NOX1 Inhibitor, NoxA1ds Set 1PC X 1SET

A major focus of breast cancer research is to understand the mechanisms responsible for disease progression and drug resistance. Toward that end, it has been found that approximately two thirds of all human breast carcinomas overexpress the Estrogen Receptor α (ERα) protein and it remains the primary pharmacological target for endocrine therapy1,2. The normal cellular function of ERα is as a transcription factor that mediates a wide variety of physiological processes, many of which are dependent upon phosphorylation of the receptor at specific amino acid residues3,4. Indeed, ERα is known to be phosphorylated at a multitude of different sites, yet how these all correlate to disease remains unclear5. Here, we interrogated multiple sites of ERα for phosphorylation status by screening an extensive panel of different breast cancer patient samples and other non-breast cancer tissue microarray (TMA) slide samples to determine their relevance to disease.

Alzheimer’s Disease is a progressively deteriorating disease. It manifests itself with memory loss, confusion, problems with judgment, planning, concentration, and personality changes; and in it’s later stages, a decline in physical abilities. The disease’s causes, cures, and preventions are unknown; however, key proteins likely involved in the degenerative mechanism have been identified. Alzheimer’s Disease is characterized by neuronal loss, alterations in neurotransmitter systems, and the presence of neurofibrillary tangles composed of abnormally hyperphosphorylated tau proteins. A prominent feature of Alzheimer’s Disease is the formation of senile plaques in selected regions of the brain. The center of these plaques are composed mainly of fibrillary aggregates of a common, but not well understood, b amyloid peptides (Aβ). The Aβ peptides are generated from the larger amyloid-β precursor protein (APP) by the sequential action of β- and γ-secretase, and it is generally accepted that oligomeric forms of this Aβ are neurotoxic, resulting in disease progression.

"Aging: getting older, exhibiting the signs of age, the decline in the physical (and mental) well-being over time, leading to death. Since the beginning of time, man has been obsessed with trying to slow down, stop, or even reverse the signs of aging. Many have gone as far as experimenting with nutritional regimens, eccentric exercises, fantastic rituals, and naturally occurring or synthetic wonder-elements to evade the signs of normal aging. Biologically speaking, what is aging? And what does the latest research tell us about the possibility of discovering the elusive “fountain of youth”? Many advances in our understanding of aging have come from systematic scientific research, and perhaps it holds the key to immortality. Scientifically, aging can be defined as a systems-wide decline in organismal function that occurs over time. This decline occurs as a result of numerous events in the organism, and these events can be classified into nine “hallmarks” of aging, as proposed by López-Otin et al. (2013). Several of the pathologies associated with aging are a direct result of these events going to extremes and may also involve aberrant activation of proliferation signals or hyperactivity. The hallmarks of aging have been defined based on their fulfillment of specific aging related criteria, such as manifestation during normal aging, acceleration of aging if experimentally induced or aggravated, and retardation of aging if prevented or blocked, resulting in increased lifespan. The nine hallmarks of aging are genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. The biological processes underlying aging are complex. By understanding the hallmarks in greater detail, we can get closer to developing intervention strategies that can make the aging process less of a decline, and more of a recline."