Beclin 1

E-syt in Autophagosome biogenesis: What is the source of it all?

Autophagy Inhibition in Cancer: Clinical Trials Update

Lysosomal Dysfunction is Linked to Exosomal Secretion

CaMKII stimulates autophagic degradation of 'ID', a new frontier against cancer

Brain size matters: MTOR regulates autophagy and number of cortical interneurons

Polyglutamine Tracts as Autophagy Regulators

Autophagy: Pro or Anti-tumorigenic? And the role of epigenetics in this debate

By Christina Towers, PhD

Key Targets in Apoptosis, Necroptosis, and Autophagy

Cell death/recycling pathways such as apoptosis, necroptosis, and autophagy are an integral part of the growth, development, homeostasis as well as the pathophysiology in the life of living organisms. These signaling pathways are highly regulated and some of their key regulatory targets are discussed below.


Apoptosis, programmed cell death, is primarily characterized by the activation of caspases which further regulate the mass cleavage of proteins and DNA. Some of major the proteins responsible for various apoptotic events are:

TRIF/TICAM1 and mitochondrial dynamics in the innate immune response

TRIF, also known as toll like receptor adaptor molecule 1 or TICAM1, is known for its role in invading foreign pathogens as part of our innate immune response. TRIF/TICAM1 is a TIR-domain adaptor protein (toll/interleukin-1 receptor) that interacts with the Toll-like receptors (TLRs) through intracellular signaling and recognition of its TIR site.

UVRAG - A regulator of membrane trafficking in autophagy and endocytosis

UV resistance-associated gene (UVRAG) is a tumor suppressor that is commonly mutated in colon and breast cancer. While UVRAG was discovered for its ability to complement UV sensitivity in xeroderma pigmentosum cells, its main functions are in autophagy, endocytosis, and apoptosis. During autophagy UVRAG interacts with Beclin 1 to promote autophagosome formation. UVRAG can also interact with VPS16 to recruit membrane fusion machinery to mediate autophagosome maturation.