Abstract: The invention relates to multispecific antibody constructs comprising Fab fragments having mutations at the interface of the CH1 and CL domains, said mutations preventing heavy chain/light chain mispairing.

Abstract: The present disclosure relates to novel PD-1 decoy variants, compositions, and methods to confer and/or increase immune responses mediated by cellular immunotherapy, such as by adoptively transferring tumor-specific genetically-modified subsets of lymphocytes.

Abstract: The invention relates to chimeric antigen receptors (CARs) targeting a cancer-associated antigen and their use for treatment of a tumor or cancer. In particular, the invention provides compositions and methods for treating diseases associated with the antigen NGcGM3. The invention also relates to CARs specific to NGcGM3, vectors encoding the same, and recombinant T cells comprising the CARs of the present invention. The invention also includes methods of administering a genetically modified T cell expressing a CAR that comprises an antigen binding domain that binds to NGcGM3.

Abstract: The present invention is based on the surprising finding of a proteolytic cleavage function of human Malt1. More particularly, the present invention relates to enzyme and screening assays, methods for assessing cleaving activity, methods for screening, isolated polypeptides, antibodies and inhibitors of Malt1. The present invention also relates to the use of Malt1 as a proteolytic enzyme and the use of compounds comprising a peptide comprising an amino acid sequence according to any one of SEQ ID NO: 1-47 as substrates susceptible for specific proteolytic cleavage.

Abstract: The present invention provides methods for determining a putative agent that treats or prevent obesity and/or obesity related diseases comprising contacting cells with the putative agent and measuring the activity and/or level of Maf1 and/or the activity and/or level of KIAA1875. The present invention also provides the agent identified by the methods herein and methods of treating or preventing obesity and/or obesity related diseases in a subject comprising administering to the subject a therapeutically effective amount of an agent that inhibits or downregulates Maf1 and/or activates or upregulates KIAA1875.

Abstract: A method removes a part representing non-brain tissue of the MR brain image. For each generated magnetic field gradient, acquiring a current signal respectively at a first time of echo TE1 after an excitation radio frequency pulse and at a second time of echo TE2 after the radio frequency pulse. The MR brain image of an internal structure of the target. The first time of echo TE1 and the second time of echo TE2 are adjusted for correlating time of echo difference ?TE=TE2-TE1 with a fat and water mutual resonance frequency difference ?, and in that fat and water information encoded in the current signal resulting from the correlation of the second and first time of echo difference ?TE with the fat and water mutual resonance frequency difference is used as an additional input source into a multispectral analysis method for removing the part.

Abstract: The present invention provides methods for determining a putative agent that treats or prevent obesity and/or obesity related diseases comprising contacting cells with the putative agent and measuring the activity and/or level of Maf1 and/or the activity and/or level of KIAA1875. The present invention also provides the agent identified by the methods herein and methods of treating or preventing obesity and/or obesity related diseases in a subject comprising administering to the subject a therapeutically effective amount of an agent that inhibits or downregulates Maf1 and/or activates or upregulates KIAA1875.

Abstract: The present invention relates to the disclosed transgenic peptides for use in the diagnosis of an infection by intracellular Chlamydia-like bacteria. The invention also relates to a serological diagnostic test. The transgenic peptides are selected from the proteome of Parachlamydia acanthamoebae properties of binding to antibodies of infected human and animals. The test may give further insight in the role of this microorganism in pulmonary diseases and possibly in miscarriage.

Abstract: The present invention is based on the surprising finding of a proteolytic cleavage function of human Malt1. More particularly, the present invention relates to enzyme and screening assays, methods for assessing cleaving activity, methods for screening, isolated polypeptides, antibodies and inhibitors of Malt1. The present invention also relates to the use of Malt1 as a proteolytic enzyme and the use of compounds comprising a peptide comprising an amino acid sequence according to any one of SEQ ID NO: 1-47 as substrates susceptible for specific proteolytic cleavage.

Abstract: The invention provides cell-permeable peptides that bind to JNK proteins and inhibit JNK-mediated effects in JNK-expressing cells.

Abstract: Disclosed is a replication-recombinant virus, preferably an adenovirus that lacks E1a, E1b and E4 ORF 6, capable of infecting an eye and comprising a lens epithelial cell specific promoter driving an ORF encoding at least one protein, which when expressed in lens epithelial cells of an eye suppresses, at the level of the germinative epithelium of the lens of the eye, cellular proliferation which is stimulated by eye surgery and which would otherwise result in secondary cataract formation in the eye. Also disclosed is the use of the recombinant virus for the treatment of an eye, undergoing eye (e.g. cataract) surgery, in order to reduce the incidence of cellular proliferation in the eye following the surgery and thereby to prevent the formation of secondary cataracts.

Abstract: The invention provides cell-permeable peptides that bind to JNK proteins and inhibit JNK-mediated effects in JNK-expressing cells.

Abstract: The present invention provides a system for controlled transgene transcription using chimeric activator and repressor proteins functioning in a novel regulatory network. The target transgene is actively silenced in non-inducing conditions by a novel class of chimeric proteins consisting of the DNA-binding tetracycline repressor fused to distinct multimerized eukaryotic transcriptional repression domains. In the presence of a tetracycline “inducer”, the repressor does not bind to the promoters for both the target gene and for another regulatory gene encoding a transactivator (e.g., GAL4-VP16). Under these inducing conditions, the transactivator activates expression of the target transgene and of its own gene, in an additional autoregulatory positive feedback loop.

Abstract: A replication-defective recombinant virus, preferably an adenovirus that lacks E1a, E1b and E4 ORF 6, capable of infecting an eye and containing a ORF encoding a protein that when expressed in lens epithelial cells of an eye, suppresses, at the level of the germinative epithelium of the lens of the eye, cellular proliferation which is stimulated by eye surgery and which would otherwise result in secondary cataract formation in the eye is disclosed. The ORF, to be expressed, is under the control of a promoter sequence which is expressly exclusively in human lens epithelial cells. The preferred ORFs, to be expressed, include a non-phosphorylatable retinoblastoma ORF, a dominant negative mutant of a human RAS ORF and a Herpes thymidine kinase ORF.

Abstract: The present invention provides a system for controlled transgene transcription using chimeric activator and repressor proteins functioning in a novel regulatory network. The target transgene is actively silenced in non-inducing conditions by a novel class of chimeric proteins consisting of the DNA-binding tetracycline repressor fused to distinct multimerized eukaryotic transcriptional repression domains. In the presence of a tetracycline "inducer", the repressor does not bind to the promoters for both the target gene and for another regulatory gene encoding a transactivator (e.g., GAL4-VP16). Under these inducing conditions, the transactivator activates expression of the target transgene and of its own gene, in an additional autoregulatory positive feedback loop.