Oxidative stress is an imbalance between the production of reactive oxygen species (free radicals) and antioxidant defenses. [1] The body’s cells produce free radicals, which are nitrogen- or oxygen-containing molecules with an uneven number of electrons [2], during normal metabolic processes. [3] Meanwhile, cells also produce antioxidants that neutralize these free radicals to prevent excessive cell and tissue damage. In general, the body is able to maintain a balance between antioxidants and free radicals. [3] However, this balance could be disrupted under certain conditions or environmental stress or infection, and uncontrolled oxidative stress can accelerate the aging process.[3]

Since DNA was first discovered by researchers, decades of work have been done to understand its importance as it is the code of life itself. While DNA is the cornerstone of life, it is not immune to damages, and as so it is vital for DNA to repair itself for normal cell function to be maintained. Though, DNA is not always able to repair itself and this leads to some diseases such as various cancers. Fortunately, DNA repair pathways are capable of being tools to provide therapies to combat these diseases.

The G2/M cycle checkpoint prevents cells with genomic DNA damage from entering mitosis (M phase). The main safeguards conferred by this checkpoint is to ensure that DNA is free of major lesions or replication errors, and there are enough organelles, metabolites, and other cellular cargo in the parent cell prior to division so the daughter cells can be adequately provided for once mitosis is complete. Failures at this checkpoint are associated with aberrant cellular growth and cancer progression.

The Cyclin B-CDK1 complex plays an important regulatory role during the G2 transition, at which time CDK1 is maintained inactivated by the tyrosine kinases Wee1 and Myt1. When the cells enter the M phase, the kinase Aurora A and the cofactor Bora act together to activate PLK1, which in turn activates the activity of phosphatase CDC25 and downstream CDC2, effectively driving the cells into mitosis. When the DNA is damaged, it activates the DNA-PK/ATM/ATR kinase and eventually inactivates the Cyclin B-CDK1 complex. Stopping cell cycle progression allows the cell enough time to attempt to repair any DNA or cellular damage, and if all else fails, to induce apoptosis to prevent risk to the entire organism.

ABclonal Technology provides a wide selection of cell cycle checkpoint antibody products for every phase of a cell's life. Please see a small sample of our offerings below.

In some ways, the heart is quite a vulnerable organ. Cardiac complications such as heart attack, cardiac arrest, or heart failure are common. But interestingly, of the many diseases that may affect the heart, cancer is not one of them. For example, we often hear about cancer in the prostate, breast, colon, skin, etc., but rarely of the heart. How is this vital organ different?

The Hippo signal is very conservative in evolution. It regulates organ size and tissue stability by regulating cell proliferation, apoptosis, and stem cell renewal. The core process of Hippo signaling is a kinase tandem process, Mst1/2 and Sav1 form a complex, phosphorylate and activate Lats1/2; Lats1/2 kinase then phosphorylates and inhibits transcriptional coactivators Yap and Taz. Yap and Taz are the most important effectors downstream of the Hippo pathway. Upon dephosphorylation, Yap and Taz translocate to the nucleus and interact with TEAD1-4 or other transcription factors (such as CTGF) to induce gene expression, thereby initiating cell proliferation and inhibiting apoptosis.