Abstract: The present invention provides methods of screening an agent for activity using teleosts. Methods of screening an agent for angiogenesis activity, toxic activity and an effect cell death activity in teleosts are provided.

Abstract: The present invention provides a transgenic non-human animal and method for using the same in evaluating a therapeutic agent for use in the treatment of Schizophrenia. More specifically, the invention is directed to a transgenic non-human animal which is incapable of expressing functional EDG2 protein. A theraupeutic agent is administered to the transgenic non-human animal incapable of expressing functional EDG2 protein and the effect of the agent on the animal is evaluated.

Abstract: The present invention relates to compositions and methods relating to the characterization and function of CYT28. Specifically, the present invention provides transgenic animals comprising disruptions in a CYT28 gene and methods of treating diseases conditions, such as pain. The present invention further relates to agents that modulate CYT28 and methods of screening for agents that modulate CYT28 for the treatment of diseases and conditions such as pain.

Abstract: Genetic evidence that an imbalance in the activity of serine proteases can cause severe skin disease has recently been presented. The serine protease SCCE is preferentially expressed in cornifying epithelia. Increased expression of SCCE in psoriasis has previously been reported. Increased SCCE expression also in chronic lesions of atopic dermatitis is described herein. Transgenic mice expressing human SCCE in suprabasal epidermal keratinocytes were found to develop pathological skin changes with increased epidermal thickness, hyperkeratosis, dermal inflammation, and severe pruritus. The results strengthen the idea that SCCE may be involved in the pathogenesis of inflammatory skin diseases, and may offer a new therapeutic target.

Abstract: Provided are methods and compositions corresponding to a genetic locus associated with nociceptive pain. In addition, method of identifying or modulating nociceptive pain and associated disorders is also provided.

Abstract: Methods for producing nondestructive nerve alterations and/or compressions in animals are provided. The animals provide a model of persistent neurogenic and neuropathic pain in humans. Also provided is a method for screening agents for activity in the treatment of persistent neuropathic pain, as well as methods for use in developing agents for treatment of neuropathic pain. Also provided are methods for detecting and monitoring physiologic changes in persistent pain.

Abstract: The present invention provides a knockout animal artificially modified to inhibit ?-TTP gene expression. This animal is useful as a tool for understanding mechanisms for the development of familial isolated vitamin E deficiency and other diseases induced by oxidative stress (e.g., arteriosclerosis, diabetes). It is also useful as a tool for developing a therapeutic agent for these diseases.

Abstract: A gene activation/inactivation and site-specific integration system has been developed for mammalian cells. The invention system is based on the recombination of transfected sequences by FLP, a recombinase derived from Saccharomyces. In several cell lines, FLP has been shown to rapidly and precisely recombine copies of its specific target sequence. For example, a chromosomally integrated, silent ?-galactosidase reporter gene was activated for expression by FLP-mediated removal of intervening sequences to generate clones of marked cells. Alternatively, the reverse reaction can be used to target transfected DNA to specific chromosomal sites. These results demonstrate that FLP can be used, for example, to mosaically activate or inactivate transgenes for a variety of therapeutic purposes, as well as for analysis of vertebrate development.

Abstract: A transgenic zebrafish animal model is disclosed. The model can be used for study of hematopoetic cell differentiation, control, and screening of therapeutic agents and can include a transgenic zebrafish expressing a heterologous Ikaros protein.

Abstract: An animal model is provided which is genetically engineered to express human serum albumin, and such animals may be advantageously used in assessing drugs, vaccines or other therapeutic compounds that may be used in humans. In addition, an animal model is provided which does not manufacture its own albumin and which has been injected with human serum albumin. Through the use of these animal models, drugs and other chemicals can be more accurately assessed in physiological environments that reflect the conditions to be expected in humans, and such models will be useful in assessing new drugs and evaluating toxic substances for potential dangers as carcinogens, mutagens, etc. Other applications include evaluating immunological properties of various albumin-engineered proteins which might be administered to humans as therapeutics or vaccines, and research of disease states, such as genetic diseases, to provide further insight in treating these diseases.

Abstract: The invention provides genetically-modified non-human mammals and genetically-modified animal cells containing a disrupted RAMP1, RAMP2, or RAMP3 gene. Also provided by the invention are methods of screening for agents that modulate the activity or expression of a RAMP and methods of treating mammals to modulate liver function and/or muscle metabolism.

Abstract: The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising mutations in a glucagon receptor gene. Such transgenic mice are useful as models for disease and for identifying agents that modulate gene expression and gene function, and as potential treatments for various disease states and disease conditions. The present invention also relates to diabetes and diabetic condition, as it demonstrates the role of the glucagon receptor in diabetes and diabetic conditions. The present invention further relates to weight gain and weight related conditions, such as obesity, and demonstrates the role of the glucagon receptor in weight gain and weight related conditions, such as obesity.

Abstract: We report the use of telomerase-immortalized human microvascular endothelial cells in the formation of functional capillary blood vessels in vivo. Previously we showed the superior in vitro survival of human telomerase reverse transcriptase (hTERT)-transduced human endothelial cells. Here we show that retroviral-mediated transduction of hTERT in human dermal microvascular endothelial cells (HDMEC) results in cell lines that form microvascular structures when subcutaneously implanted in severe combined immunodeficiency (SCID) mice. The human origin of xenografted microvaculature was confirmed both by basement membrane immunoreactivity with anti-human type IV collagen staining and visualization of fluorescent vessels containing HDMEC that were co-transduced with hTERT and green fluorescent protein (eGFP). The lack of human vascular structures after implantation of HT1080 fibrosarcoma cells, 293 human embryonic kidney cells or human skin fibroblasts demonstrated the specificity of HDMEC at forming capillaries.

Abstract: Transgenic flies displaying altered phenotypes due to expression of the Abeta and C99 portions of the human APP gene are disclosed. Use of these flies in a method to identify Drosophila genes and the human homologs of these Drosophila genes, that are potentially involved in Alzheimer's Disease, is also disclosed. The use of said human homologs as drug targets for the development of therapeutics to treat Alzheimer's Disease and other conditions associated with defects in the APP pathway, as well as pharmaceutical compositions comprising substances directed to these genes, are also disclosed.

Abstract: The present invention concerns products and methods particularly useful for activating and analyzing non-dividing cell nuclei. The featured products include activating egg extracts, cytostatic factor (CSF) extracts, kits containing these extracts, and a microchamber microscope slide useful in analyzing nucleus activation.

Abstract: The invention is directed to an isolated gene and protein product, designated Hepp, which has a role in mammalian hematopoiesis and neural function, and is further directed to a genetically modified non-human mammal that is homozygous or heterozygous for a disruption in the endogenous Hepp gene.

Abstract: The present invention relates to novel transcription control elements derived from a mouse eosinophil peroxidase gene. The novel transcription control elements described in the disclosure may comprise isolated polynucleotides, expression cassettes, vectors, recombinant cells, and transgenic animals.

Abstract: A method is provided for measuring in vivo in a transgenic non-human multicellular organism the activity of a cellular enzyme, which organism is transgenic by virtue of comprising one or more nucleic acid constructs encoding a binding domain and a binding partner thereof wherein: (i) the binding domain and/or binding partner comprise a site subject to post-translational modification by the cellular enzyme; (ii) modification of the site by the enzyme affects the interaction between the binding domain and the binding partner; and (iii) the binding domain and the binding partner each comprise a detectable label such that when the binding domain and binding partner interact, a detectable physical characteristic of one or both of the labels is altered, which method comprises measuring the interaction between the binding domain and the binding partner by measuring changes in the physical characteristic in one or more cells of the transgenic organism. A transgenic non-human multicellular organism is also provided.

Abstract: The invention provides genetically-modified non-human mammals and genetically-modified animal cells containing a functionally disrupted PDE11A gene. Also provided by the invention are methods of screening for agents that modulate PDE11A to modulate spermatogenesis, methods of treating mammals to modulate spermatogenesis, and methods of modulating cAMP and cGMP signal transduction in cells that express PDE11A.

Abstract: A mammal is provided, in which the LKB1 gene can be deleted phase-specifically and tissue-specifically. These mammals are highly useful as tools to reveal the onset mechanism for diseases caused by LKB1 gene deficiency, such as Peutz-Jeghers syndrome and cancers, as well as to develop therapeutic agents, methods, and so on for the diseases.