Bax

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

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. 

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.

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

p53, the protein product of the tp53 gene, is one of the most widely studied tumor suppressor proteins in cancer research.  p53 is unique in that it demonstrates both tumor suppressive and tumor progressive properties depending on whether it is functional or mutated.  The most common mutation in the p53 protein that leads to lack of tumor suppression activity is a missense mutation, however frameshift or nonsense mutations are also common.  In fact, mutant p53 has exhibited dominant negative inhibition of the wild type version of the protein, demonstrating the fact that the p53 pat

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

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.

Similar to other cell processes, the balance between cell survival and cell death is an important equilibrium that when altered expression of genes can lead to a variety of disease.

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