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Related Concept Videos

Phosphoinositides and PIPs01:42

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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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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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Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
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Protein Kinases and Phosphatases02:54

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Proteins undergo chemical modifications that trigger changes in the charge, structure, and conformation of the proteins. Phosphorylation, acetylation, glycosylation, nitrosylation, ubiquitination, lipidation, methylation, and proteolysis are various protein modifications that regulate protein activity. Such modifications are usually enzyme-driven.
Protein kinases
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IP3/DAG Signaling Pathway01:11

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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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PIP-on-a-chip: A Label-free Study of Protein-phosphoinositide Interactions
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Phosphoinositide dynamics in virus-associated malignancies.

Mingchuan Li1, Wenbin Zhong1, Emilio Hirsch2

  • 1Guangzhou Institute of Cancer Research, the Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou 510095, China; State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou 510095, China.

Trends in Cell Biology
|October 2, 2025
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Summary

Human oncoviruses manipulate phosphoinositides (PPIn) metabolism to promote virus replication and cancer development. This review details how oncoviruses dysregulate PPIn, driving oncogenic signaling and tumorigenesis.

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cancerkinaselipid transport proteinphosphatasephosphoinositidevirus-associated cancer

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Identification of Inositol Phosphate or Phosphoinositide Interacting Proteins by Affinity Chromatography Coupled to Western Blot or Mass Spectrometry
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Single-molecule Super-resolution Imaging of Phosphatidylinositol 4,5-bisphosphate in the Plasma Membrane with Novel Fluorescent Probes
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Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Virus-associated cancers represent a significant global health burden.
  • Human oncoviruses cause cancer by altering host cell functions, particularly membrane signaling and trafficking.
  • Phosphoinositides (PPIn) are critical regulators of membrane dynamics and signal transduction, crucial in cancer progression.

Purpose of the Study:

  • To review how human oncoviruses manipulate phosphoinositide metabolism.
  • To elucidate the role of PPIn dysregulation in oncovirus-driven tumorigenesis.

Main Methods:

  • Literature review of studies on oncoviruses and phosphoinositide metabolism.
  • Analysis of mechanisms by which oncoviruses alter host PPIn pathways.
  • Synthesis of findings linking PPIn dysregulation to oncogenic signaling.

Main Results:

  • Oncoviruses actively exploit and dysregulate host phosphoinositide metabolism.
  • Altered PPIn metabolism by oncoviruses facilitates viral replication and persistence.
  • This metabolic reprogramming activates oncogenic signaling pathways, promoting malignant transformation.

Conclusions:

  • Oncoviruses utilize phosphoinositides as key targets to sustain their life cycle.
  • Manipulation of PPIn metabolism by oncoviruses is a critical step in long-term host cell transformation and tumorigenesis.