Caspase 3

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. 

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

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 root of Parkinson’s disease (PD) points to a poorly regulated electron transport chain leading to mitochondrial damage, where many proteins need to work cohesively to ensure proper function.  The two key players of this pathway are PINK1, also known as PTEN or PARK6, and Parkin, also known as PARK2 - where PINK1 acts as an upstream effector of Parkin to regulate mitochondrial dynamics.  Mitochondria must maintain a healthy equilibrium and do so by undergoing a series of fission and fusion event

The process of autophagy, or lysosome-mediated degradation of damaged proteins and organelles in the cytosol, is a vital cellular process that acts as a quality control mechanism for proteins and organelles. The misregulation of autophagy can lead to an imbalance of cellular homeostasis and the subsequent development of disease.  Therefore, the study of autophagy is at the forefront of neuroscience and cancer research, among others.

Proliferating cell nuclear antigen (PCNA) plays a crucial role in nucleic acid metabolism as it pertains to DNA replication and repair.  Most noted for its activation of subunits of DNA polymerase, it has also been found to interact with cell-cycle progression proteins.  Modifications of PCNA as a result of cellular response put PCNA in a pivotal position with DNA replication, DNA damage, and chromatin structure and function.  In response to DNA damage, PCNA is ubiquitinated and becomes part of the RAD-6 dependent DNA repair pathway, where it acts as a substrate with a variety of p

GFP, or green fluorescent protein, is a chemiluminescent protein derived from Aequorea jellyfish that was first discovered by Osamu Shimomura.  It was soon after established that the emission spectra of GFP was right around 509nm, or the ultraviolet color range.  The GFP gene is often used to form expression constructs in order to closely follow protein behavior, cellular differentiation, protein localization and more.  The following articles employed a GFP antibody in conjunction with various other GFP construct techniques to strengthe

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.

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