Mechanisms of NF-kappaB Signaling in diffuse large cell lymphoma

弥漫性大细胞淋巴瘤中 NF-κB 信号传导机制

• 批准号: 231828635
• 负责人: Professor Dr. Jürgen Ruland
• 金额: --
• 依托单位: Institut für Klinische Chemie und Pathobiochemie
• 依托单位国家: 德国
• 项目类别: Research Grants
• 财政年份: 2013
• 资助国家: 德国
• 起止时间: 2012-12-31 至 2016-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/231828635?language=en
• 关键词: Mechanisms; NF; kappaB; Signaling; diffuse

Diffuse large B cell lymphoma (DLBCL) is a clinically and genetically heterogeneous disease caused by various alterations in distinct signaling pathways. A subtype of DLBCL termed ABC (activated B-cell)-type DLBCL is characterized by constitutive activation of NF-kappaB signaling, which is essential for ABC-DLBCL cell growth. The NF-kappaB activating mechanisms involve a molecular complex composed of CARD11, BCL10 and MALT1 (CBM complex). Under physiological conditions, this complex relays signals from antigen receptors to NF-kappaB. In the next funding period we want to analyze mechanisms and consequences of aberrant CBM signaling during lymhpomagenesis.

弥漫性大B细胞淋巴瘤（DLBCL）是一种临床和遗传异质性疾病，由不同信号通路的各种改变引起。称为ABC（活化B细胞）型DLBCL的DLBCL亚型的特征在于NF-κ B信号传导的组成性活化，这对于ABC-DLBCL细胞生长是必需的。NF-κ B的激活机制涉及由CARD 11、BCL 10和MALT 1组成的分子复合物（CBM复合物）。在生理条件下，该复合物将信号从抗原受体传递到NF-κ B。在下一个资助期，我们希望分析在胚胎发育过程中异常CBM信号传导的机制和后果。

项目成果

Lymphomagenic CARD11/BCL10/MALT1 signaling drives malignant B-cell proliferation via cooperative NF-κB and JNK activation

• DOI: 10.1073/pnas.1507459112
• 发表时间: 2015-12-29
• 期刊: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
• 影响因子: 11.1
• 作者: Knies, Nathalie;Alankus, Beguem;Ruland, Juergen
• 通讯作者: Ruland, Juergen