Related Experiment Video

Updated: Mar 7, 2026

Assessing Autophagic Flux by Measuring LC3, p62, and LAMP1 Co-localization Using Multispectral Imaging Flow Cytometry
11:39

Assessing Autophagic Flux by Measuring LC3, p62, and LAMP1 Co-localization Using Multispectral Imaging Flow Cytometry

Published on: July 21, 2017

32.4K

Human CLEC16A regulates autophagy through modulating mTOR activity

Rachel Chun Yee Tam1, Michelle Wing Man Li1, Yan Pan Gao2

  • 1Department of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR.

Experimental Cell Research
|February 23, 2017
PubMed

Insights

The protein CLEC16A inhibits autophagy, a cellular process implicated in autoimmune diseases. It does this by activating the mTOR pathway, suggesting a new target for treating autoimmune conditions.

Area of Science:

  • Cell Biology
  • Immunology
  • Molecular Biology

Background:

  • The protein CLEC16A is genetically associated with autoimmune disorders, but its precise function in these conditions is unclear.
  • Autophagy, a cellular degradation process, is increasingly recognized for its role in the development of autoimmune diseases.

Purpose of the Study:

  • To investigate the functional role of CLEC16A in autophagy and its potential connection to autoimmune disease pathogenesis.
  • To elucidate the molecular mechanism by which CLEC16A influences autophagy.

Main Methods:

  • Ectopic expression and siRNA silencing of CLEC16A in human cells.
  • Quantitative proteomics and immunoblotting analyses.
  • Cellular localization studies using microscopy.

Main Results:

  • CLEC16A was found to inhibit starvation-induced autophagy in human cells.
  • CLEC16A appears to regulate autophagy by activating the mTOR pathway.
  • Overexpression of CLEC16A enhanced mTOR activity and reduced autophagy, while CLEC16A deficiency augmented the autophagic response.
  • CLEC16A localizes to cytosolic vesicles and the Golgi apparatus, potentially positioning it to modulate mTOR signaling.

Conclusions:

  • CLEC16A negatively regulates autophagy through the mTOR pathway, particularly at the Golgi apparatus.
  • These findings suggest a functional link between CLEC16A, autophagy modulation, and the development of autoimmune diseases.
Keywords:
AutophagyCLEC16AConfocal microscopyQuantitative proteomicsmTOR signaling

More Related Videos

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy07:20

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

Published on: January 31, 2025

1.3K
Activating Autophagy by Aerobic Exercise in Mice08:44

Activating Autophagy by Aerobic Exercise in Mice

Published on: February 3, 2017

12.8K

Related Concept Videos

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
5.0K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

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...
6.0K
Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
6.0K
Delivery Pathways to the Lysosome01:36

Delivery Pathways to the Lysosome

Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
Endocytosis
In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...
10.4K
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
4.8K
Anaphase Promoting Complex00:50

Anaphase Promoting Complex

The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
3.5K