Technologies
Sub Categories
Therapeutic
Histone deacetylases (HDACs) mediate regulation of gene expression via changes in nucleosome conformation. Dysregulation of histone acetylation, can lead to the development of cancers. There is renewed interest in capitalizing new breakthroughs in epigenetic research to address oncology therapy. Epigenetic regulation and subsequent gene expression or silencing represents a tightly orchestrated interplay among enzymes responsible for modifying the tails of histones, around which nuclear DNA is wrapped.
Histone deacetylases (HDACs) mediate regulation of gene expression via changes in nucleosome conformation. Dysregulation of histone acetylation, involving CBP, a neuroprotective transcription factor with histone acetyltransferase activity, has been found in Huntington’s disease (HD), Alzheimer’s disease (AD), and Rubinstein-Taybi syndrome. In a cellular model of AD, cell death was accompanied by loss of CBP function and histone deacetylation.
G9a is overexpressed in various human cancer including leukemia, prostate cancer, hepatocellular carcinoma and lung cancer. Inhibitors of G9a are candidates for cancer treatment. A new family of G9A inhibitors have been recently identified and characterized. Through the characterization of these inhibitors, insight has been gained on the mechanistic contribution of G9a in the deregulation of the cell cycle in cancer and methyltransferase G9a regulation of a crucial step in cellular degradation.
Tuberculosis (TB) is a bacterial infection which primarily affects the lungs and central nervous system. One third of the world's population is infected with the bacteria Mycobacterium tuberculosis, the causative agent of TB. There are approximately 500,000 cases of drug-resistant TB reported annually, 6.6% of which are extensively drug resistant. To make matters worse, the number of annual TB cases is increasing due to population growth, along with the frequency of multidrug resistant TB (MDR-TB).
Histone deacetylases (HDACs) are enzymes that remove acetyl groups from histones, increasing their positive charge and encouraging high-affinity binding between histones and the DNA backbone. The increased DNA binding condenses DNA structure, preventing transcription.
Src family kinases (SFKs) are associated with normal cellular homeostasis and their activity is elevated in some pathological conditions such as cancer and acute inflammation. In many human cancers, SFKs have been found to be overactive and transforming. In addition, elevated SFK activity is associated with tumor growth, survival, migration, and metastasis. Recent clinical trials have used SFK inhibitors in the treatment of breast canser and non-small cell lung cancer.
Tuberculosis (TB) is an infectious disease that claims millions of lives worldwide each year. According to the World Health Organization, every country surveyed has disease strains that are resistant to a single anti-TB drug. The emergence of single, multi-drug and extensively drug-resistant tuberculosis incidences highlights the urgent need for the discovery and implementation of novel anti-TB therapeutics.
Decitabine is used for cancer treatment and other hematological disorders. The UIC inventors have developed a novel formulation of Decitabine. This formulation has improved oral absorption, decreased inter-individual variability, and improved efficacy against cancer cell resistance.
There is no cure for herpes and current medications only treat the symptoms of the virus. UIC inventors have developed ZnO based micro‐nano particles that multivalently bind to HSV-1, rendering them un-infectable.
Although Tularemia and Anthrax are rare according to the records in US, the diseases themselves are highly incapacitating to infected persons and have been used as biological weapons in the past. For the national security, the development of their specific antibiotics is particularly necessary. Scientists in Center for Pharmaceutical Biotechnology have found a lead compound based on a computational high-throughput screening targeting Francisella tularensis FabI.