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In a recent paper published in Nature, Carrieri et al. have identified in mouse a neuron-specific antisense lncRNA transcribed in the opposite strand of Uchl1 mRNA. Antisense Uchl1 specifically promotes the translation of UCHL1 under rapamycin treatment. To do so, the lncRNA only requires a SINEB2 repeat and a small region with sequence complementarity to the regulated mRNA.
The transcription factor Foxp3 plays an indispensible role in the differentiation of regulatory T (Treg) cells and the expression of their suppressive functions. In a recent article published in Nature, Ouyang et al. demonstrate that Treg cell differentiation is also enabled by transcriptional networks controlled by another Forkhead box family member, Foxo1.
Why stem cell numbers decline with age is a major question in regenerative biology and medicine. Skeletal muscle has emerged as a powerful paradigm to address this issue. Recently, genetic and cell marking strategies were used to uncover a new and causal relationship between muscle stem cells and differentiated fibers that constitute their niche and provoke their loss.
Maintenance of hematopoietic stem cells (HSCs) in vitro has been believed to be difficult due to a lack of complete understanding of HSC quiescence maintained by the niche. Recent evidence suggests that in vitro maintenance of human and mouse long-term HSCs (LT-HSCs) is possible through dual inhibition (2i) of both GSK-3 and mTOR in the absence of cytokines, serum, or feeder cells.
T lymphocytes express clonal receptors, called T cell receptors (TCRs), which specifically recognize antigens presented in combination with major histocompatibility molecules (MHC). To date, T cell antigens can be broadly categorized into two classes: peptides and lipids. A recent paper published in Nature by Kjer-Nielsen and colleagues reveals that a unique population of T lymphocytes expresses TCRs that recognize a completely new and unexpected class of antigens, vitamin metabolites.
Protein homeostasis in higher eukaryotes is balanced by a dynamic network of adaptive mechanisms, including the unfolded protein response (UPR) and autophagy. In a paper recently published in Cell Research, Zhu and co-workers uncover a novel biological function of the unspliced form of the UPR transcription factor XBP1 in the modulation of autophagy through the control of FoxO1 turnover.
