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Changchun Xiao

Researcher at Scripps Research Institute

Publications -  62
Citations -  8667

Changchun Xiao is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: microRNA & Cellular differentiation. The author has an hindex of 29, co-authored 56 publications receiving 7823 citations. Previous affiliations of Changchun Xiao include Harvard University & Scripps Health.

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Regulation of the Germinal Center Response by MicroRNA-155

TL;DR: It is shown that the evolutionarily conserved microRNA-155 has an important role in the mammalian immune system, specifically in regulating T helper cell differentiation and the germinal center reaction to produce an optimal T cell–dependent antibody response.
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Lymphoproliferative disease and autoimmunity in mice with increased miR-17-92 expression in lymphocytes

TL;DR: The genomic region encoding the miR-17-92 microRNA (miRNA) cluster is often amplified in lymphoma and other cancers, and cancer cells carrying this amplification have higher expression of miRNA in this cluster, and this mechanism probably contributed to the lymphoproliferative disease and autoimmunity ofmiR- 17-92-transgenic mice and contributes to lymphoma development in patients with amplifications of this coding region.
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MicroRNA Control in the Immune System: Basic Principles

TL;DR: MicroRNA (miRNA) control has emerged as a critical regulatory principle in the mammalian immune system and severely compromises immune development and response and can lead to immune disorders like autoimmunity and cancer.
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MiR-150 controls B cell differentiation by targeting the transcription factor c-Myb

TL;DR: It is shown that miR-150 indeed controls c-Myb expression in vivo in a dose-dependent manner over a narrow range of miRNA and c- myb concentrations and that this dramatically affects lymphocyte development and response.
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TAK1, but not TAB1 or TAB2, plays an essential role in multiple signaling pathways in vivo

TL;DR: The studies suggests that TAK1 acts as an upstream activating kinase for IKKbeta and JNK, but not IKKalpha, revealing an unexpectedly specific role of TAK 1 in inflammatory signaling pathways.