Rapid antimicrobial susceptibility testing (AST) is a method for quickly determining the most effective antibiotic therapy for patients with bacterial infections. These techniques enable the detection and quantification of antibiotic-resistant and susceptible bacteria metabolites at concentrations near or below ng/mL in complex media. Employing bacterial metabolites as a sensing platform, the system integrates machine learning data analysis processes to differentiate between antibiotic susceptibility and resistance in clinical infections within an hour. With the results, a clinician can prescribe appropriate medicine for the patient's bacterial infection.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a serious threat to human health without effective treatment. There is an urgent need for both real-time tracking and precise treatment of the SARS-CoV-2 infected cells to mitigate and ultimately prevent viral transmission. However, selective and responsive triggering and tracking of the therapeutic processin infected cells remains challenging.

Researchers at the University of California, Davis have developed a technology to expedite COVID-19 diagnosis and treatment using viral spike protein (S-protein) targeted peptides Zika virus envelop protein.

A breakthrough technology using insulin-secreting cells and stem cells to enhance wound healing and reduce scar formation.

Researchers at the University of California, Davis have developed multi-specific antibody molecules including bi-specific and tri-specific antibodies that could serve to co-localize effector T-cells, target tumor B-cells and would simultaneously enhance anti-tumor activity and proliferation, whilst minimizing potential systemic toxicities

Aberrant splicing contributes to the etiology of many inherited diseases. Pathogenic variants impact pre-mRNA splicing through a variety of mechanisms. Most notably, variants remodel the cis-regulatory landscape of pre-mRNAs by ablation or creation of splice sites, and auxiliary splicing regulatory sequences such as exonic or intronic splicing enhancers (ESE and ISE, respectively) and splicing silencers (ESS and ISS, respectively). Splicing-sensitive variants cripple the integrity of the gene, resulting in the production of a faulty message that is either unstable or encodes an internally deleted protein. Antisense oligonucleotides (ASOs) are a promising therapeutic modality for rescuing pathogenic aberrant splicing patterns as their direct base pairing abilities make them highly customizable and specific to targets. Although challenges such as toxicity, delivery and stability represent barriers to the clinical translation of ASOs, solutions to these challenges exist, as exemplified by the recent FDA approval of multiple ASO drugs.Generally, ASO's that target splicing mutations are limited to mutations in and around splicing enhancers and exonic mutations are commonly not targeted because of the idea that the mutation causes a significant change in protein function. 

Brief description not available

Brief description not available

Researchers at UC Irvine have identified Tetracosapentaenoic acid (24:5 n-3) for treatment of age-related eye disorders such as age-related macular degeneration (AMD), diabetic retinopathy and glaucoma. Lipids such as very long chain polyunsaturated acids (VLC-PUFAs) and docosahexaenoic acid (DHA) play a critical role in the eye during the human lifespan. Aging causes decrease in these lipids leading to age related eye disorders. Increased lipids or lipid precursors in the eye may improve retina function and overall vision health.

Researchers at UC Irvine have identified and tested the FDA approved thrombin inhibitor Dabigatran etexilate for treatment of pain related conditions, seizure conditions and exogenously induced chemical neurotoxicity. Dabigatran etexilate stabilizes function of neuronal Kv7 potassium channels which are low-voltage gated potassium channels that regulate neuronal firing. Kv7 channels generate reversible high frequency firing of neurons in response to various neurotransmitters and hormones. This transient hyperactivity sensitizes neurons so that they can facilitate responses to essential information. Dabigatran etexilate stabilizes the function of Kv7 channels. As it is already FDA approved, this treatment will be well tolerated.

