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Results demonstrate that social isolation stress during adolescence attenuates an exercise-induced increase in neurogenesis. This effect is most pronounced in the ventral hippocampus. TLX is necessary for the pro-neurogenic effects of exercise during adolescence.
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This study demonstrated that deletion of Tlx impairs motor, cognitive and anxiety-related behaviours during adolescence and adulthood in male and female mice with most effects occurring during adolescence rather than adulthood, independent of housing conditions.
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This study demonstrated that Nr2e1 could be regulated by retinoic acid, which would aid a better understanding of the mechanism underlying RA-induced brain abnormality.
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Nr2e1 deficiency augments palmitate-induced oxidative stress. Nr2e1 deficiency also resulted in decreases in antioxidant enzymes and expression level of Nrf2.
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TLX is essential for SOX2-mediated in vivo reprogramming of astrocytes and itself is also sufficient to induce neurogenesis in the adult striatum.
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TLX, an essential regulator of NSC proliferation and self-renewal, inhibits miR-219 processing. miR-219 suppresses mouse NSC proliferation downstream of TLX.
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At high glucose concentrations in vitro, AdipoR1 regulated the survival of neural stem cells through the p53/p21 pathway and the proliferation- and differentiation-related factors of neural stem cells via TLX.
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role in regulating STAT1 signaling and host defense
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Nr2e1 regulates processes involved in neurite development and terminal retinal cell differentiation.
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we have provided new candidate interacting partners and numerous well-developed testable hypotheses for understanding the pathways by which Nr2e1 functions to regulate neocortex development.
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TLX overexpression promotes beta cell proliferation and decreases cell apoptosis causes significant expression changes of 225 genes.
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data suggest that miR-378 is a novel miRNA that regulates NSC proliferation and differentiation via targeting TLX
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NR2E1 regulates CBX7 and restrains senescence in neural stem cells.
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TLX functions as a potent suppressor of oncogene-induced senescence in prostate cancer via its transcriptional co-regulation of the CDKN1A (p21(WAF1) (/) (CIP1) ) and SIRT1 genes
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MiR-9 and TLX form a feedback regulatory loop to coordinate the proliferation.
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These results suggest a strong association between hippocampal neurogenesis and cognition, as well as significant contributions of TLX to hippocampal neurogenesis, learning, and memory.
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Results of the current study suggest aggression displayed by TLX null and heterozygous mice involves 5-HT(2A/C) receptors.
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By interacting with its cofactors, Tlx represses its target genes and plays an important role in the maintenance of adult neural stem cells. (Review)
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Interaction of NSD1 with the NR2E/F subfamily including COUP-TFI, COUP-TFII, EAR2 and TLX requires an F/YSXXLXXL/Y motif. Interactions of NSD1 with liganded NRs require an overlapping LXXLL motif.