As a scientist (or at least, a guy who likes science and works for a bioscience-oriented company), I am invested in the power of scientific research in improving the quality of human life across all arenas. It is particularly gratifying when our customers, who are all primarily research scientists, derive direct benefit from ABclonal's products in their published research. In this case, our business development director had a customer recently defend her thesis based on a publication that used several ABclonal catalog antibodies. I enjoyed reading her group's article that may lead to more effective treatment strategies for diabetes patients going forward, so let's get to it.

With the holiday season upon us, it is a time to relax and be among loved ones again as we recharge for the push into the new year. Along the way, we have learned quite a bit about medical advances and new discoveries into life processes, information that will be used to drive the next stages of innovation. One of the great perks of having been in an academic setting was the constant immersion in ideas and collaboration, but even though some of us are no longer connected directly to academia, the vast interconnectivity provided by the internet means that we are never too far away from good information that could teach us something new and exciting.

What is STAT5B?

STAT5B belongs to the STAT (signal transducer and activator of transcription) protein family, a group of latent cytosolic transcription factors activated by Janus kinase (JAK) tyrosine kinases. The JAK-STAT signaling pathway is responsible for many important biological processes including cell proliferation, differentiation, apoptosis, and is also involved in the modulation of a variety of cytokines to control the immune response. 

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]

The term apoptosis was first used in 1972 to describe a morphologically distinct form of cell death. Since those early experiments and observations, apoptosis has become one of the focal points for biological research, with myriad laboratories and research groups continuing to work to further elucidate the components and pathways that drive this programmed cell death. As a fundamental biological pathway, apoptosis has benefits and adverse effects for the host organism. For example, many therapeutic strategies involve the activation of apoptosis to kill cancer cells, while other treatments seek to prevent apoptosis to preserve precious cells in key tissues. 

Reaching the golden years doesn’t always feel so golden. As we age, disease, injury, and other stress factors from the environment will damage our bodies' cells. Most cells may be able to repair that damage, while our immune system usually clears those damaged cells through a process called apoptosis.^[1] However, if cellular repair and clearance is not effective, the residual damaged cells will further weaken the immune system and deteriorate other biological processes. Is there a possibility that we can avoid this cellular damage and improve the health of older people? A cellular state known as senescence might hold the key to this question.^{[1, 2]} During senescence, the damaged cells irreversibly stop dividing and resist being removed. ^[3] Researchers have shown that determining senescence biomarkers could lead to new therapies for the inflammatory disease caused by senescence in older people.^[4]