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Related Concept Videos

Lipids as Anchors01:32

Lipids as Anchors

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In the plasma membrane, the lipids forming the bilayer can also act as an anchor to tether proteins to the membrane. The three main types of lipid anchors found in eukaryotes are – prenyl groups, fatty acyl groups, and glycosylphosphatidylinositol or GPI groups. Prenyl and fatty acyl groups act as anchors on the cytosolic surface of the membrane, whereas GPI anchors proteins on the extracellular side.
The carboxy-terminal of most of the prenylated proteins, such as Ras proteins, contains...
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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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Export of Misfolded Proteins out of the ER01:32

Export of Misfolded Proteins out of the ER

5.4K
After folding, the ER assesses the quality of secretory and membrane proteins. The correctly folded proteins are cleared by the calnexin cycle for transport to their final destination, while misfolded proteins are held back in the ER lumen. The ER chaperones attempt to unfold and refold the misfolded proteins but sometimes fail to achieve the correct native conformation. Such terminally misfolded proteins are then exported to the cytosol by ER-associated degradation or ERAD pathway for...
5.4K
GPI Anchoring of Proteins in the ER Membrane01:29

GPI Anchoring of Proteins in the ER Membrane

5.8K
GPI-anchoring is a post-translational, reversible protein modification that is ubiquitous in eukaryotes. Such proteins are primarily present on the exoplasmic leaflet of the plasma membrane.
GPI-anchor structure
A sequence of 11 enzymatic reactions results in the synthesis of the complete GPI anchor consisting of a hydrophobic and a hydrophilic portion. The hydrophobic portion comprises phosphatidylinositol, while the hydrophilic part comprises polar groups like phosphoethanolamine,...
5.8K
Protein Modifications in the RER01:26

Protein Modifications in the RER

7.4K
Modification of secretory and transmembrane proteins entering the rough ER begins in the ER lumen. These modifications aid in protein folding and stabilize the acquired tertiary structure. Protein modifications in the rough ER co-occur at different stages of protein folding.
Broadly, these modifications can be categorized into four main categories — glycosylation, formation of disulfide bonds, assembly of protein subunits, and specific proteolytic cleavages like removal of signal...
7.4K
Directing Proteins to the Rough Endoplasmic Reticulum01:34

Directing Proteins to the Rough Endoplasmic Reticulum

18.3K
The organelle-specific signaling sequences direct proteins synthesized in the cytosol to their final destination like ER, mitochondria, peroxisomes, etc. Some of the proteins directed to ER are then trafficked via vesicles to other organelles within the cell or the extracellular environment through the Golgi complex. For example, the rough ER synthesizes soluble proteins for transportation to the lysosomes or secretion out of the cell. It can also synthesize transmembrane proteins that can...
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Related Experiment Video

Updated: Mar 22, 2026

Metabolic Mapping: Quantitative Enzyme Cytochemistry and Histochemistry to Determine the Activity of Dehydrogenases in Cells and Tissues
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IDH1-Driven Reductive Carboxylation Supports Anchorage Independence

    Cancer Discovery
    |April 30, 2016
    PubMed
    Summary

    Adaptation to anchorage-independent growth depends on isocitrate dehydrogenase 1 (IDH1) altering citrate metabolism. This metabolic shift is crucial for cancer cells to thrive without attachment.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Cancer Research

    Background:

    • Anchorage-independent growth is a hallmark of cancer, enabling cell survival and proliferation without substrate attachment.
    • Metabolic reprogramming is essential for cancer cells to meet their increased bioenergetic and biosynthetic demands.
    • The role of specific metabolic enzymes in facilitating anchorage-independent growth remains an active area of investigation.

    Discussion:

    • This study investigates the role of isocitrate dehydrogenase 1 (IDH1) in adapting cancer cells to anchorage-independent growth.
    • IDH1 activity influences citrate metabolism, a key node in cellular energy production and biosynthesis.
    • The findings highlight a critical metabolic vulnerability associated with anchorage-independent growth.

    Key Insights:

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    • Isocitrate dehydrogenase 1 (IDH1) is indispensable for cancer cells to adapt to anchorage-independent growth.
    • IDH1 modulates citrate metabolism, providing essential building blocks and energy for non-adherent cells.
    • Targeting IDH1 could represent a novel therapeutic strategy against cancers exhibiting anchorage-independent phenotypes.

    Outlook:

    • Further research should explore the precise downstream targets of IDH1-mediated metabolic alterations in anchorage-independent cells.
    • Investigating the therapeutic potential of IDH1 inhibitors in combination with other anti-cancer agents is warranted.
    • Understanding these metabolic adaptations may reveal new biomarkers for aggressive cancer subtypes.