Provided herein are nucleic acid-cleaving catalytic nucleic acid probes, biosensors and lateral flow biosensor devices and methods and kits of using the probes, biosensors and lateral flow biosensor devices for detecting an analyte present on or generated from a microorganism in a test sample, including Helicobacter pylori and methods for determining whether a subject has a Helicobacter pylori infection.

Disclosed herein are methods of using an immobilized substrate, immobilized ligand, and a fusion protein of an enzyme for the substrate and a receptor for the ligand, where the immobilized substrate can react to form an immobilized product that has a different mass than the immobilized substrate, and using this transformation to indirectly determine the binding of the receptor and the ligand. These methods can be used for high-throughput screening for possible modulators (e.g., inhibitors or activators) of the ligand-receptor interaction.

Provided is a compound that comprises the structure:

##STR00001##

where SIG is a signaling molecule and R.sup.3 is a formyl, a succinyl, a methyl succinyl, or a myristoyl. Also provided is a kit is provided that comprises the above compound, with instructions for determining the presence of the enzyme. Additionally, a method is provided for determining whether a sample has an enzyme that removes a succinyl, a methyl succinyl, a formyl, or a myristoyl moiety from an -amino of a lysine. Also provided is a method of determining whether a molecule inhibits an enzyme that removes a succinyl, a methyl succinyl, a formyl, or a myristoyl moiety from an -amino of a lysine.

Methods, reagents, and kits for the reversible immobilization of glycoproteins to a solid support, the release and capture of a glycan portion of the glycoprotein, and the subsequent release and capture of the polypeptide portion of the glycoprotein are provided. The disclosure also provides suitable solid support materials, surface chemistries, and devices for use in the disclosed methods. The methods, reagents, kits, and devices provided herein are useful for the analysis of protein glycosylation, for example, in a diagnostic context, in the context of proteoglycomics, and in the context of producing glycosylated proteins for therapeutic purposes.

The present invention relates generally to glutaminase inhibitors of Formula I, Formula II, or Formula III, as well as pharmaceutical compounds containing them and methods of their use.

The present invention is based on the surprising finding of the property of promoting myelination of activators of histone deacetylase (HDAC) 1 and 2. In particular, such activators have the capacity of accelerating and increasing remyelination after lesions to the myelin of nerve cells of the peripheral and central nervous systems. The present inventor found that HDAC2 deacetylates eEF1A1 and thereby prevents the latter from removing outside the nucleus key inducers of myelin genes transcription. The HDAC1/2 activators are useful in the treatment of diseases associated with demyelination, such as Multiple Sclerosis.

The invention relates to a compound of Formula I:
F.sub.1X.sub.1-L.sub.1-X.sub.2P.sub.1X.sub.3-G.sub.1(Formula I).

A method for characterizing the risk a subject will develop an autoimmune and/or alloimmune disease following tissue transplant includes obtaining a biological sample from the subject, wherein the subject has received the tissue transplant determining in the biological sample a level of at least one protein selected from Tables 1-4, comparing the measured level of the at least one protein to a control value, and characterizing a subject as at greater risk of developing an autoimmune disease and/or alloimmune disease if the level of at least one protein determined is increased or decreased compared to the control value.

It has been discovered that NAD+-dependent histone deacetylase SIRT6 is critical for suppression of PDAC by controlling the expression of Lin28b, which is a negative regulator of let-7 microRNA. Specifically, SIRT6 loss results in histone hyperacetylation at the Lin28b promoter, Myc recruitment, and pronounced induction of Lin28b and downstream let-7 target genes, HMGA2, IGF2BP1, and IGF2BP3. This invention relates generally to agents and methods of reducing expression or activity of Lin28b to treat (aggressive) PDAC in a subject.

The present disclosure provides methods in which adherent cells are treated with small molecules, cultured, lysed, and then analyzed by mass spectrometry to measure the activities of endogenous enzymes. The implementation of this method relies on the use of surfaces that are nanopatterned with cell adhesion ligands to mediate cell attachment and a peptide that is a substrate for the desired enzyme activity in the lysate.