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NFkB1

The role of STING/TMEM173 in gamma and encephalitis Herpes Simplex Virus (HSV)

Stimulator of interferon genes (STING), also known as TMEM173, promotes the production of the interferon’s IFN-alpha and IFN-beta.  STING possesses three functional domains: a cytoplasmic C-terminal tail, a central globular domain, and four N-terminal transmembrane motifs that attach it to the ER.  The role of STING in the immune response is specific to its ability to sense nucleic acids, particularly dsDNA.

Pathway Highlight: Three key factors that contribute to cellular heterogeneity in apoptosis

Have you ever wondered why cells in the same population respond differently to an apoptotic stimulus? Apoptosis, a form of programmed cell death, is vital for the removal of unwanted or damaged cells. As with most cellular processes, too much or too little activation can be detrimental and lead to various diseases including autoimmune disorders and cancer.

Pathway Highlight: Which caspase substrates contribute to the morphological features associated with apoptosis?

Apoptosis, or programmed cell death, is controlled by a caspase signal cascade that activates downstream signals to induce the morphological changes used to differentiate apoptosis from other forms of cell death.  Novus Biologicals offers a variety of antibodies and tools to detect the different morphological indicators of cell death. 

The use of apoptosis antibodies and controls in cell death research

Apoptosis is a method of programmed cell death that is notably characterized by a morphological change in cellular nuclei and membrane appearance.  Not to be confused with necrosis, apoptosis is a pathway that is induced by a variety of factors that activate cysteine proteases known as caspases to lead the cell to its ultimate death versus natural death of a cell.

NFkB and p62 Both Activate and Regulate Inflammation

Nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB) is a protein complex that regulates DNA transcription and is a critical regulator of cell survival. NFkB has long been known as a primer of inflammation, however researchers are now finding that NFkB may also regulate over-inflammation via a novel mitophagy pathway (Minton, 2016).