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Rest in Peace: Is the Receptor Interacting Protein (RIP) Kinase-3 (RIPK3) a Protector or Offender?

CD95 Mediates Neurovascular Development

How to switch from apoptotic to necroptotic cell death? Answer: Autophagy!

By Christina Towers, PhD.

Apoptosis and Necroptosis Part II: Inhibitors of apoptosis proteins (IAPs); Key regulators of the balance between necroptosis, apoptosis and survival

In the first installment of this two-part blog post titled "Apoptosis and Necroptosis: Important factors to identify both types of programmed cell death", the mechanisms by which cell death occurs and ways to identify these pathways were discussed. In this next segment, we focus on the molecular factors regulating the choice between programmed cell death and survival signaling.

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.

Apoptosis and Necroptosis Part I: Important factors to identify both types of programmed cell death

Different types of cell death have classically been identified by discrete morphological changes. The hallmarks of apoptosis include cell shrinkage, nuclear fragmentation and membrane blebbing whereas necroptosis is characterized by cell swelling and plasma membrane breakdown. While these two forms of cell death are clearly distinct, substantial crosstalk occurs between them.  Accordingly, it is becoming increasingly important to understand how these processes differ and to understand ways to differentiate them in cellular populations. 

Article Review: Dual effects of carbon monoxide on pericytes and neurogenesis in traumatic brain injury

Traumatic brain injury (TBI) currently contributes to nearly 30% of all injury deaths in the United States.  Characterized by an abrasive head injury that interrupts normal brain function, TBI can range from mild to severe.  Mild symptoms can present themselves as excessive tiredness, difficulty concentrating and lack of clear thinking.  Severe cases of TBI are hallmarked by unusual behavior, seizures and loss of consciousness.  Research has shown that on a molecular level TBI triggers various mechanisms of cell death alongside attempted tissue recovery, therefore Choi et al sought

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.

The role of MHC Class II RT1B and immune response post brain injury

The major histocompatibility complex (MHC) is responsible for binding peptide fragments arising from pathogens in order to display them on the cell surface for recognition from immune cells.  Once recognized, the foreign pathogen is typically evaded. The MHC complex is broken into two categories, MHC Class I proteins and MHC Class II proteins.  MHC complex I and II proteins are all very different and contain specific molecules to bind different peptides – in fact, they have been described as the most polymorphic genes there are.

The role of c-Fos in the regulation of the JC virus gene transcription

c-Fos is a member of the AP-1 transcription factor family under the Fos protein family umbrella, alongside Fra-1, Fra-2 and Fos-B.  Also in the AP-1 transcription family are the Jun proteins, c-Jun, Jun-B and Jun-D.  Each member of the AP-1 transcription family is a phosphonuclear protein composed of a carboxy-terminal leucine zipper domai

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