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Phosphoinositides and PIPs01:42

Phosphoinositides and PIPs

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Phosphoinositides are a group of phospholipids containing a glycerol backbone with two fatty acid chains and a phosphate attached to a myoinositol sugar ring. The inositol head group extends into the cytoplasm, where it is modified by adding phosphate groups to form phosphatidylinositol phosphates or PIPs.
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Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the  phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and...
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The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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piRNA - Piwi-interacting RNAs02:57

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PIWI-interacting RNAs, or piRNAs, are the most abundant short non-coding RNAs. More than 20,000 genes have been found in humans that code for piRNAs while only 2000 genes have been found for miRNAs. piRNAs can act at the transcriptional and post-transcriptional levels and have a vital role in silencing transposable elements present in germ cells. They are also involved in epigenetic silencing and activation. Previously, they were thought to function only in germ cells but new evidence suggests...
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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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Many receptor binding ligands are hydrophilic; they do not cross the cell membrane but bind to cell-surface receptors. Thus, their message must be relayed by second messengers present in the cell cytoplasm. There are several second messenger pathways, each with its own way of relaying information. For example, the G protein-coupled receptors can activate both phosphoinositol and cyclic AMP (cAMP) second messenger pathways. The phosphoinositol pathway is active when the receptor induces...
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Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
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STeerING PI4P for innate immune activation.

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  • 1Section of Infection and Immunity, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, USA.

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STING protein activation relies on specific lipid enrichment in cellular compartments. The ARMH3-PI4KB-PI4P pathway drives this lipid accumulation, crucial for STING function.

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Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • STING (stimulator of interferon genes) protein is a key mediator of innate immunity.
  • STING undergoes transport through various cellular organelles, including the ER, Golgi, and endosomes, prior to lysosomal degradation.
  • STING activation is critical for mounting immune responses against pathogens and endogenous nucleic acids.

Purpose of the Study:

  • To investigate the molecular mechanisms regulating STING activation.
  • To identify the cellular pathways and lipid compositions involved in STING localization and function.
  • To elucidate the role of specific lipid-modifying pathways in STING signaling.

Main Methods:

  • Cellular fractionation and biochemical assays to track STING localization.
  • Lipidomic analysis to determine the composition of cellular membranes.
  • Genetic manipulation of the ARMH3-PI4KB-PI4P pathway components.
  • STING activation assays under various cellular conditions.

Main Results:

  • STING protein localizes to and is activated within the trans-Golgi network and endosomes.
  • The ARMH3-PI4KB-PI4P pathway is essential for the enrichment of cholesterol and sphingomyelin in these compartments.
  • This lipid enrichment is critical for STING activation, irrespective of whether it is triggered by cGAS-dependent or -independent pathways.
  • Dysregulation of this pathway impairs STING-mediated immune signaling.

Conclusions:

  • The ARMH3-PI4KB-PI4P pathway critically regulates STING activation by controlling the lipid microenvironment of the trans-Golgi network and endosomes.
  • Cholesterol and sphingomyelin enrichment in these organelles is a prerequisite for effective STING signaling.
  • These findings reveal a novel mechanism linking lipid metabolism to innate immune activation via STING.