays a role in the generation and maintenance of memory CD8 1 T cells. We analyzed here a role for Bcl6 in the generation of long-term memory CD4 1 T cells. Naive CD45RB 1 CD4 1 T cells from Bcl6-deficient DO11.10 (KJ1.26 1 ) transgenic mice were transferred into BALB/c mice and immunized with ovalbumin peptide and LPS. Long-term memory KJ1.26 1 CD4 1 T cells from wild-type mice were detected in the spleen, lungs and liver during 10 weeks after immunization; however, Bcl6-deficient KJ1.26 1 CD4 1 T cells were vanished completely in those organs 4 weeks after immunization. Since memory CD4 1 T cells can be generated from effector CD4 1 T cells, properties of Bcl6-deficient effector CD4 1 T cells were compared with those wild-type effector CD4 1 T cells 10 days after immunization. Numbers of IFN-g-non-producing CD45RB 2 , CD62L 1 or IL-7Ra 1 effector CD4 1 T cells in the spleen, lungs and liver were similar between Bcl6-deficient and wild-type CD4 1 T cells. However, the percentage of apoptotic cells in Bcl6-deficient effector CD4 1 T cells was higher than that in wild-type effector CD4 1 T cells. At the late effector phase, the number of IFN-g-non-producing cells and the percentage of apoptotic cells in Bcl6-deficient CD4 1 T cells were smaller and higher than those in wild-type CD4 1 T cells, respectively. These data suggest that Bcl6 in CD4 1 T cells plays a role in protection of memory precursor CD4 1 T cells from apoptosis and may involve in survivability of long-term memory CD4 1 T cells.
82 citations
TL;DR: Bcl6 is required for maintaining the Bcl-X(L) up- regulation in B cells stimulated with LPS plus IL-21 and IL-4, and the up-regulation may partially rescue the B cells from apoptosis induced by IL- 21.
12 citations
TL;DR: Ncx participates in cell death of enteric neurons, and motor abnormality of the gastrointestinal tract in Ncx-/- mice may be attributed to the large number of neuronal cells.
11 citations
TL;DR: In ileum, BDF1 mice have cholinergic and adrenergic dominant contraction patterns, whereas Ncx-/- mice have relaxation-dominant patterns because of nonadrenergic, noncholinergic nerves.
3 citations
TL;DR: It is suggested that Nczf functions as a sequence-specific transcription repressor to regulate neural crest cell development.
Abstract: The Nczf gene, which is identified as a target gene of Ncx, encodes a novel Kruppel-associated box (KRAB) zinc finger protein, which functions as a sequence-specific transcriptional repressor. We generated a fusion protein of the zinc finger domain of Nczf and glutathione S-transferase to identify Nczf-binding consensus DNA sequences with random oligonucleotides of 15 and 35 bases. The consensus binding sequence of core nucleotides contains (A/T/C)CTTT(A/G)TTNT. In a gel mobility shift assay, the probe containing these sequences bound to the fusion protein. In silico analysis, these consensus sequences were found on regulatory regions of the endothelin receptor B and the microphthalmia-associated transcription factor genes, which are involved in neural crest development. These results suggest that Nczf functions as a sequence-specific transcription repressor to regulate neural crest cell development.
3 citations