Abstract: A rail vehicle front end has a center buffer coupling with a free coupling end section such that the free coupling end section is connectable to a further center buffer coupling of a further rail vehicle front end. The center buffer coupling extends along a longitudinal axis in a rest position. The center buffer coupling is mounted in such a way that the free coupling end section can be pivoted with respect to the longitudinal axis. The rail vehicle front end has a front panel that radially surrounds the center buffer coupling at least in sections such that a front opening pointing substantially in the longitudinal direction is defined between the front panel and the center buffer coupling. A cover device for covering the front opening extending between a front panel and a center buffer coupling of a rail vehicle is also disclosed.

Abstract: The invention pertains to a means for downregulating or inhibiting or mislocalizing CAR in a cardiac cell for treating/curing a patient who has suffered or is predisposed to suffering a myocardial infarction (MI) or preventing myocardial infarction or complications thereof.

Abstract: The invention pertains to a means for downregulating or inhibiting or mislocalizing CAR in a cardiac cell for treating/curing a patient who has suffered or is predisposed to suffering a myocardial infarction (MI) or preventing myocardial infarction or complications thereof.

Abstract: The invention refers to polynucleotides selected from the group consisting of a) polynucleotides encoding for the polypeptide RBM20 comprising a P638L mutation for a human polypeptide RBM20, or a P641L mutation for a rat polypeptide RBM20, b) polynucleotides with a reverse complementary sequence of the polynucleotide of a) above, and c) polynucleotides with an identity at least 50% to a polynucleotide of a) or b) above.

Abstract: The invention refers to polynucleotides selected from the group consisting of a) polynucleotides encoding for the polypeptide RBM20 comprising a P638L mutation for a human polypeptide RBM20, or a P641L mutation for a rat polypeptide RBM20, b) polynucleotides with a reverse complementary sequence of the polynucleotide of a) above, and c) polynucleotides with an identity at least 50% to a polynucleotide of a) or b) above

Abstract: The present invention relates to a conditionally inducible site-directed mutant cell, comprising a mutated allele of a gene; wherein said allele comprises a mutation that was introduced by using a suitable mutagenesis technique, a rescue allele of said mutated gene that can be conditionally inactivated, wherein said mutation in said mutated allele of said gene interferes with survival and/or causes, an adverse phenotype, such as temporal and/or local phenotypes, such as cell cycle-specific, cell-type specific, tissue-specific, protein-expression specific, tissue-development specific, organ-specific, organ-development-specific and/or embryonic lethal phenotypes. According to further aspects thereof, the present invention relates to a conditionally inducible site-directed mutant cell culture, tissue, organ, or non-human embryo, comprising a cell and a respective non-human organism, in particular a genetically deficient or Knock-outmammal, -rodent, -nematode, -fish, -plant or -insect.

Abstract: The invention provides methods and compositions for inducing and detecting signal transduction through LDL receptors, including specifically detecting a stress that alters a functional interaction of a low density lipoprotein (LDL) receptor binding polypeptide with an LDL receptor interaction domain, by (a) introducing a predetermined stress into a system which provides a physical interaction of an LDL receptor binding polypeptide with an LDL receptor intracellular binding polypeptide interaction domain, whereby the system provides a stress-biased interaction of the binding polypeptide and the interaction domain, wherein the absence of the stress, the system provides a unbiased interaction of the binding polypeptide and the interaction domain; and (b) detecting the stress-biased interaction of the binding polypeptide and the interaction domain, wherein the binding polypeptide is selected from SEMCAP-1, JIP-1, PSD-95, JIP-2, Talin, OMP25, CAPON, PIP4,5 kinase, Na channel brain 3, Mint1, ICAP-1 and APC subunit1

Abstract: The invention provides methods and compositions for inducing and detecting signal transduction through LDL receptors, including specifically detecting a stress that alters a functional interaction of a low density lipoprotein (LDL) receptor binding polypeptide with an LDL receptor interaction domain, by (a) introducing a predetermined stress into a system which provides a physical interaction of an LDL receptor binding polypeptide with an LDL receptor intracellular binding polypeptide interaction domain, whereby the system provides a stress-biased interaction of the binding polypeptide and the interaction domain, wherein the absence of the stress, the system provides a unbiased interaction of the binding polypeptide and the interaction domain; and (b) detecting the stress-biased interaction of the binding polypeptide and the interaction domain, wherein the binding polypeptide is selected from SEMCAP-1, JIP-1, PSD-95, JIP-2, Talin, OMP25, CAPON, PIP4,5 kinase, Na channel brain 3, Mint1, ICAP-1 and APC subunit

Abstract: The invention provides methods and compositions for inducing and detecting signal transduction through LDL receptors, including specifically detecting a stress that alters a functional interaction of a low density lipoprotein (LDL) receptor binding polypeptide with an LDL receptor interaction domain, by (a) introducing a predetermined stress into a system which provides a physical interaction of an LDL receptor binding polypeptide with an LDL receptor intracellular binding polypeptide interaction domain, whereby the system provides a stress-biased interaction of the binding polypeptide and the interaction domain, wherein the absence of the stress, the system provides a unbiased interaction of the binding polypeptide and the interaction domain; and (b) detecting the stress-biased interaction of the binding polypeptide and the interaction domain, wherein the binding polypeptide is selected from SEMCAP-1, JIP-1, PSD-95, JIP-2, Talin, OMP25, CAPON, PIP4,5 kinase, Na channel brain 3, Mint1, ICAP-1 and APC subunit1

Abstract: The invention provides methods and compositions for inducing and detecting signal transduction through LDL receptors, including specifically detecting a stress that alters a functional interaction of a low density lipoprotein (LDL) receptor binding polypeptide with an LDL receptor interaction domain, by (a) introducing a predetermined stress into a system which provides a physical interaction of an LDL receptor binding polypeptide with an LDL receptor intracellular binding polypeptide interaction domain, whereby the system provides a stress-biased interaction of the binding polypeptide and the interaction domain, wherein the absence of the stress, the system provides a unbiased interaction of the binding polypeptide and the interaction domain; and (b) detecting the stress-biased interaction of the binding polypeptide and the interaction domain, wherein the binding polypeptide is selected from SEMCAP-1, JIP-1, PSD-95, JIP-2, Talin, OMP25, CAPON, PIP4,5 kinase, Na channel brain 3, Mint1, ICAP-1 and APC subunit1