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Related Concept Videos

GPCRs Regulate Adenylyl Cylase Activity01:09

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Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
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G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
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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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Activation and Inactivation of G Proteins01:22

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Heterotrimeric G proteins are guanine nucleotide-binding proteins. As the name suggests, heterotrimeric G proteins are composed of three subunits: alpha, beta, and gamma. They remain GDP-bound or GTP-bound inside the cells and switch between inactive/active states. The Gα subunit possesses the nucleotide-binding pocket that binds guanine nucleotides and switches between GDP or GTP-bound states. In contrast, the Gꞵ and Gγ subunits are always bound together with high...
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G-Protein Gated Ion Channels01:21

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GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory...
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Transducer Mechanism: Nuclear Receptors01:31

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Nuclear receptors, or NRs, are unique transcription factors that regulate gene transcription and affect the cellular pathways involved in reproduction, development, or metabolism. Their ability to be stimulated by small lipophilic ligands and control vital cellular processes makes them ideal drug targets. Nearly 10-15% of currently prescribed drugs target these receptors.
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Detecting the Ligand-binding Domain Dimerization Activity of Estrogen Receptor Alpha Using the Mammalian Two-Hybrid Assay
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IQGAP1 binds to estrogen receptor-α and modulates its function.

Huseyin H Erdemir1, Zhigang Li, David B Sacks

  • 1From the Department of Laboratory Medicine, National Institutes of Health, Bethesda, Maryland 20892.

The Journal of Biological Chemistry
|February 20, 2014
PubMed
Summary

IQmotif-binding protein 1 (IQGAP1) directly binds estrogen receptors (ERα and ERβ), influencing gene transcription. This interaction suggests IQGAP1 as a potential therapeutic target for breast cancer.

Keywords:
Cell SignalingEstrogenEstrogen ReceptorIQGAP1Nuclear ReceptorsProtein-Protein InteractionsScaffold ProteinsTranscription

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Area of Science:

  • Molecular biology
  • Cellular signaling
  • Cancer research

Background:

  • Estrogen receptor (ER) is a transcription factor regulating cellular functions.
  • IQ motif-binding protein 1 (IQGAP1) acts as a scaffold, integrating signaling pathways.
  • Both ERα and IQGAP1 are implicated in breast cancer development.

Purpose of the Study:

  • To investigate the interaction between IQGAP1 and ERα/ERβ.
  • To determine the functional consequences of this interaction on estrogen-responsive gene transcription.

Main Methods:

  • In vitro protein binding assays using purified proteins and protein fragments.
  • Co-immunoprecipitation assays in cellular contexts.
  • Estradiol modulation experiments.
  • Gene knockdown studies to assess transcriptional effects.

Main Results:

  • IQGAP1 directly binds to both ERα and ERβ.
  • ERα binds to the IQ domain of IQGAP1, and IQGAP1 binds to the hinge region of ERα.
  • The IQGAP1-ERα interaction is modulated by estradiol and occurs within cells.
  • Knockdown of IQGAP1 reduces estradiol-induced transcription of key estrogen-responsive genes (pS2, progesterone receptor, cyclin D1).

Conclusions:

  • IQGAP1 binds ERα and modulates its transcriptional activity.
  • IQGAP1 plays a significant role in estrogen-mediated gene regulation.
  • IQGAP1 represents a potential therapeutic target for breast cancer treatment.