Publications by authors named "A Layoun"

Article Synopsis
  • Inactivation of mTORC1 enhances the nuclear levels of certain transcription factors involved in metabolism and cell death, particularly STAT1, which requires the mTORC1-associated protein KPNA1 for its nuclear import.
  • The study identifies a specific TOS motif in protein kinase C delta (PKCδ) that facilitates its interaction with mTORC1, suggesting that PKCδ's regulation is influenced by mTORC1 activity.
  • Disruption of this TOS motif leads to increased nuclear PKCδ levels, heightening STAT1 activity and apoptosis, indicating that mTORC1 plays a role in controlling the nuclear entry of PKCδ and consequently affects apoptosis signaling pathways.
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Iron homeostasis is tightly regulated to provide virtually all cells in the body, particularly red blood cells, with this essential element while defending against its toxicity. The peptide hormone hepcidin is central to the control of the amount of iron absorbed from the diet and iron recycling from macrophages. Previously, we have shown that hepcidin induction in macrophages following Toll-like receptor (TLR) stimulation depends on the presence of myeloid differentiation primary response gene 88 (MyD88).

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During infection and inflammation, circulating monocytes leave the bloodstream and migrate into tissues, where they differentiate into macrophages. Macrophages express surface Toll-like receptors (TLRs), which recognize molecular patterns conserved through evolution in a wide range of microorganisms. TLRs play a central role in macrophage activation which is usually associated with gene expression alteration.

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Hepcidin is an antimicrobial peptide hormone that plays a central role in the metabolism of iron and its expression in the liver can be induced through two major pathways: the inflammatory pathway, mainly via IL-6; and the iron-sensing pathway, mediated by BMP-6. GATA-proteins are group of evolutionary conserved transcriptional regulators that bind to the consensus motif-WGATAR-in the promoter region. In hepatoma cells, GATA-proteins 4 and 6 in conjunction with the co-factor friend of GATA (FOG) were shown to modulate the transcription of HAMP.

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