Akt

The IKK complex, or inhibitor of NFkB kinase, is composed of IKK alpha and IKK beta.  These kinases are at the core of the NFkB signaling cascade.  The NFkB family is made up of transcription factors that are kept inactive in the cytoplasm through inhibitory IkB proteins.

AMP-activated protein kinase (AMPK) is best known as a sensor of oxidative stress.  AMPK is activated by increased intracellular AMP levels, which are a result of alterations in cellular metabolism from causes such as hypoxia, changes in ATP, senescence and more.  In cell stress models, AMPK can protect cells from reduced ATP production by altering ATP biosynthetic pathways.  Furthermore, AMPK has implications in reducing inflammatory reactions in apoptosis pathways.

Autophagy is a crucial cellular process that clears the cell of protein aggregates, toxins, and damaged cell products. Accumulation of toxins, damaged cell products and unwanted proteins has been proven to play a role in aging and many forms of disease and cancer.

Autophagy is a crucial intracellular pathway that manages the degradation and recycling of long-lived proteins in the cell. The LC3 (or light chain 3) family is composed of three members, LC3A, LC3B and LC3C. Upon autophagy induction, LC3 is cleaved, causing the release of a C-terminal glycine that is required for phospholipid conjugation.  This process is vital to the formation of the autophagosome, a double membrane structure that delivers proteins to the lysosome during autophagy.

Hypoxia inducible factor 1 (HIF-1) is a protein that plays an essential role in hypoxia, or low levels of cellular oxygen.

NFkB is a transcription factor that plays a role in the expression of genes involved in immune response, inflammation, metastasis, cell survival and more. RelA (p65) is one member of the NFkB mammalian family, alongside other subunits.

Beta tubulin III, also known as Tuj-1, is a class III member of the beta tubulin protein family. Beta tubulins are one of two structural components that form our microtubule network.

Autophagy is an essential process that maintains cellular homeostasis and carries out lysosome-mediated degradation of unwanted proteins in the cytoplasm.  Because of this regulatory function, autophagy is often examined when looking at disease pathways.  While our immune system initiates the removal of viruses and pathogens through the autophagic pathway, viruses, such as HIV, have developed a way to evade this process through inhibition.  Therefore, developing a reliable way to examine the molecular process of this inhibition and interaction is very desired.  The central autophagy

The mammalian forkhead O class transcription factors (FOXO) regulate diverse cellular processes such as metabolism, cell cycle, and apoptosis. Activity of these transcription factors can be regulated by diverse post-translational modifications including phosphorylation, acetylation, and ubiquitination (1). These modifications can alter nuclear transport, DNA binding, and protein-protein interactions to alter transcriptional activity. The best studied member of the FOXO family is FOXO1.

Programmed cell death via apoptosis is a key controlled physiological process instigated by the cell death receptor family, their ligands, and the caspase cysteine protease family. All caspases exist in a precursor form that contains a prodomain, and large and small catalytic subunits. A cleavage event adjacent to an aspartate liberates one large and one small subunit, which are now free to associate into an active a2b2 tetramer. Caspases are activated by triggers such as ligand-receptor interactions, growth factor deprivation, and cell function inhibitors.