The present application relates to a quantitative kit for myxovirus resistance protein 1. Specifically, a kit comprising latex particles coated with a myxovirus resistance protein 1 antibody is disclosed. Myxovirus resistance protein 1 in human serum and plasma samples and latex particles cross-linked with a myxovirus resistance protein 1 antibody are specifically binded to form a complex, which leads to an increase in absorbance. By detecting changes in immunoturbidity, a higher sensitivity and a wider detection range are reached.

The present invention relates to a method for screening an inhibitor of ATP11C or CDC50A, comprising determining (a) exposure of phosphatidylserine on cell surface, (b) engulfment of cells by macrophages, or (c) cleavage of ATP11C by caspase. The present invention also relates to a method for inducing engulfment of cells by macrophages, comprising inhibiting ATP11C or CDC50A.

Disclosed herein are methods, and kits for use in said methods, that aid in the diagnosis and evaluation of a pediatric subject for traumatic brain injury (TBI), using ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), glial fibrillary acidic protein (GFAP), or a combination thereof. Also disclosed herein are methods, and kits for use in said methods, that aid in determining whether a pediatric subject would benefit from and thus receive an imaging procedure, such as MRI or head computerized tomography (CT) scan based on the levels of GFAP, UCH-L1 or GFAP and UCH-L1.

The present disclosure relates to an inhibitor of Dynamin 2 for use in the treatment of centronuclear myopathies. The present disclosure relates to pharmaceutical compositions containing Dynamin 2 inhibitor and to their use for the treatment of centronuclear myopathies. It also deals with a method for identifying or screening molecules useful in the treatment of a centronuclear myopathy.

The present invention relates to a marker composition for diagnosing rheumatoid arthritis, comprising angiotensinogen (ACT) as a marker, a method for providing information necessary to determine the occurrence of rheumatoid arthritis using the marker composition, a composition for determining the occurrence of rheumatoid arthritis, comprising an agent for measurement of the expression level of the marker, and a kit for determining the occurrence of rheumatoid arthritis, comprising a device for measurement of the expression level of the marker. The method for providing information for use in determining the occurrence of rheumatoid arthritis provided by the present invention can be widely utilized to determine the occurrence of various joint diseases, including rheumatoid arthritis since it is possible to measure the expression levels of proteins of which the expression levels are changed at the time of the occurrence of rheumatoid arthritis, and to more objectively and accurately determine the occurrence of rheumatoid arthritis when the method is used.

Disclosed herein are Ral-antagonist compounds that covalently bind to binding sites in RalA, and efficaciously inhibit Ral activity. The compounds include aryl sulfonyl fluoride compounds of the general structure of wherein X and Y are independently C or N, and R.sub.4 is C.sub.1-C.sub.4 alkyl, —OCH.sub.3, —OCH.sub.2CH.sub.3, —OCH(CH.sub.3).sub.2, —(SO.sub.2)CH.sub.3, —OH, or halo. These compounds expand Ral-inhibiting therapeutic options for treating Ral-driven cancers and one embodiment of the present disclosure is directed to the use of such compounds to treat cancer.

Disclosed herein are compositions comprising a CT20 peptide and methods of using the disclosed compositions to treat cancers expressing chaperonin containing TCP (CCT).

The invention provides compositions and methods for binding Ras in a nucleotide free state (apo RAS) and inhibiting Ras signaling. In one embodiment, the invention provides monobodies that specifically bind apo RAS and methods of use. Thus, in diseases and conditions where a reduction of Ras signaling is beneficial, such inhibitory compositions act as therapeutics.

A method for treating cancer in a human subject includes initiating a cancer therapy on the human subject, preparing a biological sample from the human subject; (i) mixing the biological sample with an antibody or aptamer that specifically binds to an MEST protein, or (ii) obtaining mRNA of a nucleotide sequence encoding the MEST protein from the biological sample, and synthesizing and amplifying cDNA from the mRNA, detecting the MEST protein bound to the antibody or aptamer, or an expression of the cDNA, determining if the detected MEST or a level of the expression is higher than that in a normal human subject, determining responsiveness of the cancer to the cancer therapy by the detected MEST or the level of the expression, and continuing the cancer therapy to treat the cancer if it is determined that there is the responsiveness of the cancer to the cancer therapy.

Provided herein are methods of identifying a subject having a poly-ADP ribose polymerase (PARP) inhibitor-sensitive tumor by detecting a genomic gain in chromosome 1q21 and/or chromosome 20q13.3 in a tumor sample from the subject. Also provided are methods of identifying a subject having a PARP inhibitor-sensitive tumor by detecting gene amplification of a CHD1L gene or an RTEL1 gene in a tumor sample from the subject. Further provided are methods of treating a tumor with a genomic gain in chromosome 1q21 and/or chromosome 20q13.3 in a subject by administering an effective dose of a PARP inhibitor.