autophagy

Another study done on p62 further emphasizes autophagy's role in tumor suppression.

Strong induction of apoptosis and autophagy has also been seen.

The role of autophagy in cancer is one that has been highly researched and reviewed.

Therefore, this data supports the development of therapies that will encourage autophagy.

In order to maintain homeostasis conditions, autophagy must not be disrupted.

Thus these experiments shown autophagy's role as a tumor suppressor.

In cancerous cells, autophagy is used as a way to deal with stress on the cell.

Thus, these qualities about autophagy can be used and manipulated as a strategy for cancer prevention.

In both cases, autophagy is observed to markedly increase.

However, recent research has been able to show that autophagy is more likely to be used as a tumor suppressor according to several models.

A number of proteins involved in autophagy are known to be present in the genome.

While almost an exclusive term for this process, autophagy nonetheless has occasionally made its way into more common usage.

Alternatively, autophagy has also been shown to play a huge role in tumor cell survival.

This leads to a decrease in Atg1 kinase activity and decreased autophagy.

Another database specializing in human autophagy (http://autophagy.lu/) is also publicly available.

This in turn reduces lysosomal degradative ability and blocks autophagy.

Several experiments have been done with mice and varying Beclin1, a protein that regulates autophagy.

Unveiling the roles of autophagy in innate and adaptive immunity.

However, except for autophagy, the mammalian orthologs of Atg18p do not share similar functions.

Thus, to induce autophagy, p53 is degraded through proteasomes.

Noncovalent interactions are important for its cargo targeting functions in selective autophagy.

ATG16L1 is a component of a large protein complex essential for autophagy.

Autophagy then occurs at an accelerated rate.

Ca is seen to be increasingly important for endo-lysosomal function, e.g. trafficking and autophagy.

Research suggests that autophagy is required for the lifespan-prolonging effects of caloric restriction.