Analysis of the mechanism of mature B cell differentiation controlled by survival signals from BCR and BAFF-R
Analysis of the mechanism of mature B cell differentiation controlled by survival signals from BCR and BAFF-R
批准号:
23590575
负责人:
SASAKI YOSHITERU
金额:
$3.41万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2011
资助国家:
日本
项目状态:
已结题
起止时间:
2011 至 2013
中文摘要
来自BCR和BAFF-R的信号控制成熟B细胞的分化以及它们的存活。在本研究中,我研究了BCR和BAFF-R信号在成熟B细胞分化中的作用,发现PI 3激酶的靶分子之一Akt,其传递来自BCR的存活信号在B1细胞发育中起重要作用,并且经典NF-κ B途径在成熟B2和MZ B细胞产生中的主要功能是控制BAFF-κ B的强度。R介导的替代性NF-κ B信号传导。我还研究了一种新的泛素连接酶复合物LUBAC在B细胞中的功能,发现LUBAC在B1细胞的发育和抗体应答中起重要作用,并且是CD 40和TACI激活经典NF-κ B途径所必需的,而不是BCR。
英文摘要
Signals from BCR and BAFF-R control the differentiation of mature B cells as well as their survival. In this research I investigated the roles of signals from BCR and BAFF-R in the differentiation of mature B cells and found that Akt, one of the target molecule of PI3 kinase, which transmits the survival signal from BCR plays an important role in B1 cell development and that the main function of the canonical NF-kappaB pathway in the generation of mature B2 and MZ B cells is the control of the strength of BAFF-R mediated alternative NF-kappaB signaling. I also examined the function of a novel ubiquitin ligase complex, LUBAC in B cells and discovered that LUBAC plays important roles in the development of B1 cells and the antibody responses and is required for the activation of the canonical NF-kappaB pathway by CD40 and TACI but not by BCR.
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Canonical NF-κB pathway controls the strength of BAFF-R signaling through the induction of p100NF-κB2
经典 NF-κB 通路通过诱导 p100NF-κB2 控制 BAFF-R 信号强度
DOI:
--
发表时间:
2011
期刊:
影响因子:
--
作者:
[大洞将嗣, 黒崎知博, 佐々木義輝]
通讯作者:
佐々木義輝
Defective immune reponses in mice lacking LUBAC-mediated linear ubiquitination in B cells
B 细胞中缺乏 LUBAC 介导的线性泛素化的小鼠的免疫反应有缺陷
DOI:
--
发表时间:
2013
期刊:
EMBO J .
影响因子:
--
作者:
[Sasaki, Y., Sano, S., Nakahara, M., Murata, S., Kometani, K., Aiba, Y., Sakamoto, S., Watanabe, Y., Tanaka, K., Kurosaki, T. and Iwai, K.]
通讯作者:
K.
Canonical NF-kB pathway controls the strength of BAFF-R signaling through the induction of p100NF-kB2
规范 NF-kB 通路通过诱导 p100NF-kB2 控制 BAFF-R 信号强度
DOI:
--
发表时间:
期刊:
影响因子:
--
作者:
[大洞将嗣, 高柳広, 佐々木 義輝]
通讯作者:
佐々木 義輝
Defective immune reponses in mice lacking LUBAC-mediated linear ubiquitination in B cells.
B 细胞中缺乏 LUBAC 介导的线性泛素化的小鼠的免疫反应有缺陷。
DOI:
--
发表时间:
2013
期刊:
EMBO Journal
影响因子:
11.4
作者:
[Sasaki, Y., Sano, S., Nakahara, M., Murata, S., Kometani, K., Aiba, Y., Sakamoto, S., Watanabe, Y., Tanaka, K., Kurosaki, T. and Iwai, K.]
通讯作者:
K.
B細胞の発生・機能における直鎖状ポリユビキチン鎖の機能解析
B 细胞发育和功能中线性多聚泛素链的功能分析
DOI:
--
发表时间:
2013
期刊:
影响因子:
--
作者:
[Yoshikawa, S., Egawa, M., Oh-hora, M., Adachi, T., Horiguchi, K., Li, L., Ohta, T., Kawano, Y., Minagishi, Y. and Karasuyama, H., 佐々木義輝]
通讯作者:
佐々木義輝
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