The present invention relates to the use of the editing profile of PDE8A pre-mRNA as a specific bio marker of ADARs activities in evolved primate, particularly in Human tissues. The present invention also relates to an in vitro method for predicting in Human an alteration of the mechanism of the ADARs catalysed pre-mRNA editing of target genes, by analysing the PDE8A pre-mRNA editing profile in a peripheral tissue sample containing cells expressing said PDE8A pre-mRNA, such as blood sample. The present invention is also directed to an in vitro method for the screening of potential therapeutic compound and to predict and assess therapeutic efficacy and/or efficiency or to diagnose potential severe brain or peripheral drug side effects implementing said PDE8A pre-mRNA editing profile as specific biomarker. The present invention is further directed to a method for determining the PDE8A pre-mRNA editing profile in Human, particularly by capillary electrophoresis single-strand conformation polymorphism (CE-SSCP) method after amplification by a nested PCR. Finally the invention relates to particular nucleic acid primers implemented in said nested PCR and kit comprising such sets of primers and human cells capable of expressing PDE8A and ADARs.

Methods and kits are disclosed for measuring activity of a methyltransferase or a radical SAM enzyme or for screening for an inhibitor of a methyltransferase or a radical SAM enzyme, where the methods and kits comprise, respectively, deaminase TM0936 for a MTase coupled assay and deaminase PA3170 for a radical SAM coupled assay.

The present disclosure relates to the use of anti-PAD4 autoantibodies as a clinical biomarker for rheumatoid arthritis (RA) treatment. The disclosure further provides an assay to detect anti-PAD4 autoantibodies, assay kits for the detection of anti-PAD4 autoantibodies, as well as computer implemented diagnostic methods.

The present disclosure relates to the use of PAD proteins, such as PAD1, or PAD1 and PAD4, or antigenic fragments thereof as clinical biomarker for diagnostic and prognostic information in rheumatoid arthritis (RA) patients. The disclosure further provides methods and compositions for the detection of autoantibodies against PAD proteins, such as anti-PAD1, or anti-PAD1 and anti-PAD4, in a biological sample.

A method for measuring anti-PAD2 antibodies in a subject with an inflammatory or autoimmune disease, and to determine if the subject has a better prognosis for developing a more severe form of inflammation based on anti-PAD2 antibody levels. Methods for the therapeutic use of anti-PAD2 antibodies are also described.

Uses and a composition including a peptidylarginine deiminase 2 (PADI2) as an active ingredient are disclosed. A peptidylarginine deiminase 2 (PADI2) is useful for preventing or alleviating cellular senescence.

Anti-tumour immune responses to modified self-epitopes. The present invention relates to the use of tumour-associated epitopes in medicine and in particular in the treatment of cancer. The epitopes stimulate an immune reaction against the tumour and have a modification selected from deimination of arginine to citrulline, nitration of tyrosine, oxidation of tryptophan and deamination of glutamine or asparagine. The invention also relates to nucleic acids comprising sequences that encode such epitopes for use in the treatment of cancer.

The invention relates to a nucleic acid molecule encoding a novel selection marker. Said marker is a guanidinobutyrase from Kluyveromyces lactis, which, when expressed in Saccharomyces, allows the growth of the yeast in the presence of guanidinobutyrate as the sole nitrogen source. Said marker can be used in a method for producing a microorganism having an altered genome. The invention further relates to a set of constructs, comprising a first construct comprising a recognition site for an endonuclease, a first region of homology with a target gene of a microorganism, and a first part of a nucleotide sequence encoding the selection marker, and a second construct comprising a second part of the nucleotide sequence encoding the selection marker, a second region of homology with the target gene of the microorganism, and a copy of the endonuclease recognition site. The invention further relates to methods for altering a target gene in a microorganism, to methods for producing a microorganism, and to microorganisms that are produced by the methods of the invention.

Disclosed are new approaches to detecting adenosine deaminase (ADA) deficiency. There is provided a method of determining ADA activity, comprising: dividing a sample obtained from blood into two portions, adding an ADA inhibitor to one portion, measuring levels of ADA activity in both portions, and determining the ADA activity. Also provided is a method of measuring ADA substrate, comprising: measuring an ADA substrate in a sample obtained from blood of subject, and comparing this to at least one control sample obtained from blood and comprising an ADA inhibitor, and a known quantity of the ADA substrate. Multiplexed methods of measuring ADA enzymatic activity along with other metabolic markers are also provided. The methods are particularly useful for the analysis of samples obtained from dried blood spots (DBSs), and may be incorporated into existing newborn screening programs. Associated diagnostic methods, control samples, and apparatuses are also disclosed.

Disclosed herein are methods of aiding in a diagnosis of a traumatic brain injury (TBI) in a subject suspected of having sustained or known to have sustained an injury to the head, by detecting at least one biomarker, wherein the at least one biomarker is ubiquitin carboxy terminal hydrolase L1 (UCH-L1).