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Epithelial-Mesenchymal Transition (EMT) is the trans-differentiation of stationary epithelial cells into motile mesenchymal cells. During EMT, epithelial cells lose their junctions and apical-basal polarity, reorganize their cytoskeleton, undergo a change in the signaling cascade that defines cell shape and reprograms gene expression. Collectively, these changes increase the motility of individual cells and enables the development of an invasive phenotype.

The Hedgehog (Hh) family of secreted proteins is involved in a number of developmental processes, one of which is the development of cancer. Past data suggests that the Sonic hedgehog (Shh) receptor is composed of two transmembrane proteins, Patched and Smoothened.  The Hedgehog (Hh) signaling pathway is vital to the development of many tissues during embryogenesis, however, it also has an important role after development.  After development, Hh signaling regulates stem cells and their regenerative function.  When the Hh pathway is awry, signaling may turn oncogenic in nature.

The p53-binding protein 1 (53BP1) is a DNA damage response factor, which is recruited to nuclear structures at the site of DNA damage.  DNA double-strand breaks (DSBs) are mutations that are detrimental to cell viability and genome stability, and must be repaired either through homologous recombination (HR) or non-homologous end joining (NHEJ). 53BP1 specifically promotes both NHEJ as well as the inhibition of HR repair, yet the decision making on a molecular level between these two routes not clearly understood.

xCT is a sodium independent glutamate transporter that regulates the exchange of extracellular l-cystine and intracellular l-glutamate across the plasma membrane. This process is critical to glutathione production and protection from subsequent oxidative stress.

Epigenetics is the process of heritable change in gene activity despite alteration of the hosts DNA sequence, essentially causing a change in a phenotype without a change in the genotype of a host. To change the gene sequence without interfering with the DNA is accomplished by histone and DNA methylation.  Gene silencing in DNA methylation is carried out by DNA methyltransferases 1, 2 and 3a/b (DNMT1, DNMT2, DNMT3A/B). On a broad level, DNMT’s methylate the fifth carbon of cytosine residues in DNA within CG dinucleotides.

Epigenetics is the study of heritable change in gene activity despite alteration of the hosts DNA sequence.  Change in gene activity done independently of the DNA sequence is achieved by way of histone and DNA methylation.  Gene silencing in DNA methylation is carried out by DNA methyltransferases 1, 2 and 3a/b (DNMT1, DNMT2, DNMT3A/B). On a broad level, DNMTs methylate the fifth carbon of cytosine residues in DNA within CG dinucleotides.

Niemann-Pick type C1 (NPC1) mediates low-density cholesterol transport from late endosomes and lysosomes to other areas of the cell via receptor mediation endocytosis.  Although cholesterol moves freely inside the cell, it cannot independently export out of the lysosome, which is where NPC1 steps in.

Fanconi anemia (FA) is a genetically inherited disorder that yields cytogenetic instability, hypersensitivity to DNA crosslinking compounds and defective DNA repair. A variety of genes have been identified within the FA pathway that are referred to as the Fanconi anemia complementation group.  One member of this group, FANCD2, is monoubiquitinated in response to DNA damage.  At this point, FANCD2 specifically localizes to the nucleus to represent the site of DNA repair, often times to the DNA replication fork.

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

MHC molecules (also known as major histocompatibility complex molecules) assist in the presentation of antigens to T cells in order to eradicate foreign pathogens.  These molecules are highly polymorphic, meaning that they exist in multiple variants in order to avoid pathogens evading their activation of the immune response.  MHC Class I molecules in particular deliver cytosolic peptides to the cell surface so that they can continue on through the cytosol and ultimately the endoplasmic reticulum (ER).