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B-cell conditional deficient mice for the Med1 subunit display robust somatic hypermutation.
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High MED1 expression is associated with metastasis in breast Cancer.
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Data, including data from studies using cells from transgenic/knockout mice, suggest that Med1 plays role in enamel formation; Med1 induces Alpl via stimulation of Notch1 signaling by forming Notch1-RBP-Jk complex on Alpl promoter. (Med1 = mediator complex subunit 1; Alpl = alkaline phosphatase, liver-bone-kidney; Notch1 = Notch gene homolog 1; RBP-Jk = kappa J region recombining binding protein suppressor of hairless)
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MED1 in macrophages has an antiatherosclerotic role via PPARgamma-regulated transactivation.
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Cardiomyocyte-specific ablation of Med1 causes lethal dilated cardiomyopathy in mice.
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Med1 deletion disrupted cardiac mitochondrial and metabolic gene expression patterns
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Med1 and Med12, two subunits of the mediator complex implicated in transcription initiation and long-range enhancer/promoter loop formation, are dynamically recruited to the IgH locus enhancers.
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We conclude that MED1 regulates the temporal progression of primary spermatocytes through meiosis, with its absence resulting in abbreviated pre-leptotene, leptotene, and zygotene stages, and a prolonged pachytene stage.
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These results demonstrate that Med1 is a master regulator in adult stem cells to govern epithelial cell fate
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The novel function of MED1 in keratinocytes.
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PRDM16 deficiency in BAT reduces MED1 binding at PRDM16 target sites and causes a fundamental change in chromatin architecture at key brown fat-selective genes
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Collectively, these observations strongly suggest that MED1 has an important affect on mitochondrial function.
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Clk2 phosphorylation of PGC-1alpha disrupts its interaction with Mediator subunit 1, which leads to a suppression of PGC-1alpha activation of peroxisome proliferator-activated receptor alpha target genes in fatty acid oxidation and ketogenesis.
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hyperactivated ERK and/or AKT signaling pathways promoted MED1 overexpression in prostate cancer cells.
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Med1 phosphorylation by its association with AMPK regulates liver cell proliferation and fatty acid oxidation, most likely as a downstream effector of PPARalpha and AMPK
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Tshb gene transcription was attenuated in MED1 mutant mice in which the nuclear receptor-binding ability of MED1 was specifically disrupted.
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Med1 is a context-dependent GATA-1 coregulator that also exerts specialized functions in erythroid cells to control GATA-1-independent, cell-type-specific genes.
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MED1 has roles in maintaining quiescence of keratinocytes and preventing depletion of the follicular stem cells.
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Hyperlipidemia in MED1(deltaLiv) mice in response to fasting is due to the accumulation of VLDL, which suggests that MED1 plays a pivotal role in the regulation of plasma triglyceride and cholesterol levels.
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Med1 is implicated in adipogenesis, lipid metabolic and biosynthetic processes, glucose metabolism, and mitochondrial metabolic pathways
