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Related Concept Videos

Cotranslational Protein Translocation01:20

Cotranslational Protein Translocation

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Translocation of proteins across membranes is an ancient process that occurs even in bacteria and archaebacteria. In fact, the components of the translocation machinery are still conserved between prokaryotes and eukaryotes.
Sec61 channel partners for cotranslational translocation
During cotranslational translocation, the Sec61 channel partners with the signal recognition particle (SRP), the signal recognition particle receptor (SR), and the ribosomes to transport the nascent polypeptide chain...
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Protein Transport to the Thylakoids01:22

Protein Transport to the Thylakoids

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Thylakoids are membrane-bound sac-like structures within the chloroplast that serve as sites for photosynthesis. Thylakoid lumen contains many electron transport proteins and is enclosed by a thylakoid membrane rich in the light-harvesting complex. Proteins targeted to the thylakoids are transported as precursors and are sorted by the general TOC/TIC import pathway. Once the precursor reaches the stroma, stromal processing peptidases remove their transit signal and expose thylakoid signal...
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Tail-anchoring of Proteins in the ER Membrane01:45

Tail-anchoring of Proteins in the ER Membrane

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Tail-anchored, or TA, proteins are estimated to make up to 3-5% of membrane proteins found in the eukaryotic cell. Such proteins have a single transmembrane domain located approximately 30 amino acid residues upstream from the C-terminal end. As a result, the signal recognition particle (SRP) cannot guide a TA protein to the ER membrane for cotranslational insertion. Hence, they are integrated into the ER membrane post-translationally using their C-terminal end as the anchor. TA proteins...
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Recycling Endosomes and Transcytosis00:58

Recycling Endosomes and Transcytosis

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The recycling endosome, also known as the endosomal recycling compartment (ERC), is a part of the slow-recycling process of the endocytic pathway. Molecules internalized through receptor-mediated endocytosis are either degraded in the lysosomes or are recycled to the plasma membrane through the fast- or slow-recycling route.
The recycling endosome is not a single organelle but an extensively tubulated network of recycling pathways. It functions in storing molecules or transporting them across...
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Post-translational Translocation of Proteins to the RER01:27

Post-translational Translocation of Proteins to the RER

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A sizable fraction of proteins destined for ER are first synthesized in the cell cytosol and then transported across the ER membrane–a process called post-translational translocation. Similar to cotranslationally translocated proteins, these proteins also use the Sec translocon complex to enter the ER lumen.
Targeting proteins to the ER
Hsp40 and Hsp70 chaperone molecules bind the translated proteins in the cytosol to prevent their folding. The chaperone binding helps to keep the signal...
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Protein Translocation Machinery on the ER Membrane01:28

Protein Translocation Machinery on the ER Membrane

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The translocon complex situated on the ER membrane is the main gateway for the protein secretory pathway. It facilitates the transport of nascent peptides into the ER lumen and their insertion into the ER membrane.
Sec61 protein conducting channel
In eukaryotes, the translocon complex comprises a core heterotrimeric translocator channel called the Sec61 complex. This channel includes three transmembrane proteins, Sec61α, Sec61β, and Sec61γ, and is the largest subunit of the...
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Utilizing pHluorin-tagged Receptors to Monitor Subcellular Localization and Trafficking
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TRPC6 channel translocation into phagosomal membrane augments phagosomal function.

Vladimir Riazanski1, Aida G Gabdoulkhakova1, Lin S Boynton1

  • 1Department of Pharmacological and Physiological Sciences and Department of Medicine, University of Chicago, Chicago, IL 60637;

Proceedings of the National Academy of Sciences of the United States of America
|November 26, 2015
PubMed
Summary
This summary is machine-generated.

Defects in cystic fibrosis (CF) lung immunity impair bacterial killing. Enhancing TRPC6 channel function in alveolar macrophages (AMs) can restore microbicidal activity, offering a potential therapeutic strategy for CF lung infections.

Keywords:
TRPC6alveolar macrophagecystic fibrosisphagosomeroscovitine

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Expression and Purification of the Human Lipid-sensitive Cation Channel TRPC3 for Structural Determination by Single-particle Cryo-electron Microscopy
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Expression and Purification of the Human Lipid-sensitive Cation Channel TRPC3 for Structural Determination by Single-particle Cryo-electron Microscopy
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"Phagosome Closure Assay" to Visualize Phagosome Formation in Three Dimensions Using Total Internal Reflection Fluorescent Microscopy TIRFM
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Area of Science:

  • Immunology
  • Cell Biology
  • Respiratory Medicine

Background:

  • Cystic Fibrosis (CF) involves lung immune defects and bacterial infections.
  • Alveolar macrophages (AMs) are crucial for pathogen clearance via phagocytosis.
  • Phagosomal acidification, driven by V-ATPases, is essential for bacterial killing.

Purpose of the Study:

  • To investigate the role of TRPC6 channels in AM phagosomal function.
  • To determine if TRPC6 can restore microbicidal activity in CF models.
  • To explore methods for enhancing TRPC6 channel function.

Main Methods:

  • Studied TRPC6 channel function in alveolar macrophages (AMs).
  • Investigated TRPC6 translocation and activity modulation by (R)-roscovitine.
  • Assessed the impact of TRPC6 on phagosomal acidification and bacterial killing.

Main Results:

  • TRPC6 channels shunt the proton pump-generated transmembrane potential in AMs.
  • TRPC6 enhances bacterial killing in compromised CF AMs and boosts non-CF AM function.
  • (R)-roscovitine treatment promotes TRPC6 translocation to the cell surface, enhancing its activity.

Conclusions:

  • TRPC6 channel activity is critical for restoring phagosomal microbicidal function.
  • Enhancing TRPC6 vesicular insertion may be a therapeutic approach for CF lung infections.
  • TRPC6 modulation offers a potential strategy to improve innate immunity in CF.