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Induction and activation of the transcription factor NFATc1 (NFAT2) integrate RANKL signaling in terminal differentiation of osteoclasts.
Regulation of cancer cell metabolism
Interest in the topic of tumour metabolism has waxed and waned over the past century, but it has become clear that many of the signalling pathways that are affected by genetic mutations and the tumour microenvironment have a profound effect on core metabolism, making this topic once again one of the most intense areas of research in cancer biology.
OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis
OPGL is a new regulator of lymph-node organogenesis and lymphocyte development and is an essential osteoclast differentiation factor in vivo.
Negative Regulation of PKB/Akt-Dependent Cell Survival by the Tumor Suppressor PTEN
Integral role of IRF-5 in the gene induction programme activated by Toll-like receptors
The transcription factor IRF-5 is identified as a new, principal downstream regulator of the TLR–MyD88 signalling pathway and a potential target of therapeutic intervention to control harmful immune responses.
Modulation of oxidative stress as an anticancer strategy
The controversial role of ROS in tumour development and in responses to anticancer therapies is addressed, and the idea that targeting the antioxidant capacity of tumour cells can have a positive therapeutic impact is elaborate.
BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis.
Regulation of oxidative stress by ATM is required for self-renewal of haematopoietic stem cells
It is shown that ATM has an essential function in the reconstitutive capacity of haematopoietic stem cells (HSCs) but is not as important for the proliferation or differentiation of progenitors, in a telomere-independent manner.
Immunologic Self-Tolerance Maintained by Cd25+Cd4+Regulatory T Cells Constitutively Expressing Cytotoxic T Lymphocyte–Associated Antigen 4
- Takeshi Takahashi, Tomoyuki Tagami, S. Sakaguchi
- Biology, MedicineJournal of Experimental Medicine
- 17 July 2000
Interference with this role of CTLA-4 suffices to elicit autoimmune disease in otherwise normal animals, presumably through affecting CD25+CD4+ T cell–mediated control of self-reactive T cells.
Severe impairment of interleukin-1 and Toll-like receptor signalling in mice lacking IRAK-4
It is shown by gene-targeting that IRAK-4, an IRAK molecule closely related to the Drosophila Pelle protein, is indispensable for the responses of animals and cultured cells to IL-1 and ligands that stimulate various TLRs.