Abstract: The present invention provides methods and compositions for treating atherosclerosis in a subject comprising the use of therapeutic compounds to reduce Reelin in the circulation of the subject, thereby reducing the adhesion of leukocytes to the vascular wall. The invention also provides methods and compositions for reducing leukocyte adhesion to the vascular wall in a subject.

Abstract: The present invention provides methods and compositions for treating atherosclerosis in a subject comprising the use of therapeutic compounds to reduce Reelin in the circulation of the subject, thereby reducing the adhesion of leukocytes to the vascular wall. The invention also provides methods and compositions for reducing leukocyte adhesion to the vascular wall in a subject.

Abstract: The present invention provides methods and compositions for treating atherosclerosis in a subject comprising the use of therapeutic compounds to reduce Reelin in the circulation of the subject, thereby reducing the adhesion of leukocytes to the vascular wall. The invention also provides methods and compositions for reducing leukocyte adhesion to the vascular wall in a subject.

Abstract: The present invention provides methods and compositions for treating atherosclerosis in a subject comprising the use of therapeutic compounds to reduce Reelin in the circulation of the subject, thereby reducing the adhesion of leukocytes to the vascular wall. The invention also provides methods and compositions for reducing leukocyte adhesion to the vascular wall in a subject.

Abstract: The subject matter described here relates to the use of compounds and methods for the increase of progranulin expression. The methods may take place in vitro, ex vivo such as in isolates from adult mammalian tissue, or in vivo. Compounds and methods described herein may find use in the treatment of frontotemporal dementia.

Abstract: The present invention provides methods and compositions for treating atherosclerosis in a subject comprising the use of therapeutic compounds to reduce Reelin in the circulation of the subject, thereby reducing the adhesion of leukocytes to the vascular wall. The invention also provides methods and compositions for reducing leukocyte adhesion to the vascular wall in a subject.

Abstract: The subject matter described here relates to the use of compounds and methods for the increase of progranulin expression. The methods may take place in vitro, ex vivo such as in isolates from adult mammalian tissue, or in vivo. Compounds and methods described herein may find use in the treatment of frontotemporal dementia.

Abstract: Cycling of ApoE4 isoform is promoted in a person in need thereof by contacting the person with an effective amount of a pharmaceutically-acceptable modulator of intracellular ApoE4 transport vesicle pH.

Abstract: Cycling of ApoE4 isoform is promoted in a person in need thereof by contacting the person with an effective amount of a pharmaceutically-acceptable modulator of intracellular ApoE4 transport vesicle pH.

Abstract: The invention provides methods and compositions for modeling and detecting LDL receptor transmembrane signaling by detecting proteolysis of an LDL receptor transmembrane domain. The method comprises the steps of: a) providing a sample comprising a cell membrane comprising (i) a polypeptide comprising an LDL receptor transmembrane domain fused to a C-terminal tail, and (ii) a protease which specifically cleaves the domain and thereby releases the tail from the membrane; b) incubating the sample under conditions wherein the protease cleaves the domain and thereby releases the tail from the membrane; and c) detecting a resultant released tail.

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 modeling and detecting LDL receptor transmembrane signaling by detecting proteolysis of an LDL receptor transmembrane domain. The method comprises the steps of: a) providing a sample comprising a cell membrane comprising (i) a polypeptide comprising an LDL receptor transmembrane domain fused to a C-terminal tail, and (ii) a protease which specifically cleaves the domain and thereby releases the tail from the membrane; b) incubating the sample under conditions wherein the protease cleaves the domain and thereby releases the tail from the membrane; and c) detecting a resultant released tail.

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