Various plasmids from Michael Rape's lab, including but not limited to:pQE-UbcH5c/pET-Ube2D3-6xHispET28-E2NpET28-UEV1ApET28a-UBE2S-6xHISpET28a-E2R1-6xHIS 

Various ubiquitin plasmids from Michael Rape lab, including but not limited to: pCS2-no his-ubiquitin wtpCS2-no his-ubiquitin all RpET30a-ubiquitin (no tag)pET30a-ubiquitin K0 (no tag) 

Lipoxygenases (LOX) are enzymes that catalyze the peroxidation of certain fatty acids. The cell membrane is mostly made of lipids (which include fatty acids), and peroxidation can cause damage to the cell membrane. The human genome contains six functional LOX genes that encode for six LOX enzyme variants, or isozymes. The role that each LOX isozyme plays in health and disease varies greatly, spanning issues such as asthma, diabetes, and stroke. LOX enzymes are extremely difficult to target due to high hydrophobicity. Potential leads are often ineffective because they are either not readily soluble or not selective for a particular LOX enzyme.  Studies have implicated human epithelial 15-lipoxygenase-2 (h15-LOX-2, ALOX15B) in various diseases. h15-LOX-2 is highly expressed in atherosclerotic plaques and is linked to the progression of macrophages to foam cells, which are present in atherosclerotic plaques. h15-LOX-2 mRNA levels are also highly elevated in human macrophages isolated from carotid atherosclerotic lesions in symptomatic patients. Children with cystic fibrosis had reduced levels of h15-LOX-2, which affects the lipoxin A4 to leukotriene B4 ratio. Furthermore, the interactions of h15-LOX-2 and PEBP1 changes the substrate specificity of h15-LOX-2 from free polyunsaturated fatty acids (PUFA) to PUFA-phosphatidylethanolamines (PE), leading to the generation of hydroperoxyeicosatetraenoic acid (HpETE) esterified into PE (HpETE-PE). Accumulation of these hydroperoxyl membrane phospholipids has been shown to cause ferroptotic cell death, which implicates h15-LOX-2 in neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s diseases.  

Various plasmid constructs and cell lines for E3 Ligase project from Julia Schaletzky lab, including but not limited to:  pET28-ubiquitin wtpET28-ubiquitin deltaGGpLentiX1hygropLentiX1 blastpLentiX1 puropLentiX1 neopCS2-6xHIS-Htt-73QpCS2-6xHIS-Htt-23QpInducer Htt-23Q-GFPpInducer Htt-73Q-GFP

Researchers at the University of California, Davis (UC Davis) have developed a simplified procedure to synthesize complex glycosphingosine compounds for the chemical preparation of glycosphingolipids.

Researchers from UC San Diego developed an invention that enables protein expression to be upregulated using specific proteins and/or peptide sequences derived from SARS-CoV-2 proteins that are engineered to recognize specific mRNA transcripts by fusion to RNA-targeting modules such as CRISPR/Cas systems. They anticipate that these proteins can be fused or tethered to any engineered RNA-targeting moiety/module such as PUF/Pum, and pentatricopeptide proteins.

α-Fetoprotein (AFP) is a fetal glycoprotein produced by the majority of human hepatocellular carcinoma tumors and other tumor types. Delineating differences between fetal 'normal' AFP (nAFP) and tumor-derived AFP (tAFP), investigators at UCSF and the Parker Institute for Cancer Immunotherapy have uncovered a novel role for tAFP in altering metabolism via lipid-binding partners. They have developed a pharmaceutical composition comprising AFP bound by a fatty acid which, depending on the fatty acid used, can have an immunosuppressive effect allowing for the treatment of inflammatory diseases.  AFP bound to other fatty acids can eliminate the immune suppressive impact and have a neutral effect which allows for the development of dendritic cell (DC) vaccines presenting AFP epitopes which could be used to treat and prevent tumor AFP-expressing cancers.  

Listeria monocytogenes has been used as a therapeutic vaccine in more than 20 cancer clinical trials and administered to more than 1800 patients. However, Listeria monocytogenes vaccines have been less immunogenic in clinical trials. In rare cases, live bacteria were found in patients’ blood or on implants, after the administration of live vaccines. Additionally, even attenuated vaccine strains still caused severe adverse events and consequently put clinical trials on hold. Due, in part, to the safety and efficacy concerns of using Listeria monocytogenes as a live vector for cancer immunotherapy, there is a need for safer and more potent strains of Listeria monocytogenes.  UC Berkeley researchers have created a Listeria monocytogenes mutant strain that will likely be a safer and potentially more potent platform for the future development of cancer therapeutics. The strain is auxotrophic for adenosine, a purine nucleoside with extremely low levels in blood and healthy cells. The strain cannot grow in the host cell cytosol and is significantly attenuated in the mouse infection model. The improvement in the safety of this invention is further demonstrated by the poor growth of the mutant strain in host extracellular environments such as mouse gallbladders and human blood. Although attenuated, the invented strain elicits a robust effector CD8+ T cell response in mice and protects mice against lethal-dose challenges of wild-type L. monocytogenes. More importantly, the immunogenicity of this invention is more potent in mice than in previous Listeria monocytogenes vaccine strains. Another facet of this invention is that because of the high concentration of adenosine in tumor microenvironments, the mutant strain could potentially survive and multiply in tumors.  

Researchers at the University of California, Davis have developed a unique peptide that induces cell differentiation by inhibiting cellular protein CHD4, a promising approach to target dedifferentiated cancer cells and for cell therapy.

Researchers at the University of California, Davis have developed a virally derived homolog to increase the inflammatory response desirable in cancer immunotherapy.

Researchers at the University of California, Davis have developed a viral peptide therapeutic that targets MYC-based cancerous tumors.

Delivery technologies such as lipid nanoparticles (LNP) offer significant advantages over the delivery of free RNA for various RNA therapeutic, vaccine, and basic science applications. UC Berkeley researchers developed a new class of lipid nanoparticle (LNP) which is effective in delivering various types of nuclei acids in different tissues.  The LNP was successfully tested in in-vivo mouse models and therefore poses a significant promise in the gene editing field. The lipid formulation was packaged together with CRISPR Cas9 and a gRNA targeting the endogenous Tau locus. Tau dysrregulation is a pathological feature of Alzheimers disease, thus the invention provides a means to intervene in the development of pathological states associated with Tau aggregate formation. 

Researchers at UC Irvine have identified and tested a molecular target that regulates T cell function during chronic viral infection and cancer. The molecular target is one of the high mobility group proteins (HMGB2). HMGB2 is a DNA binding protein that regulates transcriptional processes, meaning that its modulation will have profound effects on T cell differentiation and ultimate function by altering the expression of many genes.

Researchers at the University of California, Davis (“UC Davis”) have developed fusion proteins effective in inhibiting the replication of diverse groups of viruses that can be useful in controlling vector-borne virus transmission as well as reducing vector populations.

Lipoxygenases catalyze the peroxidation of fatty acids which contain bisallylic hydrogens between two cis double bonds, such as in linoleic acid (LA) and arachidonic acid (AA). Lipoxygenases are named according to their product specificity with AA as the substrate because AA is the precursor of many active lipid metabolites that are involved in a number of significant disease states. The human genome contains six functional human lipoxygenases (LOX) genes (ALOX5, ALOX12, ALOX12B, ALOX15, ALOX15B, eLOX3) encoding for six different human LOX isoforms (h5-LOX, h12S-LOX, h12R-LOX, h15-LOX-1, h15-LOX-2, eLOX3, respectively). The biological role in health and disease for each LOX isozyme varies dramatically, ranging from asthma to diabetes or stroke. The nomenclature of the LOX isozymes is loosely based on the carbon position (e.g., 5, 12, or 15) at which they oxidize arachidonic acid to form the corresponding hydroperoxyeicosatetraenoic acid (HpETE), which is reduced to the hydroxyeicosatetraenoic acid (HETE) by intracellular glutathione peroxidases. Lipoxygenase inhibitors are difficult to formulate due to challenges with solubility and other factors, therefore new formulations are needed.