Tall or short? Blue irises or brown? Human genetic material, or deoxyribonucleic acid (DNA), include genes that provide cellular machinery with instructions to produce functional proteins. These proteins ultimately determine many traits and support our daily activities. However, due to cell aging or environmental exposure to chemicals or radiation, mutations can happen randomly within trait-encoding genes, leading to problematic gene expression and protein activity (Figure 1).
Pet dogs usually follow predictable tracks throughout their lives. Dogs, as our loyal friends, have very limited lifespans. In general, dogs have an average lifespan of 10-13 years, which only takes up a small portion of humans’ lives, not to mention that dogs of medium and large breeds have an even shorter lifespan.
In recent years, the field of cancer research has witnessed a growing interest in targeting RNA editing as a potential therapeutic strategy. Adenosine Deaminase Acting on RNA (ADAR), a key enzyme involved in RNA editing, has emerged as an attractive target for cancer therapy. In this blog post, we will explore the role of ADAR and RNA editing in cancer and the potential of ADAR inhibitors as effective cancer therapeutics, highlighting the progress made in this area and the challenges that lie ahead.
In genetics, it is common knowledge that the blueprint of life lies within the intricate structure of DNA. However, a lesser-known but equally important player in the process of gene expression is RNA. From my previous blog, we learned that RNA carries the instructions encoded in DNA and helps to synthesize proteins that dictate the functioning of living organisms.
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DNA damage is a phenomenon that can be detrimental to genomic integrity. Thankfully, our bodies have adapted many pathways to repair such DNA damage to prevent mutagenesis and cell death. There are many different topics related to DNA damage and repair, and I have recently focused on two other interesting topics related to this. In my first blog, I touched on the epigenetic role of DNA damage.
In this day and age, we have all heard this refrain over and over from a very young age. From the high taxes on cigarettes and other tobacco products to the no-smoking public campaigns, it’s been drummed into heads (and our wallets) that smoking is bad for us. But why is it so bad? And why do so many people smoke anyway knowing that it’s bad for them?
The brain is a complex organ that controls every physical movement we have or ever will make and houses our sense of self. As merely on average 3-pound organ, the brain is somehow able to govern all our sensory input coming from sight, smell, touch, taste, and hearing and assemble messages in a way that directs our thoughts, speech, movement, and internal organ functions.
There have been many methods developed for the measurement of DNA repair in a “test tube.” While these methods are powerful to reveal DNA repair capacity, it is limited by the fact that the complexities of the cell are not considered.
Extracellular vesicles (EVs) are small membranous nanoparticles secreted by all types of cells and can be found in numerous bodily fluids, including blood, urine, cerebrospinal fluid, and more. For years, scientists believed that it functioned more as a waste disposal system for cells, carrying unwanted molecules and metabolites out of the cell and into circulation to be cleared out. But it turns out that one cell’s trash could be another cell’s treasure.
Repairing DNA damage is an essential capability for humans and other multicellular organisms. Inability to repair DNA damage can lead to cells dividing randomly and the development of both benign and malignant tumors. The David Lab at UC Davis is working on understanding the molecular mechanisms of DNA repair as a first step in developing targeted therapies to prevent common cancers